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  • 1. Andreyev, HJN
    et al.
    Norman, AR
    Cunningham, D
    Oates, J
    Dix, BR
    Sun, Xiao-Feng
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Oncology.
    Zhang, Hong
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Dermatology.
    Urosevic, N
    Kirsten ras mutations in patients with colorectal cancer: The 'RASCAL II' study2001In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 85, no 5, p. 692-696Article in journal (Refereed)
    Abstract [en]

    Researchers worldwide with information about the Kirsten ras (Ki-ras) tumour genotype and outcome of patients with colorectal cancer were invited to provide that data in a schematized format for inclusion in a collaborative database called RASCAL (The Kirsten ras incolorectal-cancer collaborative group). Our results from 2721 such patients have been presented previously and for the first time in any common cancer, showed conclusively that different gene mutations have different impacts on outcome, even when the mutations occur at the same site on the genome. To explore the effect of Ki-ras mutations at different stages of colorectal cancer, more patients were recruited to the database, which was reanalysed when information on 4268 patients from 42 centres in 21 countries had been entered. After predetermined exclusion criteria were applied, data on 3439 patients were entered into a multivariate analysis. This found that of the 12 possible mutations on codons 12 and 13 of Kirsten ras, only one mutation on codon 12, glycine to valine, found in 8.6% of all patients, had a statistically significant impact on failure-free survival (P=0.004, HR 1.3) and overall survival (P=0.008, HR 1.29). This mutation appeared to have a greater impact on outcome in Dukes' C cancers (failure-free survival, P=0.008, HR 1.5, overall survival P=0.02, HR 1.45) than in Dukes' B tumours (failure-free survival, P=0.46, HR 1.12, overall survival P=0.36, HR 1.15). Ki-ras mutations may occur early in the development of pre-cancerous adenomas in the colon and rectum. However, this collaborative study suggests that not only is the presence of a codon 12 glycine to valine mutation important for cancer progression but also that it may predispose to more aggressive biological behaviour in patients with advanced colorectal cancer. ⌐ 2001 Cancer Research Campaign.

  • 2.
    Bergman-Jungeström, Malin
    et al.
    Linköping University, Department of Biomedicine and Surgery, Oncology. Linköping University, Faculty of Health Sciences.
    Wingren, Sten
    Linköping University, Department of Biomedicine and Surgery, Oncology. Linköping University, Faculty of Health Sciences.
    Catechol-O-Methyltransferase (COMT) gene polymorphism and breast cancer risk in young women2001In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 85, no 6, p. 859-862Article in journal (Refereed)
    Abstract [en]

    Oestrogen exposure has long been considered to be a main risk factor of breast cancer. More recently, interest has also focused on the possible carcinogenic influence from oestrogen metabolites, such as catechol oestrogens. O-methylation, catalysed by Catechol-O-Methyltransferase (COMT), is one pathway by which the potentially carcinogenic catechol oestrogens can be inactivated. The gene coding for COMT protein contains a single-nucleotide polymorphism (SNP), resulting in an amino acid shift Val Met, which has been shown to determine high- and low-activity configuration of the enzyme. We hypothesized that the low-activity allele, COMTMet, may be implicated in early onset breast cancer. In the present case–control study, including 126 young breast cancer patients ( 36 years) and 117 healthy female blood donors, we analysed the association between COMTMet genotype and risk of breast cancer. No significant difference in the frequency of low-/high-activity alleles was found between cases and controls, indicating that the polymorphism, as a single factor, may not contribute to breast carcinogenesis in young women.

  • 3. Bernsen, MR
    et al.
    Håkansson, Leif
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Oncology. Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Oncology UHL.
    Gustafsson, Bertil
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Neuroscience and Locomotion, Pathology. Östergötlands Läns Landsting, Centre for Laboratory Medicine, Department of Clinical Pathology and Clinical Genetics.
    Krysander, Lennart
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Plastic Surgery, Hand Surgery and Burns. Östergötlands Läns Landsting, Reconstruction Centre, Department of Plastic Surgery, Hand surgery UHL.
    Rettrup, B
    Ruiter, D
    Håkansson, Annika
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Oncology. Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Oncology UHL.
    On the biological relevance of MHC class II and B7 expression by tumour cells in melanoma metastases2003In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 88, no 3, p. 424-431Article in journal (Refereed)
    Abstract [en]

    A large number of studies have indicated that specific immune reactivity plays a crucial role in the control of malignant melanoma. In this context, expression of MHC I, MHC II and B7 molecules by melanoma cells is seen as relevant for the immune response against the tumour. For a better understanding of the biological relevance of MHC II and B7 expression by tumour cells in metastatic melanoma, we studied the expression of these molecules in melanoma metastases in relation to the inflammatory response, regression of the tumour and survival from 27 patients treated with biochemotherapy (30 mg m-2 Cisplatin and 250 mg m-2 decarbazine (dimethyl-triazene-imidazole-carboxamide, DTIC) on days 1-3 i.v., and 107 IU IFN-a2b 3 days a week s.c., q. 28d). In 19 out of 27 lesions studied, we found expression of MHC II by the tumour cells, while only in one out of II tumour biopsies obtained from untreated metastatic melanoma patients, MHC II expression was detected. Expression of B7.1 and B7.2 by tumour cells was found in nine out of 24 and 19 out of 24 lesions, respectively. In all cases where B7.1 expression was found, expression of B7.2 by the tumour cells was also seen. In general, no or only few inflammatory cells positive for B7 were found. Expression of MHC II by tumour cells was positively correlated with the presence of tumour-infiltrating lymphocytes, regression of the lesion, and with time to progression (TTP) and overall survival (OS) of the patient. However, no significant correlation between B7.1 or B7.2 expression and regression of the tumour, TTP or OS was found. In light of other recent findings, these data altogether do support a role as biomarker for MHC II expression by tumour cells, however, its exact immunological pathomechanism(s) remain to be established. ⌐ 2003 Cancer Research UK.

  • 4.
    Beskow, C
    et al.
    Department of Gynaecologic Oncology, Radiumhemmet, Karolinska University Hospital, Stockholm, Sweden..
    Kanter, L
    Department of Pathology and Cytology, Karolinska University Hospital, Stockholm, Sweden.
    Holgersson, A
    Unit of Medical Radiation Biology, Department of Oncology and Pathology, Karolinska Institutet, Stockholm, Sweden.
    Nilsson, B
    Department of Oncology and Pathology, Karolinska University Hospital, Stockholm, Sweden..
    Frankendal, B
    Department of Gynaecologic Oncology, Radiumhemmet, Karolinska University Hospital, Stockholm, Sweden..
    Åvall-Lundqvist, Elisabeth
    Department of Gynaecologic Oncology, Radiumhemmet, Karolinska University Hospital, Stockholm, Sweden..
    Lewensohn, R
    Unit of Medical Radiation Biology, Department of Oncology and Pathology, Karolinska Institutet, Stockholm, Sweden.
    Expression of DNA damage response proteins and complete remission after radiotherapy of stage IB-IIA of cervical cancer.2006In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 94, no 11, p. 1683-1689Article in journal (Refereed)
    Abstract [en]

    The primary aim of this study was to investigate if the expression of the DNA damage identifying protein DNA-PKcs known to be involved in DNA repair after treatment with ionising radiation can be used as a predictive marker for radiotherapy (RT) response in cervical cancer. Formalin-fixed primary tumour biopsies from 109 patients with cervical cancer, FIGO-stage IB-IIA, treated with preoperative brachytherapy followed by radical surgery were analysed by immunohistochemistry. In addition, correlation studies between early pathological tumour response to radiation and expression of Ku86, Ku70, Mdm-2, p53 and p21 in primary tumours were also performed. We found that tumour-transformed tissue shows positive immunostaining of DNA-PKcs, Ku86 and Ku70, while non-neoplastic squamous epithelium and tumour-free cervix glands show negative immunoreactivity. Expression of DNA-PKcs positively correlated with both Ku86 and Ku70, and a statistically significant correlation between the Ku subunits was also found. After RT, 85 patients demonstrated pathologic complete remission (pCR), whereas 24 patients had residual tumour in the surgical specimen (non-pCR). The main finding of our study is that there was no correlation between the outcome of RT and the expression of DNA-PK subunits. Positive p53 tumours were significantly more common among non-pCR cases than in patients with pCR (P=0.031). Expression of p21 and Mdm-2 did not correlate with the outcome of RT.

  • 5. Birringer, M
    et al.
    EyTina, J H
    Salvatore, B A
    Neuzil, Jiri
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Neuroscience and Locomotion, Pathology.
    Vitamin E analogues as inducers of apoptosis: Structure-function relation2003In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 88, no 12, p. 1948-1955Article in journal (Refereed)
    Abstract [en]

    Recent results show that a-tocopheryl succinate (a-TOS) is a proapoptotic agent with antineoplastic activity. As modifications of the vitamin E (VE) molecule may affect its apoptogenic activity, we tested a number of newly synthesised VE analogues using malignant cell lines. Analogues of a-TOS with lower number of methyl substitutions on the aromatic ring were less active than a-TOS. Replacement of the succinyl group with a maleyl group greatly enhanced the activity, while it was lower for the glutaryl esters. Methylation of the free succinyl carboxyl group on a-TOS and d-TOS completely prevented the apoptogenic activity of the parent compounds. Both Trolox and its succinylated derivative were inactive. a-tocotrienol (a-T3 H) failed to induce apoptosis, while ?-T3 H was apoptogenic, and more so when succinylated. Shortening the aliphatic side chain of ?-T3 by one isoprenyl unit increased its activity. Neither phytyl nor oleyl succinate caused apoptosis. These findings show that modifications of different functional moieties of the VE molecule can enhance apoptogenic activity. It is hoped that these observations will lead to the synthesis of analogues with even higher apoptogenic and, consequently, antineoplastic efficacy.

  • 6. Bjellerup, P
    et al.
    Theodorsson, Elvar
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Clinical Chemistry. Östergötlands Läns Landsting, Centre for Laboratory Medicine, Department of Clinical Chemistry.
    Jörnvall, H
    Kogner, P
    Limited neuropeptide Y precursor processing in unfavourable metastatic neuroblastoma tumours2000In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 83, no 2, p. 171-176Article in journal (Refereed)
    Abstract [en]

    Neuropeptide Y (NPY) is found at high concentrations in neural crest-derived tumours and has been implicated as a regulatory peptide in tumour growth and differentiation. Neuroblastomas, ganglioneuromas and phaeochromocytomas with significant concentrations of NPY-like immunoreactivity were investigated for different molecular forms of NPY and for significance of proNPY processing. Gel-permeation chromatography identified intact NPY (1-36) in all tumours, whereas proNPY (69 amino acids) was detected only in control adrenal tissue and malignant neuroblastomas. Purification of NPY-like immunoreactivity in tumour extracts and structural characterization revealed that both NPY (1-36) and the truncated form NPY (3-36) was present. The degree of processing of proNPY to NPY in tumour tissue was lower in advanced neuroblastomas with regional or metastatic spread (stage 3 and 4) (n = 6), (41%, 12-100%, median, range), compared to the less aggressive stage 1, 2 and 4S tumours (n = 12), (93%, 69-100%), (P = 0.012). ProNPY processing of less than 50% was correlated with poor clinical outcome (P = 0.004). MYCN oncogene amplification was also correlated to a low degree of proNPY processing (P = 0.025). In summary, a low degree of proNPY processing was correlated to clinical advanced stage and poor outcome in neuroblastomas. ProNPY/NPY processing generated molecular forms of NPY with known differences in NPY-receptor selectivity, implicating a potential for in vivo modulation of NPY-like effects in tumour tissue. (C) 2000 Cancer Research Campaign.

  • 7.
    Dabrosin, Charlotta
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Oncology. Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Oncology UHL.
    Palmer, K
    Gauldie, J
    Oestradiol enhances tumour regression induced by B7-I/IL-2 adenoviral gene transfer in a murine model of breast cancer2003In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 89, no 2, p. 385-390Article in journal (Refereed)
    Abstract [en]

    The majority of breast cancers are oestrogen dependent and although current treatment strategies have improved, approximately 50% of the patients will develop metastasis. New treatments that result in long-term systemic immunity are therefore being developed. We have previously shown that adenoviral gene transfer of B7-I/IL-2 to murine breast cancer induces a high rate of complete turnout regression and systemic immunity. Since oestrogens not only affect breast cancer but also have been shown to modulate immune function and secretion of immune-regulatory cytokines, we explored whether administration of oestradiol altered the immune response induced by an adenoviral vector expressing B7-I/IL-2. An oestrogen-dependent murine breast cancer tumour was used in ovariectomised mice, supplemented either oestradiol or placebo. We report the somewhat unexpected finding that intratumoral injection of adenovirus expressing B7-I/IL-2 induces complete turnout regression in 76% of oestradiol-supplemented mice, while only 18% of the tumours regressed in the oestrogen-depleted group. Cured mice in both groups exhibited a similar CTL response against the tumour antigen. However, intratumoral IFN-? levels, 2 days after B7-I/IL-2 injection, were significantly higher in mice treated with oestradiol compared to placebo. This may be one mechanism explaining the higher response rate of tumours in oestradiol-replenished mice.

  • 8.
    Dalen, Helge
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Neuroscience and Locomotion, Pathology. Östergötlands Läns Landsting, Centre for Laboratory Medicine, Department of Clinical Pathology and Clinical Genetics.
    Neuzil, Jiri
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Neuroscience and Locomotion, Pathology.
    a-tocopheryl succinate sensitises a T lymphoma cell line to TRAIL-induced apoptosis by suppressing NF-?B activation2003In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 88, no 1, p. 153-158Article in journal (Refereed)
    Abstract [en]

    Activation of nuclear factor-?B (NF-?B) can interfere with induction of apoptosis triggered by the tumour necrosis factor-related apoptosis-inducing ligand (TRAIL, Apo2L). Therefore, agents that suppress NF-?B activation may sensitise cells to TRAIL-dependent apoptosis. Exposure of Jurkat cells to TRAIL resulted in massive and saturable apoptosis induction, following an initial lag time. This lag was abolished by pretreatment of the cells with subapoptotic doses of a-tocopheryl succinate (a-TOS) or the proteasome inhibitor MGI32. Exposure of the cells to TRAIL led to a rapid, transient activation of NF-?B, a process that was suppressed by cell pretreatment with a-TOS or MGI32. Activation of NF-?B by TNF-a prior to TRAIL exposure increased resistance of the cells to TRAIL-mediated apoptosis. We conclude that a-TOS sensitises cells to TRAIL killing, at least in some cases, through inhibition of NF-?B activation. This further supports the possibility that this semisynthetic analogue of vitamin E is a potential adjuvant in cancer treatment, such as in the case of TRAIL-mediated inhibition of cancer.

  • 9. Dawei, X
    et al.
    Gruber, A
    Björkholm, M
    Peterson, Curt
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Medicine and Care, Clinical Pharmacology.
    Pisa, P
    Suppression of telomerase reverse transcriptase (hTERT) expression in differentiated HL-60 cells: regulatory mechanisms.1999In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 80, p. 1156-1161Article in journal (Refereed)
  • 10.
    Fredrikson, M
    et al.
    Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden..
    Hursti, T J
    Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden..
    Steineck, G
    Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden..
    Fürst, C J
    Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden..
    Börjeson, Sussanne
    Linköping University, Department of Medical and Health Sciences, Nursing Science. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre for Surgery, Orthopaedics and Cancer Treatment, Department of Oncology UHL.
    Peterson, C
    Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden..
    Delayed chemotherapy-induced nausea is augmented by high levels of endogenous noradrenaline.1994In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 70, no 4, p. 642-645Article in journal (Refereed)
    Abstract [en]

    The relation between pretreatment night-time urinary catecholamine excretion and chemotherapy-induced nausea and vomiting was studied. The first cohort included 17 women and three men with various cancer forms receiving low or moderately emetogenic chemotherapy. The second cohort included 42 women receiving cisplatinum (50 mg m-2) for ovarian cancer and ondansetron as an antiemetic (8 mg i.v. x 3 at chemotherapy and 8 mg p.o. x 3 for 5 days). Relatively higher noradrenaline, but not adrenaline, excretion was associated with an increased intensity of delayed nausea following treatment. Vomiting was not consistently related to the excretion of either catecholamine. The results indicate that noradrenaline modulates delayed nausea resulting from chemotherapy.

  • 11.
    Gentile, Massimiliano
    et al.
    Linköping University, Department of Biomedicine and Surgery, Oncology. Linköping University, Faculty of Health Sciences.
    Olsen, K.
    Linköping University, Department of Neuroscience and Locomotion, Pathology. Linköping University, Department of Molecular and Clinical Medicine, Forensic Medicine. Linköping University, Faculty of Health Sciences.
    Dufmats, Monika
    Linköping University, Department of Biomedicine and Surgery, Oncology. Linköping University, Faculty of Health Sciences.
    Wingren, Sten
    Linköping University, Department of Biomedicine and Surgery, Oncology. Linköping University, Faculty of Health Sciences.
    Frequent allelic losses at 11q24.1–q25 in young women with breast cancer: association with poor survival1999In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 80, no 5/6, p. 843-849Article in journal (Refereed)
    Abstract [en]

    Previous studies have demonstrated that the pathological features of breast cancer are more aggressive in younger women than in their older counterparts, and that young age may be an independent marker for adverse prognosis. These findings have raised the question whether these differences are also present at the molecular level. In order to characterize the genetic alterations associated with early-onset breast cancer, 102 cases selected for age under 37 at diagnosis were examined for loss of heterozygosity (LOH) at nine different loci on chromosomes 11, 13 and 17. Ninety cases (88%), exhibited LOH for at least one marker. The D17S855 marker, intragenic in the BRCA1 gene, showed a high proportion of LOH (63%), whereas the intragenic marker for the TP53 gene, HP53, exhibited LOH in 43% of the cases. On chromosome 11, frequencies of LOH peaked at the D11S969 and D11S387 markers, which expressed LOH in 53% and 48% of the informative cases, whereas D11S1818, which is proximate to the ATM gene, exhibited an LOH frequency of 24%. A statistically significant correlation was found between LOH at the D11S387 marker and poor survival (P = 0.028). No such correlation was found for the adjacent D11S969 marker, located approximately 500 kb centromeric to D11S387. We conclude that one or more as yet unidentified genes, situated in chromosome bands 11q24.1–q25, could be involved in the initiation and/or progression of breast cancer in younger women.

  • 12.
    Gnosa, Sebastian
    et al.
    Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Linköping University, Faculty of Health Sciences.
    Zhang, H.
    University of Örebro, Sweden .
    Brodin Patcha, Veronika
    Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Linköping University, Faculty of Health Sciences.
    Carstensen, John
    Linköping University, Department of Medical and Health Sciences, Division of Health and Society. Linköping University, Faculty of Health Sciences.
    Adell, G.
    Karolinska University Hospital, Sweden .
    Sun, Xiao-Feng
    Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Oncology.
    AEG-1 expression is an independent prognostic factor in rectal cancer patients with preoperative radiotherapy: a study in a Swedish clinical trial2014In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 111, no 1, p. 166-173Article in journal (Refereed)
    Abstract [en]

    BACKGROUND:

    Preoperative radiotherapy (RT) is widely used to downstage rectal tumours, but the rate of recurrence varies significantly. Therefore, new biomarkers are needed for better treatment and prognosis. It has been shown that astrocyte elevated gene-1 (AEG-1) is a key mediator of migration, invasion, and treatment resistance. Our aim was to analyse the AEG-1 expression in relation to RT in rectal cancer patients and to test its radiosensitising properties.

    METHODS:

    The AEG-1 expression was examined by immunohistochemistry in 158 patients from the Swedish clinical trial of RT. Furthermore, we inhibited the AEG-1 expression by siRNA in five colon cancer cell lines and measured the survival after irradiation by colony-forming assay.

    RESULTS:

    The AEG-1 expression was increased in the primary tumours compared with the normal mucosa independently of the RT (P<0.01). High AEG-1 expression in the primary tumour of the patients treated with RT correlated independently with higher risk of distant recurrence (P=0.009) and worse disease-free survival (P=0.007). Downregulation of AEG-1 revealed a decreased survival after radiation in radioresistant colon cancer cell lines.

    CONCLUSIONS:

    The AEG-1 expression was independently related to distant recurrence and disease-free survival in rectal cancer patients with RT and could therefore be a marker to discriminate patients for distant relapse.

  • 13.
    Gunnarsson, Cecilia
    et al.
    Linköping University, Department of Biomedicine and Surgery, Oncology. Linköping University, Faculty of Health Sciences.
    Hellqvist, Eva
    Linköping University, Department of Biomedicine and Surgery, Oncology. Linköping University, Faculty of Health Sciences.
    Stål, Olle
    Linköping University, Department of Biomedicine and Surgery, Oncology. Linköping University, Faculty of Health Sciences.
    17β-hydroxysteroid dehydrogenases involved in local oestrogen synthesis have prognostic significance in breast cancer2005In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 92, no 3, p. 547-552Article in journal (Refereed)
    Abstract [en]

    The 17β-hydroxysteroid dehydrogenase (17HSD) enzymes are involved in the local regulation of sex steroids. The 17HSD type 1 enzyme catalyses the interconversion of the weak oestrone (E1) to the more potent oestradiol (E2), whereas 17HSD type 2 catalyses the oxidation of E2 to E1. The aim of this study was to correlate the expression of these enzymes in the tumour with the recurrence-free survival of tamoxifen-treated breast cancer patients. We used real-time reverse transcriptase PCR to investigate the mRNA expression of 17HSD types 1 and 2 in tumour samples from 230 postmenopausal patients. For the patients with oestrogen receptor (ER)-positive breast cancer, we found a statistically significant positive correlation between recurrence-free survival and expression of 17HSD type 2 (P = 0.026). We examined the ratio of 17HSD types 2 and 1, and ER-positive patients with low ratios showed a significantly higher rate of recurrence than those with higher ratios (P = 0.0047), ER positive patients with high expression levels of 17HSD type 1 had a significantly higher risk for late relapse (P = 0.0051). The expression of 17HSD types 1 and 2 in breast cancer differs from the expression of these enzymes in normal mammary gland, and this study indicates that the expression has prognostic significance in breast cancer.

  • 14.
    Gustafsson, Britt
    et al.
    Huddinge Hospital, Karolinska Institute.
    Carstensen, John
    Linköping University, Department of Medical and Health Sciences, Health and Society. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre for Surgery, Orthopaedics and Cancer Treatment, Oncology Centre.
    Evidence of space-time clustering of childhood acute lymphoblastic leukaemia in Sweden1999In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 79, no 3/4, p. 655-657Article in journal (Refereed)
    Abstract [en]

    We have examined 645 recorded cases of childhood acute lymphatic leukaemia (ALL) in Sweden during 1973–89 to identify space–time clustering by using the close-pair method of Knox. The records included date of birth and of diagnosis as well as addresses at birth and at diagnosis. There was a significant excess of case pairs close in date of birth and place of birth in the 5- to 15-year age group.

  • 15.
    Hilborn, Erik
    et al.
    Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Linköping University, Faculty of Medicine and Health Sciences.
    Gacic, Jelena
    Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Linköping University, Faculty of Medicine and Health Sciences.
    Fornander, Tommy
    Karolinska Institute, Sweden.
    Nordenskjöld, Bo
    Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Oncology.
    Stål, Olle
    Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Linköping University, Faculty of Medicine and Health Sciences. Östergötlands Läns Landsting, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Oncology.
    Jansson, Agneta
    Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Linköping University, Faculty of Medicine and Health Sciences.
    Androgen receptor expression predicts beneficial tamoxifen response in oestrogen receptor-alpha-negative breast cancer2016In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 114, no 3, p. 248-255Article in journal (Refereed)
    Abstract [en]

    Background: Although the androgen receptor (AR) is frequently expressed in breast cancer, its relevance in the disease is not fully understood. In addition, the relevance of AR in determining tamoxifen treatment efficiency requires evaluation. Purpose: To investigate the tamoxifen predictive relevance of the AR protein expression in breast cancer. Methods Patients were randomised to tamoxifen 40 mg daily for 2 or 5 years or to no endocrine treatment. Mean follow-up was 15 years. Hazard ratios were calculated with recurrence-free survival as end point. Results: In patients with oestrogen receptor (ER)-negative tumours, expression of AR predicted decreased recurrence rate with tamoxifen (hazard ratio (HR) = 0.34; 95% confidence interval (CI) = 0.14-0.81; P = 0.015), whereas the opposite was seen in the AR- group (HR = 2.92; 95% CI = 1.16-7.31; P = 0.022). Interaction test was significant P &lt; 0.001. Patients with triple-negative and AR+ tumours benefitted from tamoxifen treatment (HR = 0.12; 95% CI = 0.014-0.95 P = 0.044), whereas patients with AR- tumours had worse outcome when treated with tamoxifen (HR = 3.98; 95% CI = 1.32-12.03; P = 0.014). Interaction test was significant P = 0.003. Patients with ER+ tumours showed benefit from tamoxifen treatment regardless of AR expression. Conclusions: AR can predict tamoxifen treatment benefit in patients with ER- tumours and triple-negative breast cancer.

  • 16.
    Holmberg, L
    et al.
    Kings Coll London, England .
    Wong, Y N S
    Kings Coll London, England .
    Tabar, L
    Uppsala University, Sweden .
    Ringberg, A
    University Hospital MAS, Sweden .
    Karlsson, P
    Sahlgrens University Hospital, Sweden .
    Arnesson, Lars-Gunnar
    Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Surgery in Linköping.
    Sandelin, K
    Karolinska University Hospital, Sweden .
    Anderson, H
    Lund University, Sweden .
    Garmo, H
    Kings Coll London, England .
    Emdin, S
    Umeå University Hospital, Sweden .
    Mammography casting-type calcification and risk of local recurrence in DCIS: analyses from a randomised study2013In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 108, no 4, p. 812-819Article in journal (Refereed)
    Abstract [en]

    Background: We studied the association between mammographic calcifications and local recurrence in the ipsilateral breast. less thanbrgreater than less thanbrgreater thanMethods: Case-cohort study within a randomised trial of radiotherapy in breast conservation for ductal cancer in situ of the breast (SweDCIS). We studied mammograms from cases with an ipsilateral breast event (IBE) and from a subcohort randomly sampled at baseline. Lesions were classified as a density without calcifications, architectural distortion, powdery, crushed stone-like or casting-type calcifications. less thanbrgreater than less thanbrgreater thanResults: Calcifications representing necrosis were found predominantly in younger women. Women with crushed stone or casting-type microcalcifications had higher histopathological grade and more extensive disease. The relative risk (RR) of a new IBE comparing those with casting-type calcifications to those without calcifications was 2.10 (95% confidence interval (Cl) 0.92-4.80). This risk was confined to in situ recurrences; the RR of an IBE associated with casting-type calcifications on the mammogram adjusted for age and disease extent was 16.4 (95% Cl 2.20-140). less thanbrgreater than less thanbrgreater thanConclusion: Mammographic appearance of ductal carcinoma in situ of the breast is prognostic for the risk of an in situ IBE and may also be an indicator of responsiveness to RT in younger women.

  • 17.
    Hursti, T J
    et al.
    Department of Clinical Neuroscience, Karolinska Institute, S-171 76 Stockholm, Sweden / Department of Clinical Psychology, Uppsala University, Box 1225, S-751 42 Uppsala, Sweden;.
    Åvall-Lundqvist, Elisabeth
    Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Linköping University, Faculty of Health Sciences. Department of Gynaecological Oncology, Radiumhemmet, S-171 76 Stockholm, Sweden.
    Börjeson, S
    Fredrikson, M
    Department of Clinical Psychology, Uppsala University, Box 1225, S-751 42 Uppsala, Sweden;.
    Fürst, C J
    Steineck, G
    Peterson, Curt
    Linköping University, Department of Medical and Health Sciences, Division of Drug Research. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Oncology.
    Impact of tumour burden on chemotherapy-induced nausea and vomiting.1996In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 74, no 7, p. 1114-1119Article in journal (Refereed)
    Abstract [en]

    We investigated how residual tumour burden after cytoreductive surgery was related to the occurrence of acute and delayed nausea and vomiting in 101 ovarian cancer patients receiving their first chemotherapy course. The anti-emetic treatment included ondansetron combined with dexamethasone or placebo. After chemotherapy all patients received ondansetron only for 5 days. Two categories of tumour burden (TB) were formed according to the diameter of the greatest residual tumour (< 2 cm = minimal TB and > or = 2 cm = large TB). Self-reports of nausea and vomiting were obtained for 15 days. Other potential predictor variables were assessed and included in multivariate analyses. Patients with large compared with minimal TB had more delayed emesis, especially on days 2-7. They also had more acute nausea. The aggravating effect associated with large residual TB was more evident in patients > or = 55 years. During the second week after the chemotherapy the occurrence of nausea was higher in patients > or = 55 years than in those < 55 years. This was seen primarily in patients with large residual TB. Predictors for no delayed emesis at all were anti-emetic treatment with dexamethasone, minimal tumour burden, low neuroticism and no history of motion sickness. The increased risk of "persistent' delayed nausea and vomiting seen in older patients with large tumour burden may have important clinical implications and warrants further attention.

  • 18.
    Håkansson, Annika
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Oncology. Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Oncology UHL.
    Gustafsson, Bertil
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Neuroscience and Locomotion, Pathology. Östergötlands Läns Landsting, Centre for Laboratory Medicine, Department of Clinical Pathology and Clinical Genetics.
    Krysander, Lennart
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Plastic Surgery, Hand Surgery and Burns. Östergötlands Läns Landsting, Reconstruction Centre, Department of Plastic Surgery, Hand surgery UHL.
    Hjelmqvist, B
    Rettrup, B
    Håkansson, L
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Oncology. Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Oncology UHL.
    Biochemotherapy of metastatic malignant melanoma. Predictive value of tumour-infiltrating lymphocytes2001In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 85, no 12, p. 1871-1877Article in journal (Refereed)
    Abstract [en]

    The therapeutic efficacy of biochemotherapy in metastatic malignant melanoma still carries a low remission rate, but with some durable responses. It would therefore be of considerable importance if patients with a high probability of responding could be identified using predictive tests. The response to interferon-alpha (IFN-a) correlates with the occurrence of CD4+ lymphocytes identified by fine-needle aspirates from melanoma metastases (Hσkansson et al, 1996). The present investigation studies a possible correlation between tumour-infiltrating CD4+ lymphocytes in malignant melanoma metastases and the therapeutic effect of biochemotherapy. A total of 25 patients with systemic and 16 with regional metastatic melanoma were analysed before initiation of biochemotherapy (cis-platinum 30 mg/m2 d.1-3, DTIC 250 mg/m2 d.1-3 i.v. and IFN-a2b 10 million IU s.c. 3 days a week, q. 28d.). A monoclonal antibody, anti-CD4, was used to identify tumour-infiltrating lymphocytes in fine-needle aspirates before start of treatment. The presence of these lymphocytes was correlated to response, time to progression and overall survival. A statistically significant correlation (P = 0.01) was found between the occurrence of CD4+ lymphocytes and tumour regression during biochemotherapy in patients with systemic disease. Out of 14 patients with moderate to high numbers of infiltrating CD4+ lymphocytes, 12 achieved tumour regression. In contrast, among patients with low numbers of these cells in metastatic lesions, 8 out of 11 had progressive disease. We also found a significantly longer time to progression (P < 0.003) and overall survival (P < 0.01) among patients with moderate to high numbers of these cells compared to patients with low numbers of these cells before initiation of biochemotherapy. Furthermore, in patients with regional disease, we found a significantly longer time to progression (P = 0.01) and a trend toward a longer overall survival time (P = 0.09). Based on these results and as previously shown with IFN-a therapy alone, there seems to be a need for CD4+ lymphocytes infiltrating the tumours before the start of biochemotherapy to make the treatment successful. Determination of these cells in fine-needle aspirates seems to be a method to predict responders to biochemotherapy, thus increasing the cost-benefit of this treatment strategy considerably, both in terms of patient adverse reactions and health care costs. ⌐ 2001 Cancer Research Campaign.

  • 19.
    Håkansson, L.
    et al.
    Linköping University, Department of Biomedicine and Surgery, Oncology. Linköping University, Faculty of Health Sciences.
    Adell, Gunnar
    Linköping University, Department of Biomedicine and Surgery, Oncology. Linköping University, Faculty of Health Sciences.
    Boeryd, B.
    Linköping University, Department of Neuroscience and Locomotion, Pathology. Linköping University, Faculty of Health Sciences.
    Sjögren, F.
    Linköping University, Department of Molecular and Clinical Medicine, Clinical Immunology. Linköping University, Faculty of Health Sciences.
    Sjödahl, R.
    Linköping University, Department of Clinical and Experimental Medicine, Surgery. Linköping University, Faculty of Health Sciences.
    Infiltration of mononuclear inflammatory cells into primary colorectal carcinomas: an immunohistological analysis1997In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 75, no 3, p. 374-380Article in journal (Refereed)
    Abstract [en]

    Local immunoregulation mediated by mononuclear tumour-infiltrating cells is considered of importance for tumour progression of colorectal cancer, although the balance between immunosuppressor and cytotoxic activities is unclear. Colorectal cancers from 26 patients were investigated using a panel of monoclonal antibodies in order to identify subsets of mononuclear inflammatory cells and to study their pattern of distribution in relation to tumour stage and cytotoxic immune reactivity against the tumour. In all but five tumours, mononuclear cells, lymphocytes or monocytes were present in fairly large numbers, particularly in the stroma. The infiltration of CD4+ mononuclear cells predominated over the CD8+ subset. Infiltration near the tumour cells was found in four cancers only. Stromal infiltration of CD11c+ macrophages was found in all but eight tumours. Small regressive areas, in which the histological architecture of the tumours was broken down, were found in 17 tumours with intense or moderate infiltration by CD4+ lymphocytes or CD11c+ macrophages. Probably this destruction of tumour tissue was caused by cytotoxic activity of the tumour-infiltrating mononuclear cells. In Dukes' class A and B tumours, CD4+ lymphocytes predominated over CD4+ cells with macrophage morphology, but the latter were increasingly found in Dukes' class C and D disease. The occurrence of MHC II-positive macrophages and lymphocytes in different Dukes' classes was similar to that of CD4+ cells. In contrast to this, CD11c+ and CD11a+ cells were more frequent in Dukes' A and B class tumours compared with Dukes' C and D. Four out of nine tumours of the latter stages showed a poor inflammatory reaction. The interpretation of our results is that the subsets of tumour-infiltrating mononuclear cells change with advancing Dukes' class and that the local immune control is gradually broken down in progressive tumour growth, even if some cytotoxic activity is still present.

  • 20.
    Ihnatko, Robert
    et al.
    Linköping University, Department of Clinical and Experimental Medicine, Division of Cell Biology. Linköping University, Faculty of Health Sciences.
    Post, Claes
    Linköping University, Department of Clinical and Experimental Medicine, Division of Cell Biology. Linköping University, Faculty of Health Sciences.
    Blomqvist, Anders
    Linköping University, Department of Clinical and Experimental Medicine, Division of Cell Biology. Linköping University, Faculty of Health Sciences.
    Proteomic profiling of the hypothalamus in a mouse model of cancer-induced anorexia-cachexia2013In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 109, no 7, p. 1867-1875Article in journal (Refereed)
    Abstract [en]

    Background:

    Anorexia-cachexia is a common and severe cancer-related complication but the underlying mechanisms are largely unknown. Here, using a mouse model for tumour-induced anorexia-cachexia, we screened for proteins that are differentially expressed in the hypothalamus, the brain’s metabolic control centre.

    Methods:

    The hypothalamus of tumour-bearing mice with implanted methylcholanthrene-induced sarcoma (MCG 101) displaying anorexia and their sham-implanted pair-fed or free-fed littermates was examined using two-dimensional electrophoresis (2-DE)-based comparative proteomics. Differentially expressed proteins were identified by liquid chromatography-tandem mass spectrometry.

    Results:

    The 2-DE data showed an increased expression of dynamin 1, hexokinase, pyruvate carboxylase, oxoglutarate dehydrogenase, and N-ethylmaleimide-sensitive factor in tumour-bearing mice, whereas heat-shock 70 kDa cognate protein, selenium-binding protein 1, and guanine nucleotide-binding protein Gα0 were downregulated. The expression of several of the identified proteins was similarly altered also in the caloric-restricted pair-fed mice, suggesting an involvement of these proteins in brain metabolic adaptation to restricted nutrient availability. However, the expression of dynamin 1, which is required for receptor internalisation, and of hexokinase, and pyruvate carboxylase were specifically changed in tumour-bearing mice with anorexia.

    Conclusion:

    The identified differentially expressed proteins may be new candidate molecules involved in the pathophysiology of tumour-induced anorexia-cachexia.

  • 21.
    Jakubowska, A
    et al.
    Pomeranian Medical University, Poland .
    Rozkrut, D
    University of Szczecin, Poland .
    Antoniou, A
    University of Cambridge, England .
    Hamann, U
    Deutsch Krebsforschungszentrum DKFZ, Germany .
    Scott, R J
    University of Newcastle, Australia Hunter Medical Research Institute, Australia .
    McGuffog, L
    University of Cambridge, England .
    Healy, S
    Queensland Institute Medical Research, Australia .
    Sinilnikova, O M
    Centre Hospital University of Lyon, France University of Lyon 1, France .
    Rennert, G
    Technion Israel Institute Technology, Israel Technion Israel Institute Technology, Israel Technion Israel Institute Technology, Israel .
    Lejbkowicz, F
    Technion Israel Institute Technology, Israel Technion Israel Institute Technology, Israel Technion Israel Institute Technology, Israel .
    Flugelman, A
    Technion Israel Institute Technology, Israel Technion Israel Institute Technology, Israel Technion Israel Institute Technology, Israel .
    Andrulis, I L
    Cancer Care Ontario, Canada Mt Sinai Hospital, Canada .
    Glendon, G
    Cancer Care Ontario, Canada Mt Sinai Hospital, Canada .
    Ozcelik, H
    Mt Sinai Hospital, Canada .
    Thomassen, M
    Odense University Hospital, Denmark .
    Paligo, M
    University Hospital Pisa, Italy .
    Aretini, P
    University Hospital Pisa, Italy .
    Kantala, J
    Karolinska University Hospital, Sweden .
    Aroer, B
    Karolinska University Hospital, Sweden .
    Von Wachenfeldt, A
    Karolinska University Hospital, Sweden .
    Liljegren, A
    Karolinska University Hospital, Sweden .
    Loman, N
    University of Lund Hospital, Sweden .
    Herbst, K
    University of Lund Hospital, Sweden .
    Kristoffersson, U
    University of Lund Hospital, Sweden .
    Rosenquist, R
    Uppsala University, Sweden .
    Karlsson, P
    Sahlgrens University Hospital, Sweden .
    Stenmark-Askmalm, Marie
    Linköping University, Department of Clinical and Experimental Medicine, Oncology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre for Diagnostics, Department of Clinical Pathology and Clinical Genetics.
    Melin, B
    Umeå University, Sweden .
    Nathanson, K L
    University of Penn, PA 19104 USA University of Penn, PA 19104 USA .
    Domchek, S M
    University of Penn, PA 19104 USA University of Penn, PA 19104 USA .
    Byrski, T
    Pomeranian Medical University, Poland .
    Huzarski, T
    Pomeranian Medical University, Poland .
    Gronwald, J
    Pomeranian Medical University, Poland .
    Menkiszak, J
    Pomeranian Medical University, Poland .
    Cybulski, C
    Pomeranian Medical University, Poland .
    Serrano, P
    Pomeranian Medical University, Poland .
    Osorio, A
    Spanish National Cancer Research Centre, Spain Spanish National Cancer Research Centre, Spain .
    Cajal, T R
    Hospital Santa Creu and Sant Pau, Spain .
    Tsitlaidou, M
    National Centre Science Research Demokritos, Greece .
    Benitez, J
    Spanish National Cancer Research Centre, Spain Spanish National Cancer Research Centre, Spain .
    Gilbert, M
    Deutsch Krebsforschungszentrum DKFZ, Germany .
    Rookus, M
    Netherlands Cancer Institute, Netherlands .
    Aalfs, C M
    University of Amsterdam, Netherlands .
    Kluijt, I
    Netherlands Cancer Institute, Netherlands .
    Boessenkool-Pape, J L
    Netherlands Cancer Institute, Netherlands .
    Meijers-Heijboer, H E J
    Vrije University of Amsterdam Medical Centre, Netherlands .
    C Oosterwijk, J
    University of Groningen, Netherlands .
    J van Asperen, C
    Leiden University of Medical Centre, Netherlands .
    J Blok, M
    University Hospital Maastricht, Netherlands .
    R Nelen, M
    Radboud University of Nijmegen Medical Centre, Netherlands .
    M W van den Ouweland, A
    Erasmus MC, Netherlands .
    Seynaeve, C
    Erasmus MC, Netherlands .
    B van der Luijt, R
    University of Medical Centre Utrecht, Netherlands .
    Devilee, P
    Leiden University of Medical Centre, Netherlands Leiden University of Medical Centre, Netherlands .
    F Easton, D
    University of Cambridge, England .
    Peock, S
    University of Cambridge, England .
    Frost, D
    University of Cambridge, England .
    Platte, R
    University of Cambridge, England .
    D Ellis, S
    University of Cambridge, England .
    Fineberg, E
    University of Cambridge, England .
    G Evans, D
    NHS Fdn Trust, England .
    Lalloo, F
    NHS Fdn Trust, England .
    Eeles, R
    Royal Marsden NHS Fdn Trust, England .
    Jacobs, C
    Guys and St Thomas NHS Fdn Trust, England .
    Adlard, J
    Yorkshire Regional Genet Serv, England .
    Davidson, R
    Yorkhill Hospital, Scotland .
    Eccles, D
    University of Southampton, England .
    Cole, T
    Birmingham Womens Hospital Healthcare NHS Trust, England .
    Cook, J
    Sheffield Childrens Hospital, England .
    Godwin, A
    University of Kansas Medical Centre, KS USA .
    Bove, B
    Fox Chase Cancer Centre, PA 19111 USA .
    Stoppa-Lyonnet, D
    Institute Curie, France Institute Curie, France University of Paris 05, France .
    Caux-Moncoutier, V
    Institute Curie, France .
    Belotti, M
    Institute Curie, France .
    Tirapo, C
    Institute Curie, France .
    Mazoyer, S
    University of Lyon 1, France .
    Barjhoux, L
    University of Lyon 1, France .
    Boutry-Kryza, N
    Centre Hospital University of Lyon, France .
    Pujol, P
    CHU Arnaud de Villeneuve, France CRCM dAurelle, France .
    Coupier, I
    CHU Arnaud de Villeneuve, France CRLCC Val dAurelle, France .
    Peyrat, J-P
    Centre Oscar Lambret, France .
    Vennin, P
    Centre Oscar Lambret, France .
    Muller, D
    CLCC Paul Strauss, France .
    Fricker, J-P
    CLCC Paul Strauss, France .
    Venat-Bouvet, L
    Centre Hospital University of Dupuytren, France .
    Johannsson, OTh
    Landspitali University Hospital, Iceland University of Iceland, Iceland .
    Isaacs, C
    Georgetown University, DC USA .
    Schmutzler, R
    University Hospital Cologne, Germany University Hospital Cologne, Germany .
    Wappenschmidt, B
    University Hospital Cologne, Germany University Hospital Cologne, Germany .
    Meindl, A
    University of Munich, Germany .
    Arnold, N
    University of Kiel, Germany .
    Varon-Mateeva, R
    Institute Human Genet, Germany .
    Niederacher, D
    University of Dusseldorf, Germany .
    Sutter, C
    University of Heidelberg Hospital, Germany .
    Deissler, H
    University Hospital Ulm, Germany .
    Preisler-Adams, S
    University of Munster, Germany .
    Simard, J
    University of Laval, Canada Centre Hospital University of Quebec, Canada .
    Soucy, P
    University of Laval, Canada Centre Hospital University of Quebec, Canada .
    Durocher, F
    University of Laval, Canada Centre Hospital University of Quebec, Canada .
    Chenevix-Trench, G
    Queensland Institute Medical Research, Australia .
    Beesley, J
    Queensland Institute Medical Research, Australia .
    Chen, X
    Queensland Institute Medical Research, Australia .
    Rebbeck, T
    University of Penn, PA 19104 USA University of Penn, PA 19104 USA .
    Couch, F
    Mayo Clin, MN USA Mayo Clin, MN USA .
    Wang, X
    Mayo Clin, MN USA .
    Lindor, N
    Mayo Clin, MN USA .
    Fredericksen, Z
    Mayo Clin, MN USA .
    S Pankratz, V
    Mayo Clin, MN USA .
    Peterlongo, P
    Fdn IRCCS Ist Nazl Tumori INT, Italy Fdn Ist FIRC Oncology Mol, Italy .
    Bonanni, B
    Ist Europeo Oncol, Italy .
    Fortuzzi, S
    Fdn Ist FIRC Oncology Mol, Italy 84 Cogentech Cancer Genet Test Lab, Italy .
    Peissel, B
    Fdn IRCCS Ist Nazl Tumori INT, Italy .
    Szabo, C
    Mayo Clin, MN USA .
    L Mai, P
    Department Health and Human Serv, MD 20852 USA .
    T Loud, J
    Department Health and Human Serv, MD 20852 USA .
    Lubinski, J
    Pomeranian Medical University, Poland .
    Association of PHB 1630 C andgt; T and MTHFR 677 C andgt; T polymorphisms with breast and ovarian cancer risk in BRCA1/2 mutation carriers: results from a multicenter study2012In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 106, no 12, p. 2016-2024Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: The variable penetrance of breast cancer in BRCA1/2 mutation carriers suggests that other genetic or environmental factors modify breast cancer risk. Two genes of special interest are prohibitin (PHB) and methylene-tetrahydrofolate reductase (MTHFR), both of which are important either directly or indirectly in maintaining genomic integrity. less thanbrgreater than less thanbrgreater thanMETHODS: To evaluate the potential role of genetic variants within PHB and MTHFR in breast and ovarian cancer risk, 4102 BRCA1 and 2093 BRCA2 mutation carriers, and 6211 BRCA1 and 2902 BRCA2 carriers from the Consortium of Investigators of Modifiers of BRCA1 and BRCA2 (CIMBA) were genotyped for the PHB 1630 Candgt;T (rs6917) polymorphism and the MTHFR 677 Candgt;T (rs1801133) polymorphism, respectively. less thanbrgreater than less thanbrgreater thanRESULTS: There was no evidence of association between the PHB 1630 Candgt;T and MTHFR 677 Candgt;T polymorphisms with either disease for BRCA1 or BRCA2 mutation carriers when breast and ovarian cancer associations were evaluated separately. Analysis that evaluated associations for breast and ovarian cancer simultaneously showed some evidence that BRCA1 mutation carriers who had the rare homozygote genotype (TT) of the PHB 1630 Candgt;T polymorphism were at increased risk of both breast and ovarian cancer (HR 1.50, 95% CI 1.10-2.04 and HR 2.16, 95% CI 1.24-3.76, respectively). However, there was no evidence of association under a multiplicative model for the effect of each minor allele. less thanbrgreater than less thanbrgreater thanCONCLUSION: The PHB 1630TT genotype may modify breast and ovarian cancer risks in BRCA1 mutation carriers. This association need to be evaluated in larger series of BRCA1 mutation carriers.

  • 22.
    Jerevall, Piiha-Lotta
    et al.
    Linköping University, Department of Clinical and Experimental Medicine, Oncology. Linköping University, Faculty of Health Sciences.
    Ma, Xiai-Jun
    bioTheranostics, San Diego, CA, USA.
    Li, Hongying
    bioTheranostics, San Diego, CA, USA.
    Salunga, Ranelle
    Massachusetts General Hospital, USA.
    Kesty, Nicole C.
    bioTheranostics, 9640 Towne Centre Dr Suite 200, San Diego, CA 92121, USA.
    Erlander, Mark G.
    Karolinska Institute, Stockholm, Sweden.
    Sgroi, Dennis
    Harvard Medical School, Boston, MA, USA.
    Holmlund, Birgitta
    Karolinska Institute, Stockholm, Sweden.
    Skoog, Lambert
    Karolinska Institute, Stockholm, Sweden.
    Fornander, Tommy
    Karolinska Institute, Stockholm, Sweden.
    Nordenskjöld, Bo
    Linköping University, Department of Clinical and Experimental Medicine, Oncology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre for Surgery, Orthopaedics and Cancer Treatment, Department of Oncology UHL.
    Stål, Olle
    Linköping University, Department of Clinical and Experimental Medicine, Oncology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Oncology UHL.
    Prognostic utility of HOXB13:IL17BR and Molecular Grade Index in early-stage breast cancer patients from the Stockholm trial2011In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 104, no 11, p. 1762-1769Article in journal (Refereed)
    Abstract [en]

    Background: A dichotomous index combining two gene expression assays, HOXB13:IL17BR (H:I) and molecular grade index (MGI), was developed to assess risk of recurrence in breast cancer patients. The study objective was to demonstrate the prognostic utility of the combined index in early-stage breast cancer.

    Methods: In a blinded retrospective analysis of 588 ER-positive tamoxifen-treated and untreated breast cancer patients from the randomized prospective Stockholm trial, H:I and MGI were measured using real-time RT-PCR. Association with patient outcome was evaluated by Kaplan-Meier analysis and Cox proportional hazard regression. A continuous risk index was developed using Cox modeling.

    Results: The dichotomous H:I+MGI was significantly associated with distant recurrence and breast cancer death. The >50% of tamoxifen-treated patients categorized as low-risk had <3% 10-year distant recurrence risk. A continuous risk model (Breast Cancer Index (BCI)) was developed with the tamoxifen-treated group and the prognostic performance tested in the untreated group was 53% of patients categorized as low-risk with an 8.3% 10-year distant recurrence risk.

    Conclusion: Retrospective analysis of this randomized, prospective trial cohort validated the prognostic utility of H:I+MGI and was used to develop and test a continuous risk model that enables prediction of distant recurrence risk at the patient level.

  • 23.
    Lee, C.K.
    et al.
    University of Sydney.
    Simes, R.J.
    University of Sydney.
    Brown, C.
    University of Sydney.
    Lord, S.
    University of Sydney.
    Wagner, U.
    University Hospital Giessen and Marburg.
    Plante, M.
    CHUQ Hotel Dieu Quebec.
    Vergote, I.
    University Hospital Leuven.
    Pisano, C.
    National Cancer Institute, Naples.
    Parma, G.
    European Institute for Oncology.
    Burges, A.
    Klinikum University of Munic.
    Bourgeois, H.
    Centre Jean Bernard SARL SORECOH.
    Hogberg, T.
    Östergötlands Läns Landsting, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Oncology.
    Bentley, J.
    Dalhousie University, Halifax, NS B3H 1V7, Canada.
    Angleitner-Boubenizek, L.
    BHS Linz, A-4020 Linz, Austria.
    Ferrero, A.
    Mauriziano Hospital, Academic Div Gynecol Oncol, Turin, Italy.
    Richter, B.
    University of Dresden, Department Gynecol and Obstet, Dresden, Germany.
    Hirte, H.
    Juravinski Cancer Centre Hamilton Health Science, Hamilton, ON, Canada.
    Gebski, V.
    University of Sydney, NHMRC Clin Trials Centre, Camperdown, NSW 1450, Australia.
    Pfisterer, J.
    Staedt Klinikum Solingen, Department Gynecol, D-42653 Solingen, Germany.
    Pujade-Lauraine, E.
    University of Paris 05, Hop University of Paris Centre, AP HP, F-75004 Paris, France.
    Friedlander, M.
    Prince Wales Hospital, Institute Oncol, Sydney, NSW 2031, Australia.
    Prognostic nomogram to predict progression-free survival in patients with platinum-sensitive recurrent ovarian cancer2011In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 105, no 8, p. 1144-1150Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Patients with platinum-sensitive recurrent ovarian cancer are a heterogeneous group, and it is not possible to accurately predict the progression-free survival (PFS) in these patients. We developed and validated a nomogram to help improve prediction of PFS in patients treated with platinum-based chemotherapy. METHODS: The nomogram was developed in a training cohort (n = 955) from the CALYPSO trial and validated in the AGO-OVAR 2.5 Study (n = 340). The proportional-hazards model (nomogram) was based on pre-treatment characteristics. RESULTS: The nomogram had a concordance index (C-index) of 0.645. Significant predictors were tumour size platinum-chemotherapy-free interval, CA-125, number of organ metastatic sites and white blood count. When the nomogram was applied without CA-125 (CA-125 was not available in validation cohort), the C-indices were 0.624 (training) and 0.594 (validation). When classification was based only on the platinum-chemotherapy-free interval, the indices were 0.571 (training) and 0.560 (validation). The calibration plot in the validation cohort based on four predictors (without CA-125) suggested good agreement between actual and nomogram-predicted 12-month PFS probabilities. CONCLUSION: This nomogram, using five pre-treatment characteristics, improves prediction of PFS in patients with platinum-sensitive ovarian cancer having platinum-based chemotherapy. It will be useful for the design and stratification of patients in clinical trials and also for counselling patients. 

  • 24.
    Lind, H
    et al.
    Clinical Cancer Epidemiology, Department of Oncology and Pathology, Karolinska Institutet, Stockholm, Sweden.
    Waldenström, A-C
    Division of Clinical Cancer Epidemiology, Department of Oncology, Institute of Clinical Sciences, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden. Department of Oncology, Sahlgrenska University Hospital, Gothenburg, Sweden.
    Dunberger, G
    Clinical Cancer Epidemiology, Department of Oncology and Pathology, Karolinska Institutet, Stockholm, Sweden.
    al-Abany, M
    Clinical Cancer Epidemiology, Department of Oncology and Pathology, Karolinska Institutet, Stockholm, Sweden. Department of Medical Physics, Karolinska University Hospital, Stockholm, Sweden.
    Alevronta, E
    Clinical Cancer Epidemiology, Department of Oncology and Pathology, Karolinska Institutet, Stockholm, Sweden.
    Johansson, K-A
    Department of Radiation Physics, Institute of Clinical Sciences, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.
    Olsson, C
    Division of Clinical Cancer Epidemiology, Department of Oncology, Institute of Clinical Sciences, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden. Department of Radiation Physics, Institute of Clinical Sciences, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.
    Nyberg, T
    Clinical Cancer Epidemiology, Department of Oncology and Pathology, Karolinska Institutet, Stockholm, Sweden.
    Wilderäng, U
    Division of Clinical Cancer Epidemiology, Department of Oncology, Institute of Clinical Sciences, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.
    Steineck, G
    Clinical Cancer Epidemiology, Department of Oncology and Pathology, Karolinska Institutet, Stockholm, Sweden. Division of Clinical Cancer Epidemiology, Department of Oncology, Institute of Clinical Sciences, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.
    Åvall-Lundqvist, Elisabeth
    Department of Oncology and Pathology, Karolinska Institutet, Stockholm, Sweden. Department of Gynecologic Oncology, Karolinska University Hospital, Stockholm, Sweden.
    Late symptoms in long-term gynaecological cancer survivors after radiation therapy: a population-based cohort study.2011In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 105, no 6, p. 737-745Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: We surveyed the occurrence of physical symptoms among long-term gynaecological cancer survivors after pelvic radiation therapy, and compared with population-based control women.

    METHODS: We identified a cohort of 789 eligible gynaecological cancer survivors treated with pelvic radiation therapy alone or combined with surgery in Stockholm or Gothenburg, Sweden. A control group of 478 women was randomly sampled from the Swedish Population Registry. Data were collected through a study-specific validated postal questionnaire with 351 questions concerning gastrointestinal and urinary tract function, lymph oedema, pelvic bones and sexuality. Clinical characteristics and treatment details were retrieved from medical records.

    RESULTS: Participation rate was 78% for gynaecological cancer survivors and 72% for control women. Median follow-up time after treatment was 74 months. Cancer survivors reported a higher occurrence of symptoms from all organs studied. The highest age-adjusted relative risk (RR) was found for emptying of all stools into clothing without forewarning (RR 12.7), defaecation urgency (RR 5.7), difficulty feeling the need to empty the bladder (RR 2.8), protracted genital pain (RR 5.0), pubic pain when walking indoors (RR 4.9) and erysipelas on abdomen or legs at least once during the past 6 months (RR 3.6). Survivors treated with radiation therapy alone showed in general higher rates of symptoms.

    CONCLUSION: Gynaecological cancer survivors previously treated with pelvic radiation report a higher occurrence of symptoms from the urinary and gastrointestinal tract as well as lymph oedema, sexual dysfunction and pelvic pain compared with non-irradiated control women. Health-care providers need to actively ask patients about specific symptoms in order to provide proper diagnostic investigations and management.

  • 25.
    Lindemann, Kristina
    et al.
    Oslo University Hospital, Norway; University of Sydney, Australia; Westmead Hospital, Australia.
    Gibbs, Emma
    University of Sydney, Australia.
    Åvall-Lundqvist, Elisabeth
    Linköping University, Department of Clinical and Experimental Medicine, Division of Surgery, Orthopedics and Oncology. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Oncology. Karolinska Institute, Sweden.
    dePont Christensen, Rene
    University of Southern Denmark, Denmark.
    Woie, Kathrine
    Haukeland Hospital, Norway.
    Kalling, Marten
    Skåne University Hospital, Sweden.
    Auranen, Annika
    Tampere University Hospital, Finland.
    Grenman, Seija
    Turku University Hospital, Finland; University of Turku, Finland.
    Hoegberg, Thomas
    Skåne University Hospital Lund, Sweden.
    Rosenberg, Per
    Region Östergötland, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Oncology. Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Linköping University, Faculty of Medicine and Health Sciences.
    Skeie-Jensen, Tone
    Oslo University Hospital, Norway.
    Hjerpe, Elisabet
    University of Southern Denmark, Denmark.
    Dorum, Anne
    Oslo University Hospital, Norway.
    Gebski, Val
    University of Sydney, Australia.
    Kristensen, Gunnar
    Oslo University Hospital, Norway; University of Oslo, Norway.
    Chemotherapy vs tamoxifen in platinum-resistant ovarian cancer: a phase III, randomised, multicentre trial (Ovaresist)2017In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 116, no 4, p. 455-463Article in journal (Refereed)
    Abstract [en]

    Background: Chemotherapy in platinum-resistant ovarian cancer (PROC) aims for palliation and prolonging of progression-free survival (PFS). This study compares Health-related Quality of Life (HRQoL) and efficacy between single-agent chemotherapy and tamoxifen in PROC. Methods: Patients with PROC were randomised (2 : 1) to chemotherapy (weekly paclitaxel 80 mg m(-2) or four weekly pegylated liposomal doxorubicin 40 mg m(-2)) or tamoxifen 40mg daily. The primary end point was HRQoL. Secondary end points were PFS by RECIST and overall survival (OS). Results: Between March 2002 and December 2007, 156 and 82 patients were randomised to chemotherapy and tamoxifen, respectively. In the chemotherapy arm, a significantly larger proportion of patients experienced a worsening in their social functioning. There was no difference in the proportion of patients experiencing improvement of gastrointestinal symptoms. Median PFS on tamoxifen was 8.3 weeks (95% CI, 8.0-10.4) compared with 12.7 weeks (95% CI, 9.0-16.3) on chemotherapy (HR, 1.54; 95% CI, 1.16-2.05; log-rank P = 0.003). There was no difference in OS between the treatment arms. Conclusions: Patients on chemotherapy had longer PFS but experienced more toxicity and poorer HRQoL compared with tamoxifen. Control over gastrointestinal symptoms was not better on chemotherapy. These data are important for patient counselling and highlight the need to incorporate HRQoL end points in studies of PROC.

  • 26.
    Löf, Marie
    et al.
    Karolinska Institute.
    Sandin, S
    Karolinska Institute.
    Hilakivi-Clarke, L
    Georgetown University.
    Weiderpass, E
    Karolinska Institute.
    Birth weight in relation to endometrial and breast cancer risks in Swedish women2007In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 96, no 1, p. 134-136Article in journal (Refereed)
    Abstract [en]

      An examination of birth weight in a Swedish cohort study of 38 566 women showed no significant association between birth weight and endometrial cancer, but supported a protective role for low birth weight for premenopausal breast cancer.

  • 27.
    Löf, Marie
    et al.
    Karolinska Institute.
    Sandin, S
    Karolinska Institute.
    Lagiou, P
    Karolinska Institute.
    Hilakivi-Clarke, L
    Georgetown University.
    Trichopoulos, D
    Karolinska Institute.
    Adami, H-O
    Karolinska Institute.
    Weiderpass, E
    Karolinska Institute.
    Dietary fat and breast cancer risk in the Swedish women's lifestyle and health cohort2007In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 97, no 11, p. 1570-1576Article in journal (Refereed)
    Abstract [en]

    We investigated whether dietary intakes of total fat, monounsaturated fat (MUFA), polyunsaturated fat (PUFA) and saturated fat (SFA) were associated with breast cancer risk in a prospective cohort of 49 261 Swedish women (30–49 years at enrolment), which yielded 974 breast cancer cases by December 2005. Further, we evaluated if associations differed by oestrogen and/or progesterone receptor tumour status. Total fat, MUFA, PUFA or SFA were not associated with risk overall. However, women in the highest MUFA and PUFA quintile intake had a reduced breast cancer risk after age 50 years (hazard ratios: 95% confidence interval=0.45: 0.25–0.99 and 0.54: 0.35–0.85, respectively) compared to women in the lowest quintile. The associations did not differ by oestrogen or progesterone receptor status. Despite the negative findings, type of fat during premenopausal years may have later differential effects on risk.

  • 28.
    Neuzil, Jiri
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Neuroscience and Locomotion, Pathology.
    Vitamin E succinate and cancer treatment: A vitamin E prototype for selective antitumour activity2003In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 89, no 10, p. 1822-1826Article in journal (Refereed)
    Abstract [en]

    Great hope has been given to micronutrients as anticancer agents, since they present natural compounds with beneficial effects for normal cells and tissues. One of these is vitamin E (VE), an antioxidant and an essential component of biological membranes and circulating lipoproteins. In spite of a number of epidemiological and intervention studies, little or no correlation between VE intake and incidence of cancer has been found. Recent reports have identified a redox-silent analogue of VE, a-tocopheryl succinate (a-TOS), as a potent anticancer agent with a unique structure and pharmacokinetics in vivo. a-TOS is highly selective for malignant cells, inducing them into apoptotic death largely via the mitochondrial route. The molecule of a-TOS may be modified so that analogues with higher activity are generated. Finally, a-TOS and similar agents are metabolised to VE, thereby yielding a compound with a secondary beneficial activity. Thus, a-TOS epitomises a group of novel compounds that hold substantial promise as future anticancer drugs. The reasons for this optimistic notion are discussed in the following paragraphs. ⌐ 2003 Cancer Research UK.

  • 29.
    Nilsson, Henrik
    et al.
    Lund University Medical Laser Center, Lund Institute of Technology, Lund, Sweden.
    Johansson, J.
    Lund University Medical Laser Center and Department of Physics, Lund Institute of Technology, Lund, Sweden.
    Svanberg, K.
    Lund University Medical Laser Center, Lund Institute of Technology and the Department of Oncology, Lund University Hospital, Lund, Sweden.
    Svanberg, S.
    Lund University Medical Laser Center and Department of Physics, Lund Institute of Technology, Lund, Sweden.
    Jori, G.
    Department of Biology, Padova University, Padova, Italy.
    Reddi, E.
    Department of Biology, Padova University, Padova, Italy.
    Segalla, A.
    Department of Biology, Padova University, Padova, Italy.
    Gust, D.
    Department of Chemistry and Biochemistry, Center for the Study of Early Events in Photosynthesis, Arizona State University, USA.
    Moore, A. L.
    Department of Chemistry and Biochemistry, Center for the Study of Early Events in Photosynthesis, Arizona State University, USA.
    Moore, T. A.
    Department of Chemistry and Biochemistry, Center for the Study of Early Events in Photosynthesis, Arizona State University, USA.
    Laser-induced fluorescence in malignant and normal tissue in mice injected with two different carotenoporphyrins1994In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 70, no 5, p. 873-879Article in journal (Refereed)
    Abstract [en]

    Laser-induced fluorescence (LIF) was used to characterise the localisation of an intravenously administered trimethylated carotenoporphyrin [CP(Me)3] and a trimethoxylated carotenoporphyrin [CP(OMe)3] in an intramuscularly transplanted malignant tumour (MS-2 fibrosarcoma) and healthy muscle in female Balb/c mice, 3, 24, 48 and 96 h post injection. The fluorescence was induced with a dye laser pumped by a nitrogen laser, emitting light at 425 nm. The fluorescence spectra were recorded in the region 455-760 nm using a polychromator equipped with an image-intensified CCD camera. The tumour/peritumoral muscle ratio was about 5:1 for CP(Me)3 and about 6:1 for CP(OMe)3 in terms of the background-free fluorescence intensity, which peaked at about 655 nm. By including the endogenous tissue fluorescence, the contrast was further enhanced by a factor of approximately 2.

  • 30.
    Nilsson, Henrik
    et al.
    Lund University Medical Laser Center, Lund Institute of Technology, Lund, Sweden.
    Johansson, J.
    Lund University Medical Laser Center and Department of Physics, Lund Institute of Technology, Lund, Sweden.
    Svanberg, K.
    Lund University Medical Laser Center, Lund Institute of Technology and the Department of Oncology, Lund University Hospital, Lund, Sweden.
    Svanberg, S.
    Lund University Medical Laser Center and Department of Physics, Lund Institute of Technology, Lund, Sweden.
    Jori, G.
    Department of Biology, Padova University, Padova, Italy.
    Reddi, E.
    Department of Biology, Padova University, Padova, Italy.
    Segalla, A.
    Department of Biology, Padova University, Padova, Italy.
    Gust, D.
    Department of Chemistry and Biochemistry, Center for the Study of Early Events in Photosynthesis, Arizona State University, USA.
    Moore, A. L.
    Department of Chemistry and Biochemistry, Center for the Study of Early Events in Photosynthesis, Arizona State University, USA.
    Moore, T. A.
    Department of Chemistry and Biochemistry, Center for the Study of Early Events in Photosynthesis, Arizona State University, USA.
    Laser-induced fluorescence studies of the biodistribution of carotenoporphyrins in mice1997In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 76, no 3, p. 355-364Article in journal (Refereed)
    Abstract [en]

    The biodistribution of two recently developed tumour markers, trimethylated (CP(Me)3) and trimethoxylated (CP(OMe)3) carotenoporphyrin, was investigated by means of laser-induced fluorescence (LIF) after i.v. injection into 38 tumour-bearing (MS-2 fibrosarcoma) female Balb/c mice. At 3, 24, 48 or 96 h after administration, the carotenoporphyrin fluorescence was measured in tumoral and peritumoral tissue, as well as in the abdominal, thoracic and cranial cavities. The fluorescence was induced by a nitrogen laser-pumped dye laser, emitting light at 425 nm, and analysed by a polychromator equipped with an image-intensified CCD camera. The fluorescence was evaluated at 490, 655 and 720 nm: the second and third wavelengths represent the carotenoporphyrin (CP)-related peaks, whereas the first one is close to the peak of the tissue autofluorescence. The tumour and the liver were the two tissue types showing the strongest carotenoporphyrin-related fluorescence, whereas the cerebral cortex and muscle consistently exhibited weak substance-related fluorescence. In most tissue types, the fluorescence intensities decreased over time. A few exceptions were observed, notably the liver, in which the intensity remained remarkably constant over the time period investigated.

  • 31.
    Osorio, A.
    et al.
    Spanish Natl Canc Res Ctr, Human Genet Grp, Madrid, Spain.
    Milne, R L
    Spanish Natl Canc Res Ctr, Genet and Mol Epidemiol Grp, Madrid, Spain.
    Pita, G.
    Spanish Natl Canc Res Ctr, Human Canc Genet Programme, Genotyping Unit, Madrid, Spain.
    Peterlongo, P.
    Fdn IRCCS Ist Nazl Tumori, Milan, Italy.
    Heikkinen, T.
    Helsinki Univ Cent Hosp, Dept Obstet and Gynaecol, Helsvinki, Finland.
    Simard, J.
    Ctr Hosp Univ Quebec, Canc Genom Lab, Canada Res Chair Oncogenet, Quebec City, PQ, Canada.
    Chenevix-Trench, G.
    Queensland Inst Med Res, Div Genet and Populat Hlth, Brisbane, Qld 4006, Australia.
    Spurdle, A B
    Queensland Inst Med Res, Div Genet and Populat Hlth, Brisbane, Qld 4006, Australia.
    Beesley, J.
    Queensland Inst Med Res, Div Genet and Populat Hlth, Brisbane, Qld 4006, Australia.
    Chen, X.
    Queensland Inst Med Res, Div Genet and Populat Hlth, Brisbane, Qld 4006, Australia.
    Healey, S.
    Queensland Inst Med Res, Div Genet and Populat Hlth, Brisbane, Qld 4006, Australia.
    Neuhausen, S L
    Univ Calif Irvine, Sch Med, Dept Epidemiol, Irvine, CA 92717 USA.
    Ding, Y C
    Univ Calif Irvine, Sch Med, Dept Epidemiol, Irvine, CA 92717 USA.
    Couch, F J
    Mayo Clin, Dept Lab Med and Pathol, Rochester, MN USA.
    Wang, X.
    Mayo Clin, Dept Lab Med and Pathol, Rochester, MN USA.
    Lindor, N.
    Mayo Clin, Dept Med Genet, Rochester, MN USA.
    Manoukian, S.
    Fdn IRCCS Ist Nazl Tumori, Milan, Italy.
    Barile, M.
    Ist Europeo Oncol, Milan, Italy.
    Viel, A.
    IRCCS, Ctr Riferimento Oncol, Aviano, PN, Italy.
    Tizzoni, L.
    Fdn Ist FIRC Oncol Mol, Milan, Italy.
    Szabo, C I
    Mayo Clin, Coll Med, Dept Lab Med and Pathol, Rochester, MN USA.
    Foretova, L.
    Masaryk Mem Canc Inst, Dept Canc Epidemiol and Genet, Brno, Czech Republic.
    Zikan, M.
    Charles Univ Prague, Fac Med 1, Dept Biochem and Expt Oncol, Prague, Czech Republic.
    Claes, K.
    Ghent Univ Hosp, Ctr Med Genet, B-9000 Ghent, Belgium.
    Greene, M H
    NCI, Clin Genet Branch, Rockville, MD USA.
    Mai, P.
    NCI, Clin Genet Branch, Rockville, MD USA.
    Rennert, G.
    Carmel Hosp, CHS Natl Canc Control Ctr, Haifa, Israel.
    Lejbkowicz, F.
    Carmel Hosp, CHS Natl Canc Control Ctr, Haifa, Israel.
    Barnett-Griness, O.
    Carmel Hosp, CHS Natl Canc Control Ctr, Haifa, Israel.
    Andrulis, I L
    Ontario Canc Genet Network, Toronto, ON, Canada.
    Ozcelik, H.
    Mt Sinai Hosp, Samuel Lunenfeld Res Inst, Fred A Litwin Ctr Canc Genet, Toronto, ON M5G 1X5, Canada.
    Weerasooriya, N.
    Ontario Canc Genet Network, Toronto, ON, Canada.
    Gerdes, A-M
    Odense Univ Hosp, Clin Genet BFG, DK-5000 Odense, Denmark.
    Thomassen, M.
    Odense Univ Hosp, Clin Genet BFG, DK-5000 Odense, Denmark.
    Cruger, D G
    Vejle Hosp, Dept Clin Genet, Vijle, Denmark.
    Caligo, M A
    Univ Pisa, Dept Oncol, Div Pathol, Pisa, Italy.
    Friedman, E.
    Chaim Sheba Med Ctr, IL-52621 Tel Hashomer, Israel.
    Kaufman, B.
    Chaim Sheba Med Ctr, IL-52621 Tel Hashomer, Israel.
    Laitman, Y.
    Chaim Sheba Med Ctr, IL-52621 Tel Hashomer, Israel.
    Cohen, S.
    Chaim Sheba Med Ctr, IL-52621 Tel Hashomer, Israel.
    Kontorovich, T.
    Chaim Sheba Med Ctr, IL-52621 Tel Hashomer, Israel.
    Gershoni-Baruch, R.
    Rambam Med Ctr, Haifa, Israel.
    Dagan, E.
    Univ Haifa, Fac Social Welf and Hlth Sci, Dept Nursing, IL-31999 Haifa, Israel.
    Jernstrom, H.
    Lund Univ, Dept Oncol, Lund, Sweden.
    Stenmark Askmalm, Marie
    Linköping University, Department of Clinical and Experimental Medicine, Oncology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Center for Diagnostics, Department of Clinical Pathology and Clinical Genetics.
    Arver, B.
    Karolinska Univ Hosp, Dept Oncol, Stockholm, Sweden.
    Malmer, B.
    Umea Univ, Dept Radiat Sci, Umea, Sweden.
    Domchek, S M
    Univ Penn, Abramson Canc Ctr, Philadelphia, PA 19104 USA.
    Nathanson, K L
    Univ Penn, Abramson Canc Ctr, Philadelphia, PA 19104 USA.
    Brunet, J.
    Hosp Dr Josep Trueta IdiBGi, Inst Catalan Oncol, Programa Consejo Genet Canc, Girona, Spain.
    Cajal, T. Ramon y
    Hosp Santa Creu and Sant Pau, Med Oncol Serv, Barcelona, Spain.
    Yannoukakos, D.
    Demokritos Natl Ctr Sci Res, IRRP, Mol Diagnost Lab, GR-15310 Athens, Greece.
    Hamann, U.
    Deutsch Krebsforschungszentrum, D-6900 Heidelberg, Germany.
    Hogervorst, F B L
    Netherlands Canc Inst, Family Canc Clin, Dept Clin Mol Genet, Amsterdam, Netherlands.
    Verhoef, S.
    Netherlands Canc Inst, Family Canc Clin, Dept Clin Mol Genet, Amsterdam, Netherlands.
    Gomez Garcia, E B
    Univ Med Ctr, Dept Genet and Cell Biol, Maastricht, Netherlands.
    Wijnen, J T
    Leiden Univ, Med Ctr, Dept Clin Mol Genet, Leiden, Netherlands.
    van den Ouweland, A.
    Erasmus Univ, Med Ctr, Dept Mol Genet, Rotterdam, Netherlands.
    Easton, D F
    Univ Cambridge, Dept Publ Hlth and Primary Care, Canc Res UK Genet Epidemiol Unit, Cambridge, England.
    Peock, S.
    Univ Cambridge, Dept Publ Hlth and Primary Care, Canc Res UK Genet Epidemiol Unit, Cambridge, England.
    Cook, M.
    Univ Cambridge, Dept Publ Hlth and Primary Care, Canc Res UK Genet Epidemiol Unit, Cambridge, England.
    Oliver, C T
    Univ Cambridge, Dept Publ Hlth and Primary Care, Canc Res UK Genet Epidemiol Unit, Cambridge, England.
    Frost, D.
    Univ Cambridge, Dept Publ Hlth and Primary Care, Canc Res UK Genet Epidemiol Unit, Cambridge, England.
    Luccarini, C.
    Univ Cambridge, Dept Oncol, Cambridge, England.
    Evans, D G
    St Marys Hosp, Acad Unit Med Genet, Manchester M13 0JH, Lancs, England.
    Lalloo, F.
    St Marys Hosp, Acad Unit Med Genet, Manchester M13 0JH, Lancs, England.
    Eeles, R.
    Inst Canc Res, Translat Canc Genet Team, London SW3 6JB, England.
    Pichert, G.
    Guys Hosp, London SE1 9RT, England.
    Cook, J.
    Sheffield Childrens Hosp, Sheffield Clin Genet Serv, Sheffield, S Yorkshire, England.
    Hodgson, S.
    Univ London, St Georges Hosp, Dept Canc Genet, London, England.
    Morrison, P J
    Belfast City Hosp, No Ireland Reg Genet Ctr, Belfast BT9 7AD, Antrim, North Ireland.
    Douglas, F.
    Newcastle Upon Tyne Hosp NHS Trust, Inst Human Genet, Ctr Life, Newcastle Upon Tyne, Tyne and Wear, England.
    Godwin, A K
    Fox Chase Canc Ctr, Philadelphia, PA 19111 USA.
    Sinilnikova, O M
    Hosp Civils Lyon, Ctr Leon Berard, Unite Mixte Genet Constitut Canc Frequents, Lyon, France.
    Barjhoux, L.
    Hosp Civils Lyon, Ctr Leon Berard, Unite Mixte Genet Constitut Canc Frequents, Lyon, France.
    Stoppa-Lyonnet, D.
    Univ Paris 05, Inst Curie, Serv Gent Oncol, INSERM,U509, Paris, France.
    Moncoutier, V.
    Univ Paris 05, Inst Curie, Serv Gent Oncol, INSERM,U509, Paris, France.
    Giraud, S.
    Hosp Civils Lyon, Ctr Leon Berard, Unite Mixte Genet Constitut Canc Frequents, Lyon, France.
    Cassini, C.
    Ctr Genet, Dijon, France.
    Olivier-Faivre, L.
    Ctr Genet, Dijon, France.
    Revillion, F.
    Ctr Oscar Lambret, Human Mol Oncol Lab, F-59020 Lille, France.
    Peyrat, J-P
    Ctr Oscar Lambret, Human Mol Oncol Lab, F-59020 Lille, France.
    Muller, D.
    CLCC Paul Strauss, Unite Oncogenet, Strasbourg, France.
    Fricker, J-P
    CLCC Paul Strauss, Unite Oncogenet, Strasbourg, France.
    Lynch, H T
    Creighton Univ, Dept Prevent Med, Omaha, NE 68178 USA.
    John, E M
    No Calif Canc Ctr, Fremont, CA USA.
    Buys, S.
    Huntsman Canc Inst, Salt Lake City, UT USA.
    Daly, M.
    Fox Chase Canc Ctr, Philadelphia, PA 19111 USA.
    Hopper, J L
    Univ Melbourne, Melbourne, Vic, Australia.
    Terry, M B
    Columbia Univ, New York, NY USA.
    Miron, A.
    Dana Farber Canc Inst, Boston, MA 02115 USA.
    Yassin, Y.
    Dana Farber Canc Inst, Boston, MA 02115 USA.
    Goldgar, D.
    Univ Utah, Dept Dermatol, Salt Lake City, UT USA.
    Singer, C F
    Med Univ Vienna, Dept OB GYN, Div Special Gynecol, Vienna, Austria.
    Gschwantler-Kaulich, D.
    Med Univ Vienna, Dept OB GYN, Div Special Gynecol, Vienna, Austria.
    Pfeiler, G.
    Med Univ Vienna, Dept OB GYN, Div Special Gynecol, Vienna, Austria.
    Spiess, A-C
    Med Univ Vienna, Dept OB GYN, Div Special Gynecol, Vienna, Austria.
    v. O. Hansen, Thomas
    Odense Univ Hosp, Dept Biochem Pharmacol and Genet, DK-5000 Odense, Denmark.
    T. Johannsson, O.
    Landspitali Univ Hosp, Dept Oncol, Reykjavik, Iceland.
    Kirchhoff, T.
    Mem Sloan Kettering Canc Ctr, Dept Med, Clin Genet Serv, New York, NY 10021 USA.
    Offit, K.
    Mem Sloan Kettering Canc Ctr, Dept Med, Clin Genet Serv, New York, NY 10021 USA.
    Kosarin, K.
    Mem Sloan Kettering Canc Ctr, Dept Med, Clin Genet Serv, New York, NY 10021 USA.
    Piedmonte, M.
    Roswell Pk Canc Inst, GOG Stat and Data Ctr, Buffalo, NY 14263 USA.
    C. Rodriguez, G.
    Evanston NW Healthcare, NorthShore Univ Hlth Syst, Evanston, IL USA.
    Wakeley, K.
    Tufts Univ, New England Med Ctr, Boston, MA 02111 USA.
    F. Boggess, J.
    Univ N Carolina, Chapel Hill, NC USA.
    Basil, J.
    St Elizabeth Hosp, Edgewood, KY USA.
    E. Schwartz, P.
    Yale Univ, Sch Med, New Haven, CT USA.
    V. Blank, S.
    NYU, Sch Med, New York, NY USA.
    E. Toland, A.
    Ohio State Univ, Ctr Comprehens Canc, Div Human Canc Genet, Dept Internal Med and Mol Virol, Columbus, OH 43210 USA.
    Montagna, M.
    IRCCS, Inst Oncol Veneto, Padua, Italy.
    Casella, C.
    Dept Oncol and Surg Sci, Padua, Italy.
    N. Imyanitov, E.
    NN Petrov Oncol Res Inst, St Petersburg, Russia.
    Allavena, A.
    Univ Turin, Dept Genet Biol and Biochem, Turin, Italy.
    K. Schmutzler, R.
    Univ Cologne, Dept Obstet and Gynaecol, Div Mol Gynaecooncol, Cologne, Germany.
    Versmold, B.
    Univ Cologne, Dept Obstet and Gynaecol, Div Mol Gynaecooncol, Cologne, Germany.
    Engel, C.
    Univ Leipzig, Inst Med Informat Stat and Epidemiol, Leipzig, Germany.
    Meindl, A.
    Tech Univ Munich, Dept Obstet and Gynaecol, Munich, Germany.
    Ditsch, N.
    Univ Munich, Dept Obstet and Gynaecol, Munich, Germany.
    Arnold, N.
    Univ Schleswig Holstein, Dept Obstet and Gynaecol, Lubeck, Germany.
    Niederacher, D.
    Univ Dusseldorf, Dept Obstet and Gynaecol, Mol Genet Lab, Dusseldorf, Germany.
    Deissler, H.
    Univ Ulm, Dept Obstet and Gynaecol, Ulm, Germany.
    Fiebig, B.
    Univ Regensburg, Inst Human Genet, Regensburg, Germany.
    Varon-Mateeva, R.
    Humboldt Univ, Inst Human Genet, Charite, Berlin, Germany.
    Schaefer, D.
    Goethe Univ Frankfurt, Inst Human Genet, Frankfurt, Germany.
    G. Froster, U.
    Univ Leipzig, Inst Human Genet, Leipzig, Germany.
    Caldes, T.
    Hosp Clin San Carlos, Madrid, Spain.
    de la Hoya, M.
    Hosp Clin San Carlos, Madrid, Spain.
    McGuffog, L.
    Univ Cambridge, Dept Publ Hlth and Primary Care, Canc Res UK Genet Epidemiol Unit, Cambridge, England.
    C. Antoniou, A.
    Univ Cambridge, Dept Publ Hlth and Primary Care, Canc Res UK Genet Epidemiol Unit, Cambridge, England.
    Nevanlinna, H.
    Helsinki Univ Cent Hosp, Dept Obstet and Gynaecol, Helsvinki, Finland.
    Radice, P.
    Fdn IRCCS Ist Nazl Tumori, Milan, Italy.
    Benitez, J.
    Spanish Natl Canc Res Ctr, Human Genet Grp, Madrid, Spain.
    Evaluation of a candidate breast cancer associated SNP in ERCC4 as a risk modifier in BRCA1 and BRCA2 mutation carriers. Results from the Consortium of Investigators of Modifiers of BRCA1/BRCA2 (CIMBA)2009In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 101, no 12, p. 2048-2054Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: In this study we aimed to evaluate the role of a SNP in intron I of the ERCC4 gene (rs744154), previously reported to be associated with a reduced risk of breast cancer in the general population, as a breast cancer risk modifier in BRCA1 and BRCA2 mutation carriers. METHODS: We have genotyped rs744154 in 9408 BRCA1 and 5632 BRCA2 mutation carriers from the Consortium of Investigators of Modifiers of BRCA1/2 (CIMBA) and assessed its association with breast cancer risk using a retrospective weighted cohort approach. RESULTS: We found no evidence of association with breast cancer risk for BRCA1 (per-allele HR: 0.98, 95% CI: 0.93-1.04, P = 0.5) or BRCA2 (per-allele HR: 0.97, 95% CI: 0.89-1.06, P = 0.5) mutation carriers. CONCLUSION: This SNP is not a significant modifier of breast cancer risk for mutation carriers, though weak associations cannot be ruled out.

  • 32.
    Pérez-Tenorio, Gizeh
    et al.
    Linköping University, Department of Clinical and Experimental Medicine, Oncology . Linköping University, Faculty of Health Sciences.
    Stål, Olle
    Linköping University, Department of Clinical and Experimental Medicine, Oncology . Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Oncology UHL.
    Members of the Southeast Sweden Breast Cancer Group,
    Activation of AKT/PKB in breast cancer predicts a worse outcome among endocrine treated patients2002In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 86, no 4, p. 540-545Article in journal (Refereed)
    Abstract [en]

    Akt/PKB is a serine/threonine protein kinase that regulates cell cycle progression, apoptosis and growth factor mediated cell survival in association with tyrosine kinase receptors. The protein is a downstream effector of erbB-2 with implications in breast cancer progression and drug resistance in vitro. We aimed to examine the role of Akt-1 in breast cancer patients, by determining whether the expression (Akt-1) and/or activation (pAkt) were related to prognostic markers and survival. The expression of erbB-2, heregulin β1 and Bcl-2 was also assessed by flow cytometry or immunohistochemistry. This study comprised 93 patients, aged < 50 who were treated with tamoxifen and/or goserelin. We found that pAkt was associated with lower S-phase fraction (P = 0.001) and the presence of heregulin β1-expressing stromal cells (P = 0.017). Neither Akt-1 nor pAkt was related with other factors Turnout cells-derived heregulin β1 was found mainly in oestrogen receptor negative (P = 0.026) and node negative (P = 0.005) cases. Survival analysis revealed that pAkt positive patients were more prone to relapse with distant metastasis, independently of S-phase fraction and nodal status (multivariate analysis; P = 0.004). The results suggest that activation of Akt may have prognostic relevance in breast cancer

  • 33.
    Rosell, Johan
    et al.
    Linköping University, Department of Clinical and Experimental Medicine, Oncology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Oncology UHL.
    Nordenskjöld, Bo
    Linköping University, Department of Clinical and Experimental Medicine, Oncology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Oncology UHL.
    Bengtsson, N-O
    Department of Oncolog, Umea University Hospital, Sweden.
    Fornander, T
    Department of Oncology, Karolinska University Hospital, Stockholm, Sweden.
    Hatschek, T
    Department of Oncology, Karolinska University Hospital, Stockholm, Sweden.
    Lindman, H
    Department of Oncology, Uppsala University Hospital, Uppsala, Sweden.
    Malmstrom, P-O
    Department of Oncology, Lund University Hospital, Lund, Sweden.
    Wallgren, A
    Department of Oncology, Sahlgrenska University Hospital, Göteborg, Sweden.
    Stål, Olle
    Linköping University, Department of Clinical and Experimental Medicine, Oncology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Oncology UHL.
    Carstensen, John
    Linköping University, Department of Medical and Health Sciences, Health and Society. Linköping University, Faculty of Health Sciences.
    Time dependent effects of adjuvant tamoxifen therapy on cerebrovascular disease: results from a randomised trial2011In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 104, no 6, p. 899-902Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Tamoxifen has been associated with an increased risk of stroke. There is, however, little information on the effect in the post-treatment period. Using data from the Swedish Breast Cancer Group adjuvant trial of 5 vs 2 years of tamoxifen treatment, we now report both short-term and long-term effects on morbidity as well as mortality because of cerebrovascular disease. METHODS: Data from the Swedish National Hospital Discharge Registry combined with information from the Swedish Cause of Death Registry was used to define events of disease. Hazard ratios (HRs) were estimated using Cox regression. RESULTS: Comparing patients randomised to 5 years of tamoxifen with patients randomised to 2 years of tamoxifen, the incidence of cerebrovascular diseases was increased (HR 1.70, 95% CI 1.05-2.75) during the active treatment phase and reduced after the active treatment period (HR 0.78, 95% CI 0.63-0.96), and the difference in HR between the two time-periods was significant (P 0.0033). The mortality from cerebrovascular diseases was increased during the treatment period (HR 3.18, 95% CI 1.03-9.87) and decreased during the post-treatment period (HR 0.60, 95% CI 0.40-0.90) with a significant difference in HR between the two periods of follow-up (P=0.0066). Similar results were seen for subgroups of cerebrovascular diseases, such as stroke and ischaemic stroke. CONCLUSION: In an adjuvant setting, tamoxifen was associated with an increased risk of cerebrovascular disease during treatment, but a decreased risk in the post-treatment period.

  • 34. Sandblom, G
    et al.
    Carlsson, Per
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Department of Health and Society, Center for Medical Technology Assessment.
    Sennfält, Karin
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Department of Health and Society, Center for Medical Technology Assessment.
    Varenhorst, Eberhard
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Division of surgery. Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Urology in Östergötland.
    A population-based study of pain and quality of life during the year before death in men with prostate cancer2004In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 90, no 6, p. 1163-1168Article in journal (Refereed)
    Abstract [en]

    In order to explore how health-related quality of life changes towards the end of life, a questionnaire including the EuroQOI form and the Brief Pain Inventory form was sent to all men with prostate cancer in the county of Östergötland, Sweden, in September 1999. Responders who had died prior to 1 January 2001 were later identified retrospectively. Of the 1442 men who received the questionnaire, 1243 responded (86.2%). In the group of responders, 167 had died within the study period, 66 of prostate cancer. In multivariate analysis, pain as well as death within the period of study were found to predict decreased quality of life significantly. Of those who died of prostate cancer, 29.0% had rated their worst pain the previous week as severe. The same figure for those still alive was 10.5%. On a visual analogue scale (range 0-100), the mean rating of quality of life for those who subsequently died of prostate cancer was 54.0 (95% confidence interval ±5.2) and those still alive was 70.0 (±1.2). In conclusion, hearth-related quality of life gradually declines during the last year of life in men with prostate cancer. This decline may partly be avoided by an optimised pain management. © 2004 Cancer Research UK.

  • 35.
    Sandblom, Gabriel
    et al.
    Linköping University, Department of Biomedicine and Surgery, Urology. Linköping University, Faculty of Health Sciences.
    Carlsson, Per
    Linköping University, Department of Behavioural Sciences, Centre for Studies of Humans, Technology and Organization. Linköping University, Faculty of Health Sciences.
    Sigsjö, Peter
    Linköping University, Department of Behavioural Sciences, Centre for Studies of Humans, Technology and Organization. Linköping University, Faculty of Health Sciences.
    Varenhorst, Eberhard
    Linköping University, Department of Biomedicine and Surgery, Urology. Linköping University, Faculty of Health Sciences.
    Pain and health-related quality of life in a geographically defined population of men with prostate cancer2001In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 85, no 4, p. 497-503Article in journal (Refereed)
    Abstract [en]

    In order to provide baseline data on pain and health-related quality of life, to explore factors predicting pain and reduced quality of life, and to find potentially undertreated cases in men with prostate cancer, we undertook a population-based questionnaire study. The questionnaire, which included the EuroQo1 instrument, the Brief Pain Inventory form and 8 specially designed questions, was sent to all men with prostate cancer in the county of ╓sterg÷tland, Sweden. Of the 1442 men included in the study, 1243 responded to the questionnaire. Altogether 42% had perceived pain during the previous week and 26% stated their quality of life to be 50% or lower on a visual analogue scale. A high rating of health care availability and short time since diagnosis were found to significantly predict lower ratings of pain (P < 0.05). Pain was found to be a significant predictive factor for decreased quality of life together with high age, low rating of health care availability and palliative treatment (P < 0.05). In conclusion, assessment and treatment of pain is essential for a good quality of life in men with prostate cancer. The monitoring of prostate cancer patients should be individualized to fit the demands of the groups with the greatest need for support.

  • 36.
    Schoemaker, N.E.
    et al.
    Antoni Van Leeuwenhoek Hospital, The Netherlands Cancer Institute, Amsterdam, Netherlands, Slotervaart Hospital, Amsterdam, Netherlands.
    Kuppens, I.E.L.M.
    Antoni Van Leeuwenhoek Hospital, The Netherlands Cancer Institute, Amsterdam, Netherlands, Slotervaart Hospital, Amsterdam, Netherlands, Dept. of Pharmacy and Pharmacology, Slotervaart Hospital, The Netherlands Cancer Institute, Louwesweg 6, 1066 EC Amsterdam, Netherlands.
    Moiseyenko, V.
    Petrov Res. Institute of Oncology, St-Petersburg, Russian Federation.
    Glimelius, B.
    Onkologiska Kliniken, Uppsala, Sweden.
    Kjaer, M.
    Aalborg Hospital, Aalborg, Denmark.
    Starkhammer, H.
    Onkologiska Kliniken, Linkoping, Sweden.
    Richel, D.J.
    Medisch Spectrum Twente, Enschede, Netherlands.
    Smaaland, R.
    Haukeland Hospital, Bergen, Norway.
    Bertelsen, K.
    Odense University Hospital, Odense, Denmark.
    Poulsen, J.P.
    Norwegian Radium Hospital, Oslo, Norway.
    Voznyi, E.
    Res. Inst. of Diagnostic and Surgery, Moscow, Russian Federation.
    Norum, J.
    Regional Hospital of Tromso, Tromso, Norway.
    Fennelly, D.
    St. Vincent Hospital, Dublin, Ireland.
    Tveit, K.M.
    Ullevaal University Hospital, Oslo, Norway.
    Garin, A.
    All-Union Cancer Research Center, Moscow, Russian Federation.
    Gruia, G.
    Aventis Pharma, Antony Cedex, France.
    Mourier, A.
    Aventis Pharma, Antony Cedex, France.
    Sibaud, D.
    Aventis Pharma, Antony Cedex, France.
    Lefebvre, P.
    Aventis Pharma, Antony Cedex, France.
    Beijnen, J.H.
    Antoni Van Leeuwenhoek Hospital, The Netherlands Cancer Institute, Amsterdam, Netherlands, Slotervaart Hospital, Amsterdam, Netherlands, Utrecht University, Faculty of Pharmaceutical Sciences, Netherlands.
    Schellens, J.H.M.
    Antoni Van Leeuwenhoek Hospital, The Netherlands Cancer Institute, Amsterdam, Netherlands, Utrecht University, Faculty of Pharmaceutical Sciences, Netherlands.
    Ten, Bokkel Huinink W.W.
    Ten Bokkel Huinink, W.W., Antoni Van Leeuwenhoek Hospital, The Netherlands Cancer Institute, Amsterdam, Netherlands.
    A randomised phase II multicentre trial of irinotecan (CPT-11) using four different schedules in patients with metastatic colorectal cancer2004In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 91, no 8, p. 1434-1441Article in journal (Refereed)
    Abstract [en]

    The purpose of this phase II trial was to compare the efficacy, safety and pharmacokinetics of four irinotecan schedules for the treatment of metastatic colorectal cancer. In total, 174 5-fluorouracil pretreated patients were randomised to: arm A (n = 41), 350 mg m-2 irinotecan as a 90-min i.v. infusion q3 weeks, arm B (n = 38), 125 mg m-2 irinotecan as a 90-min i.v. infusion weekly x 4 weeks q6 weeks, arm C (n = 46), 250 mg m-2 irinotecan as a 90-min i.v. infusion q2 weeks, or arm D (n = 49), 10 mg m -2 day-1 irinotecan as a 14-day continuous infusion q3 weeks. No significant differences in efficacy across the four arms were observed, although a shorter time to treatment failure was noted for arm D (1.7 months, P = 0.02). Overall response rates were in the range 5-11%. Secondary end points included median survival (6.4-9.4 months), and time to progression (2.7-3.8 months) and treatment failure (1.7-3.2 months). Similarly, there were no significant differences in the incidence of grade 3-4 toxicities, although the toxicity profile between arms A, B, and C and D did differ. Generally, significantly less haematologic toxicity, alopecia and cholinergic syndrome were observed in arm D, however, there was a trend for increased gastrointestinal toxicity. Irinotecan is an effective and safe second-line treatment for colorectal cancer. The schedules examined yielded equivalent results, indicating that there is no advantage of the prolonged vs short infusion schedules. © 2004 Cancer Research UK.

  • 37.
    Thiel, U
    et al.
    Technical University of Munich, Germany .
    Koscielniak, E
    Klinikum Stuttgart, Germany .
    Blaeschke, F
    Technical University of Munich, Germany .
    Grunewald, T G P.
    Technical University of Munich, Germany .
    Badoglio, M
    Hop St Antoine, France .
    Diaz, M A.
    Hospital Infantil University of Nino Jesus, Spain .
    Paillard, C
    CHU Clermont Ferrand, France .
    Prete, A
    Osped S Orsola Malpighi, Italy .
    Ussowicz, M
    Wroclaw Medical University, Poland .
    Lang, P
    University of Childrens Hospital, Germany .
    Fagioli, F
    Regina Margherita Childrens Hospital, Italy .
    Lutz, P
    Hop Hautepierre, France .
    Ehninger, G
    University Hospital Carl Gustav Carus, Germany .
    Schneider, P
    Rouen University Hospital, France .
    Santucci, A
    University of Perugia, Italy .
    Bader, P
    Goethe University of Frankfurt, Germany .
    Gruhn, B
    Jena University Hospital, Germany .
    Faraci, M
    G Gaslini Childrens Research Institute, Italy .
    Antunovic, Petar
    Linköping University, Department of Clinical and Experimental Medicine. Linköping University, Faculty of Health Sciences.
    Styczynski, J
    Coll Medical UMK, Poland .
    Krueger, W H.
    Ernst Moritz Arndt University of Greifswald, Germany .
    Castagna, L
    Ist Clin Humanitas, Italy .
    Rohrlich, P
    University of Franche Comte, France .
    Ouachee-Chardin, M
    Hop Robert Debre, France .
    Salmon, A
    CHU Nancy Brabois, France .
    Peters, C
    St Anna Childrens Hospital, Austria .
    Bregni, M
    Osped Circolo, Italy .
    Burdach, S
    Technical University of Munich, Germany .
    Allogeneic stem cell transplantation for patients with advanced rhabdomyosarcoma: a retrospective assessment2013In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 109, no 10, p. 2523-2532Article in journal (Refereed)
    Abstract [en]

    Background: Allogeneic haematopoietic stem cell transplantation (allo-SCT) may provide donor cytotoxic T cell-/NK cell-mediated disease control in patients with rhabdomyosarcoma (RMS). However, little is known about the prevalence of graft-vs-RMS effects and only a few case experiences have been reported. less thanbrgreater than less thanbrgreater thanMethods: We evaluated allo-SCT outcomes of 30 European Group for Blood and Marrow Transplantation (EBMT)-registered patients with advanced RMS regarding toxicity, progression-free survival (PFS) and overall survival (OS) after allo-SCT. Twenty patients were conditioned with reduced intensity and ten with high-dose chemotherapy. Twenty-three patients were transplanted with HLA-matched and seven with HLA-mismatched grafts. Three patients additionally received donor lymphocyte infusions (DLIs). Median follow-up was 9 months. less thanbrgreater than less thanbrgreater thanResults: Three-year OS was 20% (s. e.+/- 8%) with a median survival time of 12 months. Cumulative risk of progression was 67% (s. e.+/- 10%) and 11% (s. e.+/- 6%) for death of complications. Thirteen patients developed acute graft-vs-host disease (GvHD) and five developed chronic GvHD. Eighteen patients died of disease and four of complications. Eight patients survived in complete remission (CR) (median: 44 months). No patients with residual disease before allo-SCT were converted to CR. less thanbrgreater than less thanbrgreater thanConclusion: The use of allo-SCT in patients with advanced RMS is currently experimental. In a subset of patients, it may constitute a valuable approach for consolidating CR, but this needs to be validated in prospective trials.

  • 38. Thompson, JF
    et al.
    Siebert, GA
    Anissimov, YG
    Smithers, BM
    Doubrovsky, A
    Anderson, Chris
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Dermatology. Östergötlands Läns Landsting, Centre for Medicine, Department of Dermatology and Venerology in Östergötland.
    Roberts, MS
    Microdialysis and response during regional chemotherapy by isolated limb infusion of melphalan for limb malignancies.2001In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 85, p. 157-165Article in journal (Refereed)
  • 39. Tomasetti, M
    et al.
    Rippo, MR
    Alleva, R
    Moretti, S
    Andera, L
    Neuzil, Jiri
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Neuroscience and Locomotion, Pathology.
    Procopio, A
    α-tocopheryl succinate and TRAIL selectively synergise in induction of apoptosis in human malignant mesothelioma cells2004In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 90, no 8, p. 1644-1653Article in journal (Refereed)
    Abstract [en]

    Malignant mesothelioma (MM) is a fatal type of neoplasia with poor therapeutic prognosis, largely due to resistance to apoptosis. We investigated the apoptotic effect of α-tocopheryl succinate (α-TOS), a strong proapoptotic agent, in combination with the immunological apoptogen TNF-related apoptosis-inducing ligand (TRAIL) on both MM and nonmalignant mesothelial cells, since MM cells show low susceptibility to the clinically intriguing TRAIL. All MM cell lines tested were sensitive to α-TOS-induced apoptosis, and exerted high sensitivity to TRAIL in the presence of subapoptotic doses of the vitamin E analogue. Neither TRAIL or α-TOS alone or in combination caused apoptosis in nonmalignant mesothelial cells. Isobologram analysis of the cytotoxicity assays revealed a synergistic interaction between the two agents in MM cells and their antagonistic effect in nonmalignant mesothelial cells. TRAIL-induced apoptosis and its augmentation by α-TOS were inhibited by the caspase-8 inhibitor Z-IETD-FMK and the pan-caspase inhibitor Z-VAD-FMK. Activation of caspase-8 was required to induce apoptosis, which was amplified by α-TOS via cytochrome c release following Bid cleavage, with ensuing activation of caspase-9. Enhancement of TRAIL-induced apoptosis in MM cells by α-TOS was also associated with upregulation of the TRAIL cognate death receptors DR4 and DR5. Our results show that α-TOS and TRAIL act in synergism to kill MM cells via mitochondrial pathway, and are nontoxic to nonmalignant mesothelial cells. These findings are indicative of a novel strategy for treatment of thus far fatal MM.

  • 40. von Plessen, C
    et al.
    Bergman, B
    Andresen, O
    Bremnes, RM
    Sundström, S
    Gilleryd, M
    Stephens, RM
    Vilsvik, J
    Aasebö, U
    Sörenson, Sverre
    Haukeland University Hospital .
    Palliative chemotherapy beyond three courses conveys no survival or consistent quality-of-life benefits in advanced non-small-cell lung cancer2006In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 95, no 8, p. 966-973Article in journal (Refereed)
    Abstract [en]

    This randomised multicentre trial was conducted to establish the optimal duration of palliative chemotherapy in advanced non-small-cell lung cancer (NSCLC). We compared a policy of three vs six courses of new-generation platinum-based combination chemotherapy with regard to effects on quality of life (QoL) and survival. Patients with stage IIIB or IV NSCLC and WHO performance status (PS) 0-2 were randomised to receive three (C3) or six (C6) courses of carboplatin (area under the curve (AUC) 4, Chatelut's formula, equivalent to Calvert's AUC 5) on day 1 and vinorelbine 25mg m-2 on days 1 and 8 of a 3-week cycle. Key end points were QoL at 18 weeks, measured with EORTC Quality of Life Questionnaire (QLQ)-C30 and QLQ-LC13, and overall survival. Secondary end points were progression-free survival and need of palliative radiotherapy. Two hundred and ninety-seven patients were randomised (C3 150, C6 147). Their median age was 65 years, 30% had PS 2 and 76% stage IV disease. Seventy-eight and 54% of C3 and C6 patients, respectively, completed all scheduled chemotherapy courses. Compliance with QoL questionnaires was 88%. There were no significant group differences in global QoL, pain or fatigue up to 26 weeks. The dyspnoea palliation rate was lower in the C3 arm at 18 and 26 weeks (P<0.05), but this finding was inconsistent across different methods of analysis. Median survival in the C3 group was 28 vs 32 weeks in the C6 group (P=0.75, HR 1.04, 95% CI 0.82-1.31). One- and 2-year survival rates were 25 and 9% vs 25 and 5% in the C3 and C6 arm, respectively. Median progression-free survival was 16 and 21 weeks in the C3 and C6 groups, respectively (P=0.21, HR 0.86, 95% CI 0.68-1.08). In conclusion, palliative chemotherapy with carboplatin and vinorelbine beyond three courses conveys no survival or consistent QoL benefits in advanced NSCLC. © 2006 Cancer Research UK.

  • 41.
    Wangsa, D
    et al.
    Department of Oncology-Pathology, Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden. Genetics Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. .
    Ryott, M
    Department of Oto-Rhino-Laryngology, Head and Neck Surgery, Karolinska University Hospital, Stockholm, Sweden. .
    Åvall-Lundqvist, Elisabeth
    Department of Gynaecologic Oncology, Radiumhemmet, Karolinska University Hospital, Stockholm, Sweden.
    Petersson, F
    Department of Oncology-Pathology, Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden.
    Elmberger, G
    Department of Oncology-Pathology, Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden.
    Luo, J
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Ried, T
    Genetics Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
    Auer, G
    Department of Oncology-Pathology, Karolinska Institute, Karolinska University Hospital, Stockholm, Sweden.
    Munck-Wikland, E
    Department of Oto-Rhino-Laryngology, Head and Neck Surgery, Karolinska University Hospital, Stockholm, Sweden.
    Ki-67 expression predicts locoregional recurrence in stage I oral tongue carcinoma.2008In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 99, no 7, p. 1121-1128Article in journal (Refereed)
    Abstract [en]

    Oral tongue squamous cell carcinoma (OTSCC) is an aggressive cancer associated with poor prognosis. Methods for determining the aggressiveness of OTSCC from analysis of the primary tumour specimen are thus highly desirable. We investigated whether genomic instability and proliferative activity (by means of Ki-67 activity) could be of clinical use for prediction of locoregional recurrence in 76 pretreatment OTSCC paraffin samples (stage I, n=22; stage II, n=33; stage III, n=8; stage IV, n=13). Eleven surgical tumour specimens were also analysed for remnants of proliferative activity after preoperative radiotherapy. Ninety-seven percent of cases (n=72) were characterised as being aneuploid as measured by means of image cytometry. Preoperative radiotherapy (50-68 Gy) resulted in significant reduction of proliferative activity in all patients for which post-treatment biopsies were available (P-value=0.001). Proliferative activity was not associated with response to radiation in stage II patients. However, we report a significant correlation between high proliferation rates and locoregional recurrences in stage I OTSCC patients (P-value=0.028). High-proliferative activity is thus related to an elevated risk of recurrence after surgery alone. We therefore conclude that Ki-67 expression level is a potentially useful clinical marker for predicting recurrence in surgically treated stage I OTSCC.

  • 42.
    Wäster, Petra
    et al.
    Linköping University, Department of Clinical and Experimental Medicine, Division of Cell Biology. Linköping University, Faculty of Medicine and Health Sciences.
    Orfanidis, Kyriakos
    Linköping University, Department of Clinical and Experimental Medicine, Division of Cell Biology. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Heart and Medicine Center, Department of Dermatology and Venerology.
    Eriksson, Ida
    Linköping University, Department of Clinical and Experimental Medicine, Division of Cell Biology. Linköping University, Faculty of Medicine and Health Sciences.
    Rosdahl, Inger
    Linköping University, Department of Clinical and Experimental Medicine, Division of Cell Biology. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Heart and Medicine Center, Department of Dermatology and Venerology.
    Seifert, Oliver
    Linköping University, Department of Clinical and Experimental Medicine, Division of Cell Biology. Linköping University, Faculty of Medicine and Health Sciences. Ryhov Hospital, Sweden.
    Öllinger, Karin
    Linköping University, Department of Clinical and Experimental Medicine, Division of Cell Biology. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Diagnostics, Department of Clinical Pathology and Clinical Genetics.
    UV radiation promotes melanoma dissemination mediated by the sequential reaction axis of cathepsins-TGF-beta 1-FAP-alpha2017In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 117, no 4, p. 535-544Article in journal (Refereed)
    Abstract [en]

    Background: Ultraviolet radiation (UVR) is the major risk factor for development of malignant melanoma. Fibroblast activation protein (FAP)-alpha is a serine protease expressed on the surface of activated fibroblasts, promoting tumour invasion through extracellular matrix (ECM) degradation. The signalling mechanism behind the upregulation of FAP-alpha is not yet completely revealed. Methods: Expression of FAP-alpha was analysed after UVR exposure in in vitro co-culture systems, gene expression arrays and artificial skin constructs. Cell migration and invasion was studied in relation to cathepsin activity and secretion of transforming growth factor (TGF)-beta 1. Results: Fibroblast activation protein-a expression was induced by UVR in melanocytes of human skin. The FAP-alpha expression was regulated by UVR-induced release of TGF-beta 1 and cathepsin inhibitors prevented such secretion. In melanoma cell culture models and in a xenograft tumour model of zebrafish embryos, FAP-alpha mediated ECM degradation and facilitated tumour cell dissemination. Conclusions: Our results provide evidence for a sequential reaction axis from UVR via cathepsins, TGF-beta 1 and FAP-alpha expression, promoting cancer cell dissemination and melanoma metastatic spread.

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