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  • 1601.
    Zhang, Hong
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Dermatology.
    Arbman, Gunnar
    Sun, Xiao-Feng
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Oncology.
    Codon 201 polymorphism of DCC gene is a prognostic factor in patients with colorectal cancer2003In: Cancer Detection and Prevention, ISSN 0361-090X, E-ISSN 1873-443X, Vol. 27, no 3, p. 216-221Article in journal (Refereed)
    Abstract [en]

    The polymorphism at codon 201 of the "deleted in colorectal carcinoma" (DCC) gene has been liked to susceptibility to colorectal cancer. However, its clinicopathological significance has not been reported. We examined the codon 201 polymorphism and loss of heterozygosity (LOH) by PCR-restriction fragment length polymorphism (PCR-RFLP) in 59 colorectal cancers, 48 samples from transitional mucosa and 67 samples from normal mucosa. The frequencies of the polymorphism did not significantly differ from normal to transitional mucosa and to tumor, but LOH was increased from transitional mucosa to tumor. Almost all of the LOH cases showed the polymorphism. The polymorphism was increased from well/moderately to poorly differentiated and to mucinous carcinoma (P = 0.03). The polymorphism was more frequently seen in advanced stages than in earlier stages (P = 0.02), and further predicted worse survival (P = 0.04). The data suggest that the codon 201 polymorphism of the DCC gene was a target of LOH, and predicted prognosis in colorectal cancer patients. ⌐ 2003 International Society for Preventive Oncology. Published by Elsevier Science Ltd. All rights reserved.

  • 1602.
    Zhang, Hong
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Cell biology.
    Evertsson, Sofia
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Oncology.
    Sun, Xiao-Feng
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Oncology.
    Clinicopathological and genetic characteristics of mucinous carcinomas in the colorectal.1999In: International Journal of Oncology, ISSN 1019-6439, Vol. 14, p. 1057-1061Article in journal (Refereed)
  • 1603.
    Zhang, Hong
    et al.
    Linköping University, Department of Biomedicine and Surgery, Division of dermatology and venereology. Linköping University, Faculty of Health Sciences.
    Nordenskjöld, Bo
    Linköping University, Department of Biomedicine and Surgery, Oncology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Oncology UHL.
    Dufmats, Monika
    Linköping University, Department of Biomedicine and Surgery, Oncology. Linköping University, Faculty of Health Sciences.
    Söderkvist, Peter
    Linköping University, Department of Biomedicine and Surgery, Cell biology. Linköping University, Faculty of Health Sciences.
    Sun, Xiao-Feng
    Linköping University, Department of Biomedicine and Surgery, Oncology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Oncology UHL.
    K-ras mutations in colorectal adenocarcinomas and neighbouring transitional mucosa.1998In: European Journal of Cancer, ISSN 0959-8049, E-ISSN 1879-0852, Vol. 34, no 13, p. 2053-2057Article in journal (Refereed)
    Abstract [en]

    The K-ras gene in codons 12 and 13 was investigated using allele-specific polymerase chain reaction in matched normal mucosa (n = 106), transitional mucosa (n = 69) and tumours (n = 149) from 149 patients with colorectal adenocarcinomas. K-ras mutations in codon 12 were detected in 41/149 (28%) of tumours and 4/69 (6%) of transitional mucosa samples, but not in the normal mucosa. Further, mutation rates were increased in younger patients (P = 0.001) and in mucinous carcinomas (50%) compared with well differentiated (17%), moderately differentiated (26%) or poorly differentiated (24%) tumours. Our findings indicate that mucinous carcinoma may represent a distinct genetic entity.

  • 1604.
    Zhang, Hong
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Division of dermatology and venereology.
    Rosdahl, Inger
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Division of dermatology and venereology. Östergötlands Läns Landsting, Centre for Medicine, Department of Dermatology and Venerology in Östergötland.
    Bcl-xL and bcl-2 proteins in melanoma progression and UVB-induced apoptosis.2006In: International Journal of Oncology, ISSN 1019-6439, Vol. 28, no 3, p. 661-666Article in journal (Refereed)
    Abstract [en]

    Whether bcl-xL and bcl-2 play an essential role in melanoma progression and UVB-induced apoptosis is not completely understood. We investigated the expression of bcl-xL and bcl-2 in matched primary and metastatic melanoma tumors and melanoma cell lines from the same melanoma patients to clarify the importance of bcl-xL and bcl-2 in melanoma progression and in UVB-induced apoptosis. The expression of bcl-xL and bcl-2 proteins was examined by immunohisto(cyto)chemistry and Western blot in melanoma tumors and melanoma cells. Cellular viability and apoptosis were estimated after the melanoma cells were exposed to 30, 60 and 180 mJ/cm2 UVB. Both primary melanoma tumors and melanoma cells showed lower expression of bcl-xL and bcl-2 proteins estimated as frequency of positive cells than their matched metastatic tumors and cells in vitro. After exposure to UVB, the cell viability decreased and the number of apoptotic cells increased in both primary and metastatic melanoma cell lines. These changes were more pronounced in the primary melanoma cells than in the matched metastatic cells. After UVB exposure, the expression of bcl-xL protein decreased in primary melanoma cells in a dose- and time-dependent manner, but the expression of bcl-2 was not influenced. The expression of bcl-xL and bcl-2 proteins was increased during melanoma progression from primary to metastatic melanoma. Reduction of bcl-xL, but not bcl-2 expression was involved in UVB-induced apoptosis in primary melanoma cells.

  • 1605.
    Zhang, Hong
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Division of dermatology and venereology.
    Rosdahl, Inger
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Division of dermatology and venereology. Östergötlands Läns Landsting, Centre for Medicine, Department of Dermatology and Venerology in Östergötland.
    Deletion in p16INK4a and loss of p16 expression in human skin primary and metastatic melanoma cells.2004In: International Journal of Oncology, ISSN 1019-6439, Vol. 24, no 2, p. 331-335Article in journal (Refereed)
    Abstract [en]

    p16INK4a gene mapped at chromosome 9p21 region encodes a tumor suppressor protein p16 which is frequently inactivated in human cancers, including skin melanoma. In order to clarify the importance of p16 alterations in melanoma, we examined the deletions of p16INK4a and expression of p16 protein in eight unselected primary and metastatic melanoma cell lines from human skin melanomas. Normal skin melanocytes were used as controls. Deletions of entire exons in the p16INK4a gene were detected by PCR technique and expression of the p16 protein was examined by Western blotting and immunocytochemistry. Results showed that the fragments from exons 2A, 2C and 3 in p16INK4a gene were totally deleted in the metastatic melanoma cell line, FM28.7 and the fragment from exon 3 was deleted in the metastatic melanoma cell line, FM55M2. P16 protein was strongly expressed in two of the primary melanomas cell lines (FM55P and RaH3). The p16 protein was weakly expressed in one of the metastatic melanoma cell lines (FM55M1) and negative in the other metastasis (FM55M2) as compared to their matched primary melanoma cells (FM55P). The p16 protein was strongly expressed in normal skin melanocytes. Immunocytochemistry showed that p16 protein was mainly localized in the nuclei of the melanoma cells and normal melanocytes, if it was expressed. Deletions of p16INK4a gene was uncommon and loss of p16 protein expression was common event in melanoma, especially in the later stages of melanoma.

  • 1606.
    Zhang, Hong
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Dermatology.
    Rosdahl, Inger
    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.
    Expression of oncogenes, tumour suppressor, mismatch repair and apoptosis-related genes in primary and metastatic melanoma cells.2001In: International Journal of Oncology, ISSN 1019-6439, Vol. 19, no 6, p. 1149-1153Article in journal (Refereed)
    Abstract [en]

    Several genetic alterations have been implicated in the development of malignant melanoma, but the expression of oncogenes, tumour suppressor, mismatch repair and apoptosis-related genes and their interactions in melanoma have not been completely clarified. We simultaneously examined the expression of p73, c-erbB-2, ras, p53, Mdm2, p27, DCC, hMLH-1, hMSH-2, bcl-2, Bax and NF-kappaB, by immunocytochemistry, in both primary and metastatic melanoma cell lines derived from melanoma patients. p73 was expressed in 7/8 cell lines, but stronger expressed in the metastatic cells than in the primary melanoma cells. c-erbB-2 was detected in all 8 cell lines and ras in 2/5 metastases. p53 was found in all the cell lines and Mdm2 in 1/8 of the cell lines. In the same patient, the intensity of p27 expression was decreased from the primary to the metastatic tumours. bcl-2 was expressed in all the cell lines. Bax was absent in 5/8 cell lines. In the same patient, Bax was weakly expressed in the primary tumour but lacking in the metastases. The data demonstrate that overexpression of p73, c-erbB-2, p53 and bcl-2, and loss of Mdm2 and Bax may interact and play important roles in the development and aggressiveness of human melanoma.

  • 1607.
    Zhang, Hong
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Division of dermatology and venereology.
    Rosdahl, Inger
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Division of dermatology and venereology. Östergötlands Läns Landsting, Centre for Medicine, Department of Dermatology and Venerology in Östergötland.
    Expression of p27 and MAPK proteins involved in all-trans retinoic acid-induced apoptosis and cell cycle arrest in matched primary and metastatic melanoma cells.2004In: International Journal of Oncology, ISSN 1019-6439, Vol. 25, no 5, p. 1241-1248Article in journal (Refereed)
    Abstract [en]

    We investigated whether p27 and mitogen-activated protein kinase (MAPK) proteins were involved in all-trans retinoic acid (atRA)-induced apoptosis and cell cycle arrest. Matched primary and metastatic melanoma cells were exposed to atRA. Apoptosis and cell cycle were detected by flow cytometry. Expression of p27, Ras, B-raf, Mek and Erk proteins was examined. Results showed that atRA induced apoptosis and cell cycle arrest in both primary and metastatic melanoma cells. The primary melanoma cells were more vulnerable than their matched metastatic cells. Expression of p27 was increased, while MAPK proteins were decreased, this response was dose- and time-dependent. Alterations of these proteins were more pronounced in primary melanoma cells than in the matched metastases. These data indicate that up-regulation of p27 and down-regulation of MAPK proteins were involved in atRA-induced apoptosis and cell cycle arrest in melanoma.

  • 1608.
    Zhang, Hong
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Division of dermatology and venereology.
    Rosdahl, Inger
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Division of dermatology and venereology. Östergötlands Läns Landsting, Centre for Medicine, Department of Dermatology and Venerology in Östergötland.
    Expression profiles of Id1 and p16 proteins in all-trans-retinoic acid-induced apoptosis and cell cycle re-distribution in melanoma2005In: Cancer Letters, ISSN 0304-3835, E-ISSN 1872-7980, Vol. 217, no 1, p. 33-41Article in journal (Refereed)
    Abstract [en]

    All-trans-retinoic acid (atRA) exerts its effects via apoptosis and cell cycle re-distribution. However, the mechanisms behind the effects have not been fully understood. In this study, we used a model system of matched primary and metastatic melanoma cells to investigate whether expression of Id1 and p16 proteins were involved in atRA-induced apoptosis and cell cycle re-distribution. Melanoma cells were exposed to 0.1 or 10 μM atRA for 1-96 h. Apoptosis and cell cycle were measured by flow cytometry. Expression of Id1 and p16 proteins was examined by Western blotting and immunocytochemistry. After exposure to atRA we found a marked increase in apoptosis and cell cycle re-distribution in both primary and metastatic melanoma cells. Expression level of Id1 protein was decreased and the p16 was increased in a dose- and time-dependent (P<0.05) manner after treatment with atRA. Alterations of these proteins were more pronounced in the primary melanoma cells than the matched metastases (P<0.05). These data suggested that the alterations of Id1 and/or p16 proteins were involved in atRA-induced apoptosis and cell cycle re-distribution in melanoma. These expression profiles of Id1 and p16 proteins may provide molecular evidence for better chemotherapy primarily for early stages of melanoma.

  • 1609.
    Zhang, Hong
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Division of dermatology and venereology.
    Rosdahl, Inger
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Division of dermatology and venereology. Östergötlands Läns Landsting, Centre for Medicine, Department of Dermatology and Venerology in Östergötland.
    Expression profiles of p53, p21, bax and bcl-2 proteins in all-trans-retinoic acid treated primary and metastatic melanoma cells.2004In: International Journal of Oncology, ISSN 1019-6439, Vol. 25, no 2, p. 303-308Article in journal (Refereed)
    Abstract [en]

    We have previously shown that all-trans-retinoic acid (atRA) induces apoptosis in melanoma cells and primary melanoma cells are more sensitive to the exposure of atRA than the matched metastases. However, mechanisms behind the atRA-induced apoptosis have not been studied. In this study, we used a similar cell culture model system of matched primary and metastatic melanoma cells from the same patient to investigate whether p53 and bcl-2 family proteins were involved in atRA-induced apoptosis. The primary and metastatic melanoma cells were exposed to 0.1 and 10 micro M atRA in serum-free RPMI 1640 cell culture medium in the dark for up to 96 h. The protein expression of p53, p21, bax and bcl-2 were examined by Western blotting and immunocytochemistry. Expression of p53, p21 and bax was increased, and bcl-2 was decreased in melanoma cells after exposure to atRA at different concentrations for various periods of time. The changes of p53, p21, bax, and bcl-2 protein levels were dose- and time-dependent. The primary melanoma cells were more sensitive to the atRA treatments than cells from matched metastatic melanoma. These data indicate that p53, p21, bax and bcl-2 proteins were involved in atRA-induced apoptosis in melanoma cells. Modification of these protein levels in the tumour cells might be beneficial for early treatment of melanoma.

  • 1610.
    Zhang, Hong
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Dermatology.
    Rosdahl, Inger
    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.
    Ultraviolet A and B differently induce intracellular protein expression in human skin melanocytes - A speculation of separate pathways in initiation of melanoma2003In: Carcinogenesis, ISSN 0143-3334, E-ISSN 1460-2180, Vol. 24, no 12, p. 1929-1934Article in journal (Refereed)
    Abstract [en]

    Ultraviolet (UV) irradiation has been involved in both initiation and promotion of carcinogenesis in melanoma. Alterations of cellular proliferation proteins, such as p73, Nup88, Id1 and p27 have been considered to play critical roles in melanoma development. However, the molecular mechanisms behind melanoma carcinogenesis are still poorly understood. In this study, we used human skin melanocytes as an experimental model system to investigate effects of UV irradiation on protein expression concerning cellular proliferation. The melanocytes prepared from human foreskin were separately exposed to various doses of UVA or UVB and post-cultivated for 24 or 48 h. Total proteins were isolated from the melanocytes, and expression of p73, Nup88, Id1, p27, bcl-2 and proliferating cell nuclear antigen (PCNA) proteins was examined by western blotting and immunocytochemistry. Results showed that expression of p73 and Nup88 was enhanced by UVA irradiation in a dose- and time-dependent manner. However, expression of Id1, p27, bcl-2 and PCNA proteins was not changed upon exposure to the UVA. Id1 and p27 proteins were over-expressed by exposure to UVB, but expression of p73, Nup88, bcl-2 and PCNA proteins was not changed by the UVB irradiation. The data suggested that UVA and UVB irradiation might lead to alterations of the different intracellular proteins. UVA enhanced protein expression concerning cell growth (p73 and Nup88) and UVB might over-express proteins concerning cellular proliferation (Id1 and p27). UVA and UVB may induce initiation of melanoma via separate intracellular pathways.

  • 1611.
    Zhang, Hong
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Dermatology.
    Satyamoorthy, K
    Herlyn, M
    Rosdahl, Inger
    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.
    All-trans retinoic acid (atRA) differentially induces apoptosis in matched primary and metastatic melanoma cells - A speculation on damage effect of atRA via mitochondrial dysfunction and cell cycle redistribution2003In: Carcinogenesis, ISSN 0143-3334, E-ISSN 1460-2180, Vol. 24, no 2, p. 185-191Article in journal (Refereed)
    Abstract [en]

    All-trans retinoic acid (atRA) has been suggested to exert its cytotoxicity via apoptosis but the mechanisms behind the damage effects have not been fully understood. In this study, we investigated the cytotoxic effects of atRA in eleven primary and matched metastatic cutaneous melanoma cell lines. All the primary and metastatic melanoma cell lines examined expressed the retinoic acid receptors. The cultured melanoma cells treated with atRA showed dysfunction of mitochondria and altered cell cycle distribution, inhibited cell proliferation and apoptosis. The cytotoxic effects of atRA were dose- and time-dependent. The dysfunction of mitochondria and altered cell cycle distribution, inhibited cell proliferation and apoptosis. The cytotoxic effects of atRA were dose- and time-dependent. The dysfunction of mitochondria and induction of apoptosis were more pronounced in the primary tumor cells than in the metastatic cell lines from the same patients. The data indicate that the cytotoxic effect of atRA was mediated through dysfunction of mitochondria, alterations in cell cycle and induction of apoptosis. Melanoma in early stage may have better response to atRA adjuvant therapy than the melanoma in late stage, suggesting the early utility of atRA in melanoma chemotherapy.

  • 1612.
    Zhang, Hong
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Dermatology.
    Schneider, José
    Rosdahl, Inger
    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.
    Expression of p16, p27, p53, p73 and Nup88 proteins in matched primary and metastatic melanoma cells.2002In: International Journal of Oncology, ISSN 1019-6439, Vol. 21, no 1, p. 43-48Article in journal (Refereed)
    Abstract [en]

    Cutaneous melanoma is a tumor with high metastatic potential, but the mechanisms leading to progression are still not fully understood. In this study, we examined whether p16, p27, p53, p73 and Nup88 proteins were involved in the progression from primary to metastatic melanomas by immunocytochemistry and Western blotting in eleven melanoma cell lines from five matched primary and metastatic melanomas. We demonstrated that the primary and metastatic melanomas expressed differently p16, p27, p73 and Nup88 proteins. When expressed in the primary melanoma cells p16 and p27 were lost or reduced in almost all the metastatic melanoma cell lines. In contrast, p73 and Nup88 were expressed in most of the tested melanoma cell lines and were increased in the metastatic melanomas. p53 was expressed at the same level in both the primary and metastatic melanoma cells. These data suggest that a reduced expression of p16 and p27 and an enhanced expression of p73 and Nup88 might play an important role in the progression of melanoma from primary tumor to metastasis.

  • 1613.
    Zhang, Hong
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Dermatology.
    Sun, Xiao-Feng
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Oncology.
    Loss of p27 expression predicts poor prognosis in patients with Dukes' B stage or proximal colorectal cancer.2001In: International Journal of Oncology, ISSN 1019-6439, Vol. 19, no 1, p. 49-52Article in journal (Refereed)
    Abstract [en]

    p27 is a cyclin-dependent kinase inhibitor which regulates progression of cells from G1 into S phase in a cell cycle. Loss of the negative regulator may contribute to oncogenesis and tumor progression. The aim of this study was to examine p27 expression in normal mucosa, primary and metastatic tumors from patients with colorectal adenocarcinomas and to analyze association of p27 with patient survival and clinicopathological variables. p27 expression was estimated by immunohistochemistry in 178 primary colorectal cancers, 34 lymph node metastases and 48 normal mucosa samples from patients with colorectal adenocarcinoma. Associations of p27 with patient survival, clinicopathological characteristics and expression of p53, p73 and DCC were analyzed. Loss of p27 was found in 51% of primary tumors, 68% of metastases and 56% of normal samples. The intensity of p27 staining was similar in the matched primary tumor, metastasis and normal mucosa. In patients with Dukes' B or with proximal tumors, the loss of p27 predicted poorer prognosis (p = 0.03 and p = 0.05, respectively). However, there were no significant differences in the patients with other individual Dukes' stage or distal tumors. No relationships were found between p27 and patients' gender, age, tumor location, growth pattern and expression of p53, p73 and DCC (p > 0.05). The data suggest that loss of p27 was associated with poor prognosis in patients with Dukes' B tumor or those with proximal tumor. p27 might be a useful marker to identify the more progressive tumors in these groups.

  • 1614.
    Zhang, Hong
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Dermatology.
    Sun, Xiao-Feng
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Oncology.
    Overexpression of cyclooxygenase-2 correlates with advanced stages of colorectal cancer2002In: American Journal of Gastroenterology, ISSN 0002-9270, E-ISSN 1572-0241, Vol. 97, no 4, p. 1037-1041Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: We aimed to investigate the associations of cyclooxygenase-2 (COX-2) with pathological features and survival in patients with colorectal cancer. METHODS: The expression of COX-2 was examined by immunohistochemistry in 112 primary colorectal cancers, with 64 samples from the corresponding normal mucosa and 16 metastases in the regional lymph nodes of patients with colorectal cancer. The associations of COX-2 expression with clinico-pathological features, including survival, were analyzed. RESULTS: The frequency and intensity of COX-2 staining were remarkably increased from the normal samples (17%) to the primary tumors (72%) and to the metastases (100%). Expressions of COX-2 were 25%, 74%, 78%, and 67% in Dukes' A, B, C, and D tumors, respectively (p = 0.005), and positively related to proliferative activity (p = 0.003). COX-2 expressions were 80% in colonic tumors and 60% in rectal tumors (p = 0.03). The expression of COX-2 was positively related to the better differentiated tumors in the colon (p = 0.04). We were unable to find any relationship of COX-2 with patient age, sex, tumor growth pattern, apoptosis, and patient survival (p > 0.05). CONCLUSION: We found that the expression of COX-2 was upregulated from normal cells to primary tumors and to metastases, and related to proliferative activity, tumor location, Dukes' stage, and differentiation. These results further support the evidence that COX-2 may be involved in tumorigenesis and development of colorectal cancer. ⌐ 2002 by Am. Coll. of Gastroenterology.

  • 1615.
    Zhang, Hong
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Division of dermatology and venereology.
    Sun, Xiao-Feng
    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.
    Synnerstad, Ingrid
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Division of dermatology and venereology. Östergötlands Läns Landsting, Centre for Medicine, Department of Dermatology and Venerology in Östergötland.
    Rosdahl, Inger
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Division of dermatology and venereology. Östergötlands Läns Landsting, Centre for Medicine, Department of Dermatology and Venerology in Östergötland.
    Importance of FAS-1377, FAS-670, and FASL-844 polymorphisms in tumor onset, progression, and pigment phenotypes of Swedish patients with melanoma: a case-control analysis.2007In: Cancer Journal, ISSN 0765-7846, E-ISSN 1292-8658, Vol. 13, no 4, p. 233-237Article in journal (Refereed)
    Abstract [en]

    PURPOSE: Human skin melanoma at later stages usually has an extremely poor prognosis. It is of importance to search for biologic markers to identify and monitor individuals at risk for melanoma for early diagnosis and to avoid tumor progression. The FAS gene and its natural ligand (FASL) gene initiate the death signal cascade, playing a central role in the apoptotic signaling pathway and tumor growth and metastasis. PATIENTS AND METHODS: In this study, we analyzed polymorphisms in 229 patients with melanoma and 351 age- and gender-matched tumor-free individuals. Genomic DNAs were isolated from mononuclear cells in peripheral vein blood, and the polymorphisms were examined with polymerase chain reaction-restriction fragment length polymorphism techniques. Frequency in distribution of the polymorphisms was compared between the patients with melanoma and the healthy control subjects, and associations with patients' pigment phenotypes, age at diagnosis, and melanoma characteristics were analyzed. RESULTS AND CONCLUSIONS: The FAS-1377, FAS-670, and FASL-844 polymorphisms were not found to be markers of melanoma risk (P > 0.05). In patients with melanoma, frequencies of the FAS-1377, FAS-670, and FASL-844 polymorphisms were different between the patients aged <50 and > or =50 years (P < or = 0.025, P < or = 0.025, and P < or = 0.01). Moreover, the FAS-670 polymorphism correlated with tumor Breslow thickness (P < or = 0.01) and Clark level (P < or = 0.001) and was associated with tumors developing in sun-exposed locations (P < or = 0.001). FAS and FASL were not markers for melanoma risk but might be important in the development and progression of sun-induced melanoma independently of skin type.

  • 1616.
    Zhang, Zhiyong
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Oncology.
    Zhao, Zeng-Ren
    Adell, Gunnar
    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.
    Jarlsfelt, Ingvar
    Cui, Yong-Xing
    Kayed, Hany
    Kleeff, Jörg
    Wang, Ming-Wei
    Sun, Xiao-Feng
    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.
    Expression of MAC30 in rectal cancers with or without preoperative radiotherapy2007In: Oncology, ISSN 0890-9091, Vol. 71, no 3-4, p. 259-265Article in journal (Refereed)
    Abstract [en]

    Objective: Meningioma-associated protein (MAC30) is overexpressed in several types of cancers, but its therapeutic implication in the patients has not been studied. We examined the relationship of MAC30 with clinicopathological and biological factors in rectal cancer patients with or without radiotherapy (RT). Methods: MAC30 was immunohistochemically examined in 75 distant and 91 adjacent normal mucosa specimens, 132 primary tumours and 39 lymph node metastases from rectal cancer patients participating in a clinical trial of preoperative RT. Results: In the RT group, MAC30 was or tended to be positively correlated with infiltrated growth pattern (p = 0.02), PRL (phosphatase of regenerating liver, p = 0.01) and Ki-67 expression (p = 0.06). MAC30 at the invasive margin of the metastasis was related to poor survival (p = 0.02) in the whole group of patients. MAC30 in primary tumours was not related to recurrence and survival in the non-RT or RT group. Conclusions:MAC30 expression in metastasis was an indicator for poor survival. After RT, MAC30 seemed to be more related to aggressive morphological and biological factors, however, we did not find direct evidence that MAC30 expression was related to the outcome of patients with or without RT. Copyright © 2006 S. Karger AG.

  • 1617. Zhang, Zhi-Yong
    et al.
    Zhao, Zeng-Ren
    Jiang, Li
    Li, Jia-Chen
    Gao, Yan-Min
    Cui, Dong-Sheng
    Wang, Che-Jiang
    Schneider, Jose
    Wang, Ming-Wei
    Sun, Xiao-Feng
    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.
    Nup88 expression in normal mucosa, adenoma, primary adenocarcinoma and lymph node metastasis in the colorectum2007In: Tumor Biology, ISSN 1010-4283, E-ISSN 1423-0380, Vol. 28, no 2, p. 93-99Article in journal (Refereed)
    Abstract [en]

    Objectives: It was the aim of this study to investigate Nup88 expression in normal colorectal mucosa, adenoma, adenocarcinoma and lymph node metastasis, as well as the relationship between Nup88 expression and clinicopathological features. Methods: Nup88 expression was examined by immunohistochemistry in 84 normal mucosa samples, 32 adenomas, 181 primary adenocarcinomas, and 18 lymph node metastases from colorectal tumour patients. Results: Nup88 expression was observed in normal epithelial and tumour cells. The frequency of strong Nup88 expression was increased from normal mucosa or adenoma to primary tumour and lymph node metastasis (p < 0.0001). There was no significant difference in the expression between normal mucosa and adenoma (p = 0.41). The frequency of strong Nup88 expression was higher in ulcerated tumours (40%) than in polypoid/large fungating tumours (23%, p = 0.048). The frequency of strong Nup88 expression was significantly different among tumours with good (21%), moderate (42%) and poor differentiation (48%, p = 0.01). Nup88 expression was not related to the patients' gender, age, tumour location, size, histological type, invasive depth, lymph node status and Dukes stage (p > 0.05). Conclusion: Our results suggest that Nup88 may play a role during the development, aggressiveness and differentiation of colorectal tumours. Copyright © 2007 S. Karger AG.

  • 1618.
    Zhao, Ming
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Neuroscience and Locomotion, Pathology.
    Liu, Yawei
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Neuroscience and Locomotion, Pathology.
    Bao, Mingmin
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Cell biology.
    Kato, Yutaka
    Han, Jiahuai
    Eaton, John Wallace
    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.
    Vascular smooth muscle cell proliferation requires both p38 and BMK1 MAP kinases2002In: Archives of Biochemistry and Biophysics, ISSN 0003-9861, E-ISSN 1096-0384, Vol. 400, no 2, p. 199-207Article in journal (Refereed)
    Abstract [en]

    Vascular smooth muscle cell (VSMC) proliferation is a key event in the progression of atherosclerosis. Induction of both c-fos (through the transcription factor Elk-1) and c-jun, both immediate early genes, is important for the stimulation of VSMC proliferation and migration. It was earlier found that p38 mitogen-activated protein (MAP) kinase upregulates c-jun gene transcription through phosphorylation of two myocyte enhancer factor 2 (MEF2) family transcription factors, MEF2A and MEF2C, while big MAP kinase 1 (BMK1) may upregulate c-jun gene transcription through MEF2A, MEF2C, and also MEF2D. Here, we report that inhibition of BMK1 by a dominant negative form of MEK5 or pharmacologic inhibition of p38 by SB 203580 additively suppress serum-induced VSMC proliferation. This additive effect of p38 and BMK1 inhibition implies that these two kinases coordinately regulate MEF2 transcription factors. The exclusive activation of MEF2D by BMK1 appears required for this cooperative upregulation of c-jun in VSMC, and coactivation of p38 and BMK1 also has additive effects on the activation of a reporter gene linked to the c-jun promoter in our experimental system. Thus, coordinate activity of both the p38 and BMK1 pathways appears necessary for optimal transcription of c-jun and, pari pasu, VSMC proliferation. These results may have implications for the future design of pharmacologic agents for inhibition of VSMC growth.

  • 1619. Zhao, Zeng-Ren
    et al.
    Zhang, Zhi-Yong
    Cui, Dong-Sheng
    Jiang, Li
    Zhang, Hui-Jun
    Wang, Ming-Wei
    Sun, Xiao-Feng
    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.
    Particularly interesting new cysteine-histidine rich protein expression in colorectal adenocarcinomas2006In: World Journal of Gastroenterology, ISSN 1007-9327, E-ISSN 2219-2840, Vol. 12, no 2, p. 298-301Article in journal (Refereed)
    Abstract [en]

    Aim: To study the relationship between particularly interesting new cysteine-histidine rich protein (PINCH) expression and clinicopathological factors in Chinese colorectal cancer patients. Methods: The expression of PINCH was examined by immumohistochemistry in 141 samples of primary colorectal adenocarcinoma and 92 normal samples of colorectal mucosa. Eighty of the cases had both primary tumour and normal mucosa from the same patients. Results: PINCH was expressed in the stroma of normal mucosa and tumours. PINCH expression in tumourassociated stroma was increased compared to normal mucosa in both unmatched cases (n = 141, X2 = 85.79, df = 3, P<0.0001) and matched cases (n = 80, X2 = 45.86, df = 3, P<0.0001). Among 135 tumours with visible invasive margin, 86 (64%) showed stronger PINCH expression at the invasive margin than in the intratumoural stroma. The frequency of PINCH strong expression in mucinous and signet-ring cell carcinomas was higher (52%) compared to non-mucinous carcinomas (29%, X2= 5.13, P= 0.02). We did not find that PINCH expression was related to patient's gender, age, tumour location, tumour size, gross status, histological type, differentiation, invasion depth, lymph node status and Dukes' stage (P>0.05). Conclusion: The expression of PINCH was upregulated in colorectal cancers, and especially at the margin of tumours, and further was related to mucinous and signet-ring cell carcinomas. The results suggest that expression of PINCH may be involved in the tumourigenesis and aggressiveness of colorectal cancers. © 2006 The WJG Press. All rights reserved.

  • 1620. Zhou, Xiao-Lei
    et al.
    Eriksson, Ulrika
    Werelius, Barbro
    Kressner, Ulf
    Sun, Xiao-Feng
    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.
    Lindblom, Annika
    Definition of candidate low risk APC alleles in a Swedish population2004In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 110, no 4, p. 550-557Article in journal (Refereed)
    Abstract [en]

    Many families experience an apparently inherited increased risk of colorectal cancer (CRC) similar to the known syndromes familial adenomatous polyposis (FAP) and hereditary nonpolyposis colorectal cancer (HNPCC). Besides these high-risk syndromes, approximately 10% of all CRC cases come from families with 2 affected 1st-degree relatives, and even 1st-degree relatives to a single case of CRC are at increased risk. Risk subjects from these families frequently show polyps at colonoscopy, which suggests the APC gene as a good candidate susceptibility gene for these attenuated polypotic syndromes. We used the sensitive DHPLC technique to search for possible predisposing germline mutations in the entire APC gene in 91 risk subjects from these high- and low-risk syndromes with unknown predisposing genes. Most exons were also screened for mutations in 96 normal controls and 96 colorectal cancer cases. In our study we probably have identified the most common APC variants in a Swedish population. Among 30 germline variants identified, 1 clearly pathogenic nonsense mutation and 11 putative pathogenic variants (10 missense and one 3′ UTR) were found in 20 index patients (22%). Twelve silent as well as 5 intronic variants were considered nonpathogenic. Two of the missense variants found here, E1317Q and D1822V, have previously been related to a difference in risk of colorectal cancer. One variant, 8636C>A, located within the 3′ UTR region of the APC gene, was suggested to constitute an additional low risk allele with a similar relative risk as the Jewish 11307K mutation (OR = 1.8, 9S% CI, 0.96-3.40). The question of whether all the other variants confer an increased colorectal cancer risk warrants future large association studies. © 2004 Wiley-Liss, Inc.

  • 1621.
    Zhuang, Shi-Mei
    Linköping University, Department of Biomedicine and Surgery, Cell biology. Linköping University, Faculty of Health Sciences.
    Molecular genetic alterations in chemically-induced lymphomas1999Doctoral thesis, comprehensive summary (Other academic)
    Abstract [en]

    Lymphoma is one of the most common malignancies in humans. Its incidence has increased rapidly in the past 30 years. However, the molecular mechanisms underlying the development of lymphomas are largely unknown.

    Environmental carcinogens play an important role in tumorigenesis. 1,3-butadiene (BD) and 2~,3-dideoxycytidine (ddC) are two carcinogens to which humans are exposed. Cancer bioassays in mice have revealed that both BD and ddC induce high frequencies of lymphomas. The present study provides a genetic dissection of these chemically-induced lymphomas, with a focus on identification of potential turner suppressor loci and genetic alterations in genes involved in the pRb, p53 and Ras/Raf pathways. These pathways are important in the control of cell proliferation.

    Approximately 87% of BD-induced and 75% of ddC-induced lymphomas show allelic losses or mutations in genes examined. Similar frequencies for inactivation of the p53 pathway were observed in BD- and ddC-induced tumors, whereas disruption of the pRb pathway is more common in ddC-induced lymphomas. On the other hand, BD-induced tumors display more frequent activation of the Ras/Raf pathway. These data indicate the genotoxicity of both ddC and BD, and also confirm the carcinogenicity of these chemicals at a molecular level.

    This study also reveals that different genetic alterations occur in distinct stages of the development of BD-induced lymphomas. Ras mutations were detected in tumors derived from mice exposed to BD for only 26 weeks or at a rather low concentration (20 ppm), suggesting that ras mutations may occur early in tumor formation. In contrast, all six tumors with aberrations of p53 occurred in the high dose (625 ppm), continuous long-term exposure group, and these tumors appear to have a more aggressive phenotype, indicating that inactivation of p53 may be a late event, associated with progression of BD-induced lymphomas. Furthermore, two or more genetic alterations were found in 67% of tumors from the 625 ppm dose group and in only 46% of lymphomas derived from mice exposed to s312 ppm of BD. In addition, more than five genetic aberrations occurred only in the 625 ppm dose group. These results support the contention that there is a dose-dependent increase of genetic alterations in BD-induced tumors.

    The mutational pattern resulting from carcinogen-exposure has been observed in both human and animal turners. In the present study, the specific K-ras codon 13 CGC mutation and allelic loss of the Rafl locus on chromosome 6 were detected only in BD-induced lymphomas, while frequent allelic loss of the telomeric region of chromosome 2 was observed only in ddC-induced tumors, suggesting an agent-specific effect.

    The genome-wide screen of allelic losses revealed that multiple potential tumor suppressor genes contribute to the development of BD- and ddC-induced lymphomas. Moreover, most of the identified regions with frequent allelic losses carry unknown tumor suppressor genes, whose isolation and identification are of great interest for further investigation.

  • 1622.
    Zhuang, Shi-Mei
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Cell biology.
    Wiseman, Roger W
    Söderkvist, Peter
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Cell biology.
    Frequent mutations of the Trp53,Hras1 and beta-catenin (Catnb) genes in 1,3-butadiene-induced mammary adenocarcinomas in B6C3F1 mice2002In: Oncogene, ISSN 0950-9232, E-ISSN 1476-5594, Vol. 21, no 36, p. 5643-5648Article in journal (Refereed)
    Abstract [en]

    DNAs from 1,3-butadiene-induced mammary adenocarcinomas of B6C3F1 mice were examined for mutations in the Trp53 gene, the ras gene family and several components of the Wnt signaling pathway, including ▀-catenin (Catnb), Apc and Axin. Trp53 mutations were detected in 41% (7 out of 17) of tumors. Each tumor with a Trp53 mutation also exhibited loss of the wildtype Trp53 allele, supporting the importance of Trp53 inactivation during development of these tumors. Analyses of the Hras1, Kras2 and Aras proto-oncogenes revealed Hras1 mutations in 53% (9 out of 17) of tumors. Seven of these mutations were a G?C transversion in Hras1 codon 13, consistent with a 1,3-butadiene-specific Kras2 mutation previously reported in several other tumor types. Mutation screens in Catnb exon 2, the Apc mutation cluster region and the Catnb-binding domain of the Axin gene identified Catnb missense mutations in 3 out of 17 (18%) tumors. In total, mutations of the Trp53, Hras1 and/or Catnb genes were identified in 15 out of 17 1,3-butadiene-induced mammary adenocarcinomas. These results indicate that multiple genetic pathways are disrupted in chemically induced mammary tumors, and that studies in mouse models may help to understand the etiology of human breast cancers.

  • 1623.
    Zhuang, Shi-Mei
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Cell biology.
    Wiseman, Roger W
    Söderkvist, Peter
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Cell biology.
    Mutation analysis of the pRb pathway in 2',3'-dideoxycytidine- and 1,3-butadiene-induced mouse lymphomas2000In: Cancer Letters, ISSN 0304-3835, E-ISSN 1872-7980, Vol. 152, no 2, p. 129-134Article in journal (Refereed)
    Abstract [en]

    The pRb pathway plays a key role in controlling the G1/S transition in cell cycle progression. Aberrations of various components of the pRb pathway, such as retinoblastoma protein and its upstream actors including cyclin D1, cyclin dependence kinase-4 and p16/p15 cyclin dependent kinase inhibitors, have been reported in a variety of human tumors. Furthermore, the alterations of retinoblastoma protein and its upstream components often occur in a reciprocal manner. Previously, we have reported frequent inactivation of the Cdkn2a/Cdkn2b loci encoding p16/p15 cyclin dependent kinase inhibitors in a subset of 2',3'-dideoxycytidine- and 1,3-butadiene-induced mouse lymphomas (S.-M. Zhuang, A. Schippert, A. Haugen-Strano, R.W. Wiseman, P. Soderkvist, Inactivation of p16(INK4a)-a, p16(INK4a)-▀ and p15(INK4b) genes in 2',3'-dideoxycytidine- and 1,3-butadiene-induced lymphomas, Oncogene 16 (1998) 803-808), indicating the involvement of pRb pathway in lymphomagenesis. To investigate whether alteration of other components in pRb pathway is an alternative mechanism underlying the development of these chemically induced lymphomas, we have examined the genetic status of Rb1, Ccnd1 and Cdk4 genes that encode retinoblastoma protein, cyclin D1 and cyclin dependence kinase-4, respectively. Gross alterations of the Rb1, Ccnd1, and Cdk4 genes were not detected by Southern analysis in any of the tumors examined. In addition, single-strand conformation analysis failed to reveal point mutations in the Cdk4 amino terminal domain that is important for its association with Cdkn2a gene products. These results indicate that the mechanisms underlying the development of 2',3'-dideoxycytidine- and 1,3-butadiene-induced lymphomas involve inactivation of p16/p15 cyclin-dependent kinase inhibitors but not genomic alterations of the Rb1, Ccnd1 and Cdk4 genes. Copyright (C) 2000 Elsevier Science Ireland Ltd.

  • 1624. Åkerblom, B
    et al.
    Lindahl, Tomas
    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.
    Larsson, A
    ADP activation induces bFGF binding to platelets in vitro2002In: Upsala Journal of Medical Sciences, ISSN 0300-9734, E-ISSN 2000-1967, Vol. 107, no 3, p. 165-171Article in journal (Refereed)
    Abstract [en]

    Basic fibroblast growth factor (bFGF), is a heparin-binding factor with potent angiogenic properties in vitro and in vivo. bFGF is involved in tumour growth, but it has also been shown to reduce infarct size in experimentally induced acute myocardial infarction. Platelets are also believed to have an important role in both tumour growth and myocardial infarction. We have studied bFGF binding to platelets by flow cytometry. Platelet activation by ADP induces bFGF binding to platelets. bFGF bound to activated platelets will result in a locally high concentration of bFGF in patients with myocardial infarctions and malignant tumours. Addition of recombinant bFGF to platelet rich plasma reduced the percentage of fibrinogen positive platelets. bFGF may thus have an inhibitory effect on platelet aggregation.

  • 1625. Åkerlund, Emma
    et al.
    Erlandsson, Ulf
    Sjöberg, Folke
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Division of surgery. Östergötlands Läns Landsting, Reconstruction Centre, Department of Plastic Surgery, Hand surgery UHL.
    Huss, Fredrik
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Division of surgery. Östergötlands Läns Landsting, Reconstruction Centre, Department of Plastic Surgery, Hand surgery UHL.
    Brännskador: Antalet skadade och avlidna sjunker kontinuerligt men äldre utgör fortsatt en riskgrupp2007In: Nordisk geriatrik, ISSN 1403-2082, Vol. 10, no 3Article in journal (Refereed)
  • 1626. Åkerlund, Emma
    et al.
    Huss, Fredrik
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Division of surgery. Östergötlands Läns Landsting, Reconstruction Centre, Department of Plastic Surgery, Hand surgery UHL.
    Sjöberg, Folke
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Division of surgery. Östergötlands Läns Landsting, Reconstruction Centre, Department of Plastic Surgery, Hand surgery UHL.
    Burns in Sweden: An analysis of 24 538 cases during the period 1987-20042007In: Burns, ISSN 0305-4179, E-ISSN 1879-1409, Vol. 33, no 1, p. 31-36Article in journal (Refereed)
    Abstract [en]

    Burn care is always progressing, but there is little epidemiological information giving a clear picture of the current number of treated burns in Sweden. This study was conducted to provide an update of patients admitted to hospital with burns in Sweden. Data were obtained for all patients who were admitted to hospitals with a primary or secondary diagnosis of burns (ICD-9/10 codes) from 1 January 1987 to 31 December 2004, 24 538 patients were found. Most of the patients were male (69%), giving a male:female ratio of 2.23:1. Children in the age-group 0-4 years old predominated, and accounted for 27% of the study material. The median length of stay was 3 days. Throughout the period 740 patients (3%) died of their burns. Significant reductions in mortality, incidence, and length of stay were seen during the study, which correlates well with other studies. However, most of the reductions were in the younger age-groups. Men accounted for the improved mortality, as female mortality did not change significantly. We think that the improvement in results among patients admitted to hospital after burns is a combination of preventive measures, improved treatment protocols, and an expanding strategy by which burned patients are treated as outpatients. © 2006 Elsevier Ltd and ISBI.

  • 1627.
    Årstrand, Kerstin
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Division of clinical chemistry.
    Kullman, Anita
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Division of clinical chemistry.
    Andersson, R
    Rasmuson, T
    Kågedal, Bertil
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Division of clinical chemistry. Östergötlands Läns Landsting, Centre for Laboratory Medicine, Department of Clinical Chemistry.
    Improved method for analysis of cysteinyldopa in human serum2004In: Scandinavian Journal of Clinical and Laboratory Investigation, ISSN 0036-5513, E-ISSN 1502-7686, Vol. 64, no 6, p. 559-564Article in journal (Refereed)
    Abstract [en]

    5-S-L-Cysteinyl-L-dopa is a well-known pigment intermediate and analysis of its serum concentration is well suited for evaluation of treatment and follow-up of stage III and IV malignant melanoma. A simplified analytical method is described using organic extraction followed by clean-up on a boronate gel to capture the compound containing vicinal hydroxyls. Weak acid solution elutes the 5-S-cysteinyldopa suitable for high-performance liquid chromatography (HPLC). The absolute recoveries of cysteinyldopa and its diastereomer 5-S-D-cysteinyl-L-dopa (used as an internal standard) were 81.5±2.8% and 81.3±2.7%, respectively, and use of the internal standard for the whole procedure gave an analytical recovery of 101±0.8%. The limit of quantitation was 1.5 nmol/L and the imprecision of the method was < 5.0% over the analytical range 1.5-500 nmol/L. The method is cheap and easy to perform and compares well with other described techniques. The use of the method is illustrated by results obtained during treatment of a patient with metastatic malignant melanoma.

  • 1628.
    Åstradsson, Eva
    et al.
    Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Oncology UHL.
    Granath, Lena
    Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Oncology UHL.
    Heedman, Per-Anders
    Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Oncology UHL.
    Starkhammar, Hans
    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.
    Cancer patients hospitalised for palliative reasons. Symptoms and needs presented at a University Hospital2001In: Supportive Care in Cancer, ISSN 0941-4355, E-ISSN 1433-7339, Vol. 9, no 2, p. 97-102Article in journal (Refereed)
    Abstract [en]

    The aim of this study was to identify patients in need of palliative care in 11 different care units with a total of 256 beds at Link÷ping University Hospital and to look at their overall situation with respect to assessed symptom control and quality of life. There were 46 patients fulfilling the two criteria of incurable cancer and need for palliative care, and each was assessed with the aid of a questionnaire (five oral questions on life situation) and a single visual analogue scale (VAS) about their overall quality of life (QoL). Each patient also assessed him- or herself on the Edmonton Symptom Assessment Scale (ESAS). Total ESAS scores ranged from 20 to 639 mm (median 211). Median VAS scores (100 mm = greatest symptom severity) were as follows: nausea 6 mm, pain 9 mm, anxiety 17 mm, depression 18 mm, drowsiness 35 mm, activity 38 mm, appetite 45 mm, and sensation of well-being 46 mm. The median score for QoL was 47 and correlated well with the total ESAS score. Thirty-seven patients answered the open question "What in your current situation troubles you the most?". Seven patients answered "nothing", and 10 said "the present symptoms". Twenty patients had different concerns (existential, social, and psychological). The low number of hospitalised patients found reflects a well-functioning hospital-based home-care unit. Reduced appetite, sensation of well-being and activity were dominant, while pain and nausea were less intense. The simple QoL-VAS seemed to be comparable to ESAS, which is more useful for assessing each single symptom. The non-physical dimensions need more attention in the future in order to achieve totally satisfactory palliative care.

  • 1629.
    Öhman, Hans
    Linköping University, Department of Biomedicine and Surgery, Division of dermatology and venereology. Linköping University, Faculty of Health Sciences.
    Studies on the pH gradient in normal and ichthyotic human skin1998Licentiate thesis, comprehensive summary (Other academic)
    Abstract [en]

    In search for pathogenetic mechanisms underlying hyperkeratosis, we examined the pH gradient across the stratum corneum in normal and ichthyotic skin. Twenty students and employees, (12 men and 8 womenaged 25-69 years) served as controls. Patients with ichthyoses were recruited from the outpatient clinic (13 men aged 12-71 years). Diagnosis was made on the basis of clinical examination and serum lipid electrophoresis.

    For recording pH values, a flat glass electrode was repeatedly applied to the skin during tape stripping of volar forearm skin. Before stripping, surface pH (mean±SD) was higher in autosomal dominant ichthyosis vulgaris (IV) (5.2±0.3; n=7) than in x-linked recessive ichthyosis (XRI) (4.6±0.2; n=6) and healthy control skin (4.5±0.2; n=7). This comparision was made between men since a sex difference was observed when comparing men and women in the control group (4.5±0.2; n=7 for men and 5.3±0.5 for women).

    Removal of stratum corneum, which required 170-200 strippings in ichthyotic skin and 100-120 strippings in healthy control skin, dicsclosed markedly different pH variations in the two types of ichthyoses. The major abnormality in IV skin was that a neutral pH was attained already after half the total number of strippings through the hyperkeratotic stratum corneum, which may reflect a lack of acidickeratohyalin breakdown products in this condition.This in contrast to XRI where the pH gradient was less steep and eventually plateaued at pH 6.2-6.6 instead of at 6.7-7.0 as in normal skin. A likely explanation is the accumulation of cholesterol sulfate in lower stratum corneum which occurs in XRI.

    Our results suggest that the 'acid mantle' of normal skin, which penetrates deep into the stratum corneum, is the combined result of cornification-associated organic acids and back-diffusion of of acid material from the surface. Since comeocyte desquamation involves many pH dependent enzymes, abnormalities in the transcomeal pH gradient might play a role in the pathogenesis of ichthyoses.

  • 1630.
    Öhman, Hans
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Division of dermatology and venereology. Östergötlands Läns Landsting, Centre for Medicine, Department of Dermatology and Venerology in Östergötland.
    The pH gradient in the epidermis evaluated by serial tape stripping2006In: Handbook of non-invasive methods and the skin / [ed] Gary L. Grove ,Gregor B.E. Jemec and Jorgen Serup, Boca Raton, Florida: Taylor & Francis , 2006, 2, p. 421-427Chapter in book (Other academic)
    Abstract [en]

    Inbunden

                Handbook of Non-Invasive Methods and the Skin       

    Engelska, 2006Firmly established as the leading international reference in this field, Non-Invasive Methods and the Skin broke new ground with its comprehensive coverage of methods used in both clinical and experimental dermatology. Completely revised and updated, containing more than twice as much information, the Second Edition continues the tradition. The authors' thorough research and clear organization make this book a baseline reference for those using noninvasive biophysical methods to study the skin.  Arranged by physical modality and structured to provide educational and practical information, the second edition, like its predecessor, will prove to be of value to young researchers and senior scientists alike. The coverage of major evaluation and measurement methods share a consistent format, including scope, sources of error, application, and validity. This edition incorporates 69 revised chapters with more than 90 new chapters covering topics such as computer technique, imaging techniques, skin friction, barrier functions, and more.New chapters provide coverage of: computers, computer techniques, and image analysis imaging techniques, including clinical photography legal situations and guidelines behind instrumental use skin friction barrier functions important new techniques such as in vitro confocal microscopy, OCT, and Raman spectroscopy veterinary/animal research use of methods  The truly interdisciplinary, international panel of contributors includes experts from the specialties of dermatology, bioengineering, pathology, manufacturing engineering, medical physics, pharmacology, microbiology, neurology, surgery, obstetrics and gynecology, cardiovascular research, and pharmacy from academic institutions and hospitals in countries such as Denmark, Germany, the United Kingdom, the United States, Japan, Israel, Taiwan, and Singapore. The revision is extensive and covers a broad spectrum of methods while providing the same caliber of authoritative information that made the previous edition so popular. Application oriented, practical, and instructive, this Second Edition will meet the needs of the researchers today, and in years to come.

  • 1631.
    Öhman, Sten
    Linköping University, Department of Biomedicine and Surgery, Clinical Chemistry. Linköping University, Faculty of Health Sciences.
    Diagnostic methods for demonstration of intrathecal synthesis of immunoglobulines within the central nervous system1994Doctoral thesis, comprehensive summary (Other academic)
    Abstract [en]

    This thesis is based upon studies of quantitative and qualitative determinations of immunoglobulins A, G, and M (lgA, IgG, and IgM) in cerebrospinal fluid (CSF) and in serum. Inflammatory diseases, such as multiple sclerosis and infections (e.g. meningitis) affecting the central nervous system are characterized by intrathecal synthesis of immunoglobulins, and therefore determinations of them in CSF are important diagnostic tools.

    A non-linear relationship between the CSF/serum ratios of IgG, IgA, IgM, and albumin was found in patients with damaged blood-CSF barrier, but in whom no intrathecal synthesis orimmunoglobulins was expected. On the basis of this non-linear relationship a new kind of formula, the extended indices (lgA-EI, IgG-EI, and IgM-EI), was developed to giveimproved estimates of intrathecal synthesis.

    These formulae were evaluated together with other proposed formulae and with agarose isoelectrofocusing, to determine their diagnostic sensitivities in different neurological diseases. The main advantage with the extended indices, compared to other formulae, was a lower rate offalse positive tests, without affecting the diagnostic sensitivities for intrathecal immunoglobulin synthesis.

    A method based on ultracentrifugation is presented, where the distribution of monomeric and dimeric IgA in CSF and serum can be determined quantitatively. Both total and Ilerpes simplex virus specific lgA antibodies were estimated with respect to the physical form of lgA.

    For determination of CSF-IgM the sampling should be performed with an atraumatic Sprotte needle to minimise pre-analytical errors owing to contamination with serum or interstitial fluid.

  • 1632.
    Örtegren Kugelberg, Unn
    et al.
    Linköping University, Department of Biomedicine and Surgery, Cell biology. Linköping University, Faculty of Health Sciences.
    Yin, Lan
    Linköping University, Department of Biomedicine and Surgery, Cell biology. Linköping University, Faculty of Health Sciences.
    Öst, Anita
    Linköping University, Department of Biomedicine and Surgery, Cell biology. Linköping University, Faculty of Health Sciences.
    Karlsson, Helen
    Linköping University, Department of Molecular and Clinical Medicine, Occupational and Environmental Medicine. Linköping University, Faculty of Health Sciences.
    Nyström, Fredrik
    Linköping University, Department of Medicine and Care, Internal Medicine. Linköping University, Faculty of Health Sciences.
    Strålfors, Peter
    Linköping University, Department of Biomedicine and Surgery, Cell biology. Linköping University, Faculty of Health Sciences.
    Separation and characterization of caveolae subclasses in the plasma membrane of primary adipocytes: segregation of specific proteins and functions2006In: The FEBS Journal, ISSN 1742-464X, E-ISSN 1742-4658, Vol. 273, no 14, p. 3381-3392Article in journal (Refereed)
    Abstract [en]

    Caveolae are nearly ubiquitous plasma membrane domains that in adipocytes vary in size between 25 and 150 nm. They constitute sites of entry into the cell as well as platforms for cell signalling. We have previously reported that plasma membrane-associated caveolae that lack cell surface access can be identified by electron microscopy. We now report the identification, after density gradient ultracentrifugation, of a subclass of very high-density apparently closed caveolae that were not labelled by cell surface protein labelling of intact cells. These caveolae contained caveolin-1 and caveolin-2. Another class of high-density caveolae contained caveolin-1, caveolin-2 and specifically fatty acid transport protein-1, fatty acid transport protein-4, fatty acyl-CoA synthetase, hormone-sensitive lipase, perilipin, and insulin-regulated glucose transporter-4. This class of caveolae was specialized in fatty acid uptake and conversion to triacylglycerol. A third class of low-density caveolae contained the insulin receptor, class B scavenger receptor-1, and insulin-regulated glucose transporter-4. Small amounts of these proteins were also detected in the high-density caveolae. In response to insulin, the insulin receptor autophosphorylation and the amount of insulin-regulated glucose transporter-4 increased in these caveolae. The molar ratio of cholesterol to phospholipid in the three caveolae classes varied considerably, from 0.4 in very high-density caveolae to 0.9 in low-density caveolae. There was no correlation between the caveolar contents of caveolin and cholesterol. The low-density caveolae, with the highest cholesterol concentration, were particularly enriched with the cholesterol-rich lipoprotein receptor class B scavenger receptor-1, which mediated cholesteryl ester uptake from high-density lipoprotein and generation of free cholesterol in these caveolae, suggesting a specific role in cholesterol uptake/metabolism. These findings demonstrate a segregation of functions in caveolae subclasses.

  • 1633.
    Örtegren, Unn
    et al.
    Linköping University, Department of Biomedicine and Surgery, Cell biology. Linköping University, Faculty of Health Sciences.
    Aboulaich, Nabila
    Linköping University, Department of Biomedicine and Surgery, Cell biology. Linköping University, Faculty of Health Sciences.
    Öst, Anita
    Linköping University, Department of Biomedicine and Surgery, Cell biology. Linköping University, Faculty of Health Sciences.
    Strålfors, Peter
    Linköping University, Department of Biomedicine and Surgery, Cell biology. Linköping University, Faculty of Health Sciences.
    A new role for caveolae as metabolic platforms2007In: Trends in endocrinology and metabolism, ISSN 1043-2760, E-ISSN 1879-3061, Vol. 18, no 9, p. 344-349Article in journal (Refereed)
    Abstract [en]

    The plasma membrane of cells functions as a barrier to the environment. Caveolae are minute invaginations of the membrane that selectively carry out the exchange of information and materials with the environment, by functioning as organizers of signal transduction and through endocytosis. Recent findings of uptake of different metabolites and of lipid metabolism occurring in caveolae, point to a new general function of caveolae. As gateways for the uptake of nutrients across the plasma membrane, and as platforms for the metabolic conversion of nutrients, especially in adipocytes, caveolae are now emerging as active centers for many aspects of intermediary metabolism, with implications for our understanding of obesity, diabetes and other metabolic disorders.

  • 1634.
    Örtegren, Unn
    et al.
    Linköping University, Department of Biomedicine and Surgery, Cell biology. Linköping University, Faculty of Health Sciences.
    Karlsson, Margareta
    Linköping University, Department of Biomedicine and Surgery, Cell biology. Linköping University, Faculty of Health Sciences.
    Blazic, Natascha
    Department of Clinical Neuroscience, Sahlgrenska University Hospital/Mölndal, Göteborg University, Mölndal, Sweden.
    Blomqvist, Maria
    Department of Clinical Neuroscience, Sahlgrenska University Hospital/Mölndal, Göteborg University, Mölndal, Sweden.
    Nyström, Fredrik
    Linköping University, Department of Biomedicine and Surgery, Cell biology. Linköping University, Faculty of Health Sciences.
    Gustavsson, Johanna
    Linköping University, Department of Biomedicine and Surgery, Cell biology. Linköping University, Faculty of Health Sciences.
    Fredman, Pam
    Department of Clinical Neuroscience, Sahlgrenska University Hospital/Mölndal, Göteborg University, Mölndal, Sweden.
    Strålfors, Peter
    Linköping University, Department of Biomedicine and Surgery, Cell biology. Linköping University, Faculty of Health Sciences.
    Lipids and glycosphingolipids in caveolae and surrounding plasma membrane of primary rat adipocytes2004In: European Journal of Biochemistry, ISSN 0014-2956, E-ISSN 1432-1033, Vol. 271, no 10, p. 2028-2036Article in journal (Refereed)
    Abstract [en]

    We have made a comprehensive and quantitative analysis of the lipid composition of caveolae from primary rat fat cells and compared the composition of plasma membrane inside and outside caveolae. We isolated caveolae from purified plasma membranes using ultrasonication in carbonate buffer to disrupt the membrane, or extraction with nonionic detergent, followed by density gradient ultracentrifugation. The carbonate-isolated caveolae fraction was further immunopurified using caveolin antibodies. Carbonate-isolated caveolae were enriched in cholesterol and sphingomyelin, and the concentration was three- and twofold higher, respectively, in caveolae compared to the surrounding plasma membrane. The concentration of glycerophospholipids was similar suggesting that glycerophospholipids constitute a constant core throughout the plasma membrane. The composition of detergent-insoluble fractions of the plasma membrane was very variable between preparations, but strongly enriched in sphingomyelin and depleted of glycerophospholipids compared to carbonate-isolated caveolae; indicating that detergent extraction is not a suitable technique for caveolae preparation. An average adipocyte caveola contained about 22 × 103 molecules of cholesterol, 7.5 × 103 of sphingomyelin and 23 × 103 of glycerophospholipid. The glycosphingolipid GD3 was highly enriched in caveolae, whereas GM3, GM1 and GD1a were present inside as well as outside the caveolae membrane. GD1b, GT1b, GM2, GQ1b, sulfatide and lactosylceramide sulfate were not detected in caveolae.

  • 1635.
    Örtegren, Unn
    et al.
    Linköping University, Department of Biomedicine and Surgery, Cell biology. Linköping University, Faculty of Health Sciences.
    Scherer, Philipp
    Albert Einstein College of Medicine, New York, NY, USA.
    Strålfors, Peter
    Linköping University, Department of Biomedicine and Surgery, Cell biology. Linköping University, Faculty of Health Sciences.
    Localization of adiponectin at the plasma membrane in caveolae of human adipocytesManuscript (preprint) (Other academic)
    Abstract [en]

    The hormone adiponectin is exclusively secreted by adipocytes and it regulates whole body energy homeostasis primarily by affecting liver and muscles. The circulating level of adiponectin inversely correlates with insulin resistance and type 2 diabetes. Little is known about the secretion of adiponectin by the adipocyte, but in caveolin-1 knockout mice the amount of secreted adiponectin is severely reduced. Here we show that in human adipocytes adiponectin was associated with the plasma membrane and to a specific class of high-density-caveolae. Substantial amounts of adiponectin were also found in the microsomal and cytosolic fractions of adipocytes, while very little was associated with mitochondria, nuclei, or the fat. Adiponectin in isolated caveolae was readily degraded by added trypsin, demonstrating that adiponectin was largely bound to the cytosolic face of the caveolae membrane. The findings indicate that caveolae may have a critical role in the secretion of adiponectin by human adipocytes.

  • 1636.
    Österström, Anna
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Cell biology.
    Dimberg, Jan
    Fransén, Karin
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Cell biology.
    Söderkvist, Peter
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Cell biology.
    Expression of cytosolic and group X secretory phospholipase A2 genes in human colorectal adenocarcinomas2002In: Cancer Letters, ISSN 0304-3835, E-ISSN 1872-7980, Vol. 182, no 2, p. 175-182Article in journal (Refereed)
    Abstract [en]

    Gene expression of cytosolic phospholipase A2 (cPLA2) and protein level of secretory PLA2 group X (sPLA2-X) are upregulated in human colorectal cancer and provide cyclooxygenase-2 (COX-2) with arachidonic acid, resulting in increased levels of PGE2. Mutated ras-genes are suggested to be involved in the regulatory pathway of cPLA2 in lung cancer cells. We analysed the gene expression of cPLA2 and sPLA2-X in 42 and 38 primary colorectal tumours, respectively, with and without K-ras mutations. We found an up-regulation of cPLA2 mRNA but the induction in tumour tissues does not correlate with Ras-gene mutations. Moreover, our results cannot consistently reflect an overexpression of sPLA2-X gene in colorectal cancer tissues.

30313233 1601 - 1636 of 1636
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