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BETA
Olsson, Birgit
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Publications (10 of 15) Show all publications
Ding, Z.-Y., Zhang, H., Adell, G., Olsson, B. & Sun, X.-F. (2013). Livin expression is an independent factor in rectal cancer patients with or without preoperative radiotherapy. Radiation Oncology, 8(281)
Open this publication in new window or tab >>Livin expression is an independent factor in rectal cancer patients with or without preoperative radiotherapy
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2013 (English)In: Radiation Oncology, ISSN 1748-717X, E-ISSN 1748-717X, Vol. 8, no 281Article in journal (Refereed) Published
Abstract [en]

Background: This study was aimed to investigate the expression significance of Livin in relation to radiotherapy (RT), clinicopathological and biological factors of rectal cancer patients. Methods: This study included 144 primary rectal cancer patients who participated in a Swedish clinical trial of preoperative radiotherapy. Tissue microarray samples from the excised primary rectal cancers, normal mucosa and lymph node metastases were immunostained with Livin antibody. The proliferation of colon cancer cell lines SW620 and RKO was assayed after Livin knock-down. Results: The expression of Livin was significantly increased from adjacent (P = 0.051) or distant (P = 0.028) normal mucosa to primary tumors. 15.4% (2/13) and 39.7% (52/131) patients with Livin-negative and positive tumors died at 180 months after surgery, and the difference tended to be statistically significant (P = 0.091). In multivariate analyses, the difference achieved statistical significance, independent of TNM stage, local and distant recurrence, grade of differentiation, gender, and age (odds ratio = 5.09, 95% CI: 1.01-25.64, P = 0.048). The in vitro study indicated colon cancer cells with Livin knock-down exhibited decreased proliferation compared with controls after RT. Conclusions: The expression of Livin was was independently related to survival in rectal cancer patients, suggesting Livin as a useful prognostic factor for rectal cancer patients.

Place, publisher, year, edition, pages
BioMed Central, 2013
Keywords
Rectal cancer; Livin; Radiotherapy
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-105255 (URN)10.1186/1748-717X-8-281 (DOI)000331620900002 ()
Available from: 2014-03-14 Created: 2014-03-14 Last updated: 2017-12-05
Ding, Z.-Y., Liu, G.-H., Olsson, B. & Sun, X.-F. (2013). Upregulation of the antiapoptotic factor Livin contributes to cisplatin resistance in colon cancer cells. Tumor Biology, 34(2), 683-693
Open this publication in new window or tab >>Upregulation of the antiapoptotic factor Livin contributes to cisplatin resistance in colon cancer cells
2013 (English)In: Tumor Biology, ISSN 1010-4283, E-ISSN 1423-0380, Vol. 34, no 2, p. 683-693Article in journal (Refereed) Published
Abstract [en]

The antiapoptotic factor Livin has been considered critical for tumor progression and poor prognosis for variant types of tumors. However, there are only limited reports regarding its expression and biological functions in colon cancer. Here, we examined Livin expression in four colon cancer cell lines (HCT116, RKO, KM12C, and SW620) in the presence or absence of cisplatin that was used as a model reagent. We found the different response to cisplatin was related to endogenous Livin expression level. From among a panel of apoptosis-related factors (p53, Bcl-2, Bcl-XL, BAX, and survivin), the expression of Livin was upregulated after cisplatin treatment in a dose-dependent manner. Both immunocytochemistry and nuclear cytoplasmic fractionation indicated Livin remained in the cytoplasm after treatment with cisplatin. In an attempt to explore the mechanism, we found the elevated expression of Livin was not due to the decreased degradation by proteosome but was enhanced at the mRNA level. Besides, cisplatin treatment activated the mammalian target of rapamycin (mTOR) pathway as shown by increased phosphorylation of Akt1, mTOR, S6K, and 4E-BP1, together with the elevated Livin. The PI3K inhibitor LY294002 inhibited both the phosphorylation of mTOR and upregulation of Livin. The stable overexpression of Livin inhibited the activation of caspase-3 and led to resistance to cisplatin, while the knockdown of Livin by siRNA rendered colon cancer cells more sensitive to cisplatin. Our study, along with others, highlighted the potential of Livin for cancer therapy in colon cancer.

Place, publisher, year, edition, pages
Karger / Springer Verlag (Germany), 2013
Keywords
Livin; Apoptosis; Cisplatin; Colon cancer
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-96160 (URN)10.1007/s13277-012-0596-8 (DOI)000316364500010 ()
Available from: 2013-08-14 Created: 2013-08-14 Last updated: 2017-12-06Bibliographically approved
Shen, Y.-m., Arbman, G., Sandström, P., Gullstrand, P., Wei, Y.-Q., Zhang, H., . . . Sun, X.-F. (2012). Novel gene hBiot2 is an independent prognostic factor in colorectal cancer patients. Oncology Reports, 27(2), 376-382
Open this publication in new window or tab >>Novel gene hBiot2 is an independent prognostic factor in colorectal cancer patients
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2012 (English)In: Oncology Reports, ISSN 1021-335X, E-ISSN 1791-2431, Vol. 27, no 2, p. 376-382Article in journal (Refereed) Published
Abstract [en]

The present study investigated the expression of the novel gene hBiot2 in colorectal cancer (CRC) and its relationships with clinicopathological variables in CRC patients. The expression of hBiot2 in 163 primary CRCs together with the corresponding normal mucosa, 36 liver metastases and 5 colon cancer cell lines was examined using real-time PCR. In situ hybridization (ISH) was performed to evaluate the localization of hBiot2 expression in CRC and normal mucosa. hBiot2 expression at the RNA level was localized in the nucleus of tumor cells and normal epithelial cells. The mean expression of hBiot2 in the CRCs (243.571 +/- 564.569) was higher compared to the normal mucosa (107.252 +/- 413.635, Pandlt;0.0001) and liver metastasis samples (42.002 +/- 40.809, P=0.0002). hBiot2 expression was increased from stages I + II to III (P=0.047), and no difference in the expression was found in stages III and IV (P=0.452). A high value of hBiot2 was associated with a poorer prognosis compared with a low value independently of gender, age, tumor site, stage and differentiation (P=0.007, RR 7.519, 95% Cl 1.729-32.704). Liver metastasis, smaller tumors, non-local recurrence and primary liver surgery alone were associated with a higher value of hBiot2 compared to larger tumors, local recurrence and repeated liver surgery (P=0.003, 0.044 and 0.026, respectively). An inverse relationship was found between hBiot2 expression and the metastatic potential of the colon cancer cell lines. Thus, increased expression of hBiot2 may be an early and interim event in the development of CRC. A higher expression of hBiot2 in primary CRC patients independently indicates a poorer prognosis.

Place, publisher, year, edition, pages
Spandidos Publications, 2012
Keywords
human Biot2, colorectal cancer, prognosis, real-time PCR, in situ hybridization
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-75107 (URN)10.3892/or.2011.1521 (DOI)000298825900011 ()
Note
Funding Agencies|Swedish Cancer Foundation||Swedish Research Council||Health Research Council in Southeast Sweden||Available from: 2012-02-21 Created: 2012-02-17 Last updated: 2017-12-07
Perez-Tenorio, G., Karlsson, E., Ahnström, M., Olsson, B., Holmlund, B., Nordenskjöld, B., . . . Stål, O. (2011). Clinical potential of the mTOR targets S6K1 and S6K2 in breast cancer. Breast Cancer Research and Treatment, 128(3), 713-723
Open this publication in new window or tab >>Clinical potential of the mTOR targets S6K1 and S6K2 in breast cancer
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2011 (English)In: Breast Cancer Research and Treatment, ISSN 0167-6806, E-ISSN 1573-7217, Vol. 128, no 3, p. 713-723Article in journal (Refereed) Published
Abstract [en]

The mammalian target of rapamycin (mTOR) and its substrates S6K1 and S6K2 regulate cell growth, proliferation, and metabolism through translational control. RPS6KB1 (S6K1) and RPS6KB2 (S6K2) are situated in the commonly amplified 17q21-23 and 11q13 regions. S6K1 amplification and protein overexpression have earlier been associated with a worse outcome in breast cancer, but information regarding S6K2 is scarce. The aim of this study was to evaluate the prognostic and treatment predictive relevance of S6K1/S6K2 gene amplification, as well as S6K2 protein expression in breast cancer. S6K1/S6K2 gene copy number was determined by real-time PCR in 207 stage II breast tumors and S6K2 protein expression was investigated by immunohistochemistry in 792 node-negative breast cancers. S6K1 amplification/gain was detected in 10.7%/21.4% and S6K2 amplification/gain in 4.3%/21.3% of the tumors. S6K2 protein was detected in the nucleus (38%) and cytoplasm (76%) of the tumor cells. S6K1 amplification was significantly associated with HER2 gene amplification and protein expression. S6K2 amplification correlated significantly with high S6K2 mRNA levels, ER+ status and CCND1 amplification. S6K1 and S6K2 gene amplification was associated with a worse prognosis independent of HER2 and CCND1. S6K2 gain and nuclear S6K2 expression was related to an improved benefit from tamoxifen among patients with ER+, respectively ER+/PgR+ tumors. In the ER+/PgR- subgroup, nuclear S6K2 rather indicated decreased tamoxifen responsiveness. S6K1 amplification predicted reduced benefit from radiotherapy. This is the first study showing that S6K2 amplification and overexpression, like S6K1 amplification, have prognostic and treatment predictive significance in breast cancer.

Place, publisher, year, edition, pages
Springer Science Business Media, 2011
Keywords
mTOR; S6 kinase; 17q21-23; 11q13; Gene amplification; Tamoxifen response
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-69784 (URN)10.1007/s10549-010-1058-x (DOI)000292557100013 ()
Note
The original publication is available at www.springerlink.com: Gizeh Perez-Tenorio, Elin Karlsson, Marie Ahnström, Birgit Olsson, Birgitta Holmlund, Bo Nordenskjöld, Tommy Fornander, Lambert Skoog and Olle Stål, Clinical potential of the mTOR targets S6K1 and S6K2 in breast cancer, 2011, Breast Cancer Research and Treatment, (128), 3, 713-723. http://dx.doi.org/10.1007/s10549-010-1058-x Copyright: Springer Science Business Media http://www.springerlink.com/Available from: 2011-08-10 Created: 2011-08-08 Last updated: 2017-12-08
Karlsson, E., Ahnström, M., Bostner, J., Perez-Tenorio, G., Olsson, B., Hallbeck, A.-L. & Stål, O. (2011). High-Resolution Genomic Analysis of the 11q13 Amplicon in Breast Cancers Identifies Synergy with 8p12 Amplification, Involving the mTOR Targets S6K2 and 4EBP1. Genes, Chromosomes and Cancer, 50(10), 775-787
Open this publication in new window or tab >>High-Resolution Genomic Analysis of the 11q13 Amplicon in Breast Cancers Identifies Synergy with 8p12 Amplification, Involving the mTOR Targets S6K2 and 4EBP1
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2011 (English)In: Genes, Chromosomes and Cancer, ISSN 1045-2257, E-ISSN 1098-2264, Vol. 50, no 10, p. 775-787Article in journal (Refereed) Published
Abstract [en]

The chromosomal region 11q13 is amplified in 15-20% of breast cancers; an event not only associated with estrogen receptor (ER) expression but also implicated in resistance to endocrine therapy. Coamplifications of the 11q13 and 8p12 regions are common, suggesting synergy between the amplicons. The aim was to identify candidate oncogenes in the 11q13 region based on recurrent amplification patterns and correlations to mRNA expression levels. Furthermore, the 11q13/8p12 coamplification and its prognostic value, was evaluated at the DNA and the mRNA levels. Affymetrix 250K NspI arrays were used for whole-genome screening of DNA copy number changes in 29 breast tumors. To identify amplicon cores at 11q13 and 8p12, genomic identification of significant targets in cancer (GISTIC) was applied. The mRNA expression levels of candidate oncogenes in the amplicons [ RAD9A, RPS6KB2 (S6K2), CCND1, FGF19, FGF4, FGF3, PAK1, GAB2 (11q13); EIF4EBP1 (4EBP1), PPAPDC1B, and FGFR1 (8p12)] were evaluated using real-time PCR. Resulting data revealed three main amplification cores at 11q13. ER expression was associated with the central 11q13 amplification core, encompassing CCND1, whereas 8p12 amplification/gene expression correlated to S6K2 in a proximal 11q13 core. Amplification of 8p12 and high expression of 4EBP1 or FGFR1 was associated with a poor outcome in the group. In conclusion, single nucleotide polymorphism arrays have enabled mapping of the 11q13 amplicon in breast tumors with high resolution. A proximal 11q13 core including S6K2 was identified as involved in the coamplification/coexpression with 8p12, suggesting synergy between the mTOR targets S6K2 and 4EBP1 in breast cancer development and progression.

Place, publisher, year, edition, pages
Wiley-Blackwell, 2011
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-70514 (URN)10.1002/gcc.20900 (DOI)000294177300003 ()
Note

Funding Agencies|Swedish Cancer Foundation||Swedish Research Council||

Available from: 2011-09-12 Created: 2011-09-12 Last updated: 2017-12-08
Shen, Y.-m., Arbman, G., Olsson, B. & Sun, X.-F. (2011). Overexpression of GLUT1 in colorectal cancer is independently associated with poor prognosis. International Journal of Biological Markers, 26(3), 166-172
Open this publication in new window or tab >>Overexpression of GLUT1 in colorectal cancer is independently associated with poor prognosis
2011 (English)In: International Journal of Biological Markers, ISSN 0393-6155, E-ISSN 1724-6008, Vol. 26, no 3, p. 166-172Article in journal (Refereed) Published
Abstract [en]

Background: To investigate the expression of glucose transporter 1 (GLUT1) in colorectal cancer (CRC) and its relationship to clinicopathological variables. Methods: The expression of GLUT1 in 163 primary tumors together with the corresponding normal mucosa, and 36 liver metastases was examined using real-time PCR. Results: The mean value of GLUT1 was higher in primary tumors (50.390 +/- 68.648) than in the corresponding normal mucosa (20.437 +/- 28.703, p less than 0.0001), while there was no significant difference in GLUT1 expression between CRC and liver metastasis (50.390 +/- 68.648 vs 52.277 +/- 52.482, p = 0.190). In CRCs, GLUT1 expression was higher in poorly differentiated than in well and moderately differentiated tumors (p = 0.022), and higher in stage III + IV than in stage I + II tumors (p = 0.035). The patients with high-expressed GLUT1 had a worse prognosis than those with low-expressed GLUT1 independently of gender, age, tumor site, stage and differentiation (p = 0.026, RR 2.737, 95% CI 1.126-6.651) in stage I-III CRCs. In liver metastasis, GLUT1 expression was higher in larger tumors than in smaller ones (p = 0.025). Conclusions: Overexpression of GLUT1 in stage I-III CRCs was independently associated with poor prognosis.

Place, publisher, year, edition, pages
Wichtig Editore, 2011
Keywords
GLUT1; Colorectal cancer; Prognosis; Real-time PCR
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-73744 (URN)10.5301/JBM.2011.8550 (DOI)000297972200004 ()
Available from: 2012-01-12 Created: 2012-01-12 Last updated: 2017-12-08
Yang, L., Olsson, B., Pfeifer, D., Jönsson, J.-I., Zhou, Z.-G., Jiang, X., . . . Sun, X.-F. (2010). Knockdown of peroxisome proliferator-activated receptor-beta induces less differentiation and enhances cell-fibronectin adhesion of colon cancer cells. ONCOGENE, 29(4), 516-526
Open this publication in new window or tab >>Knockdown of peroxisome proliferator-activated receptor-beta induces less differentiation and enhances cell-fibronectin adhesion of colon cancer cells
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2010 (English)In: ONCOGENE, ISSN 0950-9232, Vol. 29, no 4, p. 516-526Article in journal (Refereed) Published
Abstract [en]

The role of peroxisome proliferator-activated receptor-beta/delta (PPAR-beta/delta) in the pathogenesis of colon cancer remains highly controversial. This study specifically silenced the PPAR-beta expression in three colon cancer cell lines with different metastatic potentials. Although PPAR-beta knockdown resulted in more malignant morphological changes, bigger colony sizes and lower carcinoembryonic antigen (CEA) secretion, and enhanced the cell-fibronectin adhesion, cell invasion and migration were unaffected. These effects were stronger in poorly metastatic cell lines compared with highly metastatic ones. Simultaneously, PPAR-beta knockdown decreased the mRNAs encoding adipocyte differentiation-related protein and liver fatty acid binding protein, and increased the mRNA of ILK, whereas the mRNAs encoding integrin-beta 1 and angiopoietin-like 4 were unchanged. Using immunohistochemistry, we determined that the intensity of PPAR-beta expression was stronger in rectal cancers with better differentiation than in those with poor differentiation, and was stronger in early-stage tumors than in advanced ones. Together, these findings consistently indicate that PPAR-beta may facilitate differentiation and inhibit the cell-fibronectin adhesion of colon cancer, having a role as an inhibitor in the carcinogenesis and progression of colorectal cancer. Interestingly, PPAR-beta seems to have a more important role in poorly metastatic cells than in highly metastatic ones.

Keywords
peroxisome proliferator-activated receptor, colon neoplasm, pathogenesis, RNA interference, differentiation
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-54059 (URN)10.1038/onc.2009.370 (DOI)000274084600005 ()
Available from: 2010-02-22 Created: 2010-02-22 Last updated: 2013-10-22
Karlsson, E., Waltersson, M. A., Bostner, J., Perez-Tenorio, G., Olsson, B., Fornander, T. & Stål, O. (2009). Comprehensive Genomic and Transcriptomic Analysis of the 11q13 Amplicon in Breast Cancer in CANCER RESEARCH, vol 69, issue 24, pp 820S-821S. In: CANCER RESEARCH (pp. 820S-821S). , 69(24)
Open this publication in new window or tab >>Comprehensive Genomic and Transcriptomic Analysis of the 11q13 Amplicon in Breast Cancer in CANCER RESEARCH, vol 69, issue 24, pp 820S-821S
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2009 (English)In: CANCER RESEARCH, 2009, Vol. 69, no 24, p. 820S-821SConference paper, Published paper (Refereed)
Abstract [en]

n/a

National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-53836 (URN)000272920702125 ()
Available from: 2010-02-05 Created: 2010-02-05 Last updated: 2010-02-05
Gunnarsson, C., Jerevall, P.-L., Hammar, K., Olsson, B., Nordenskjöld, B., Jansson, A. & Stål, O. (2008). Amplification of HSD17B1 has prognostic significance in postmenopausal breast cancer. Breast Cancer Research and Treatment, 108(1), 35-41
Open this publication in new window or tab >>Amplification of HSD17B1 has prognostic significance in postmenopausal breast cancer
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2008 (English)In: Breast Cancer Research and Treatment, ISSN 0167-6806, E-ISSN 1573-7217, Vol. 108, no 1, p. 35-41Article in journal (Refereed) Published
Abstract [en]

In situ synthesis of estrogens is believed to be of great importance for the progression of breast cancer. In postmenopausal women most estrogens are synthesized in peripheral hormone-target tissues from circulating precursor steroids, by the enzymes involved in formation of active estrogens. One of the enzymes involved in this process is 17β-hydroxysteroid dehydrogenase (17β-HSD) type 1. This enzyme catalyzes the interconversion of estrone (E1) to the biologically more potent estradiol (E2). The gene coding for 17β-HSD type 1 (HSD17B1) is located at 17q12-21. The aim of this study was to investigate altered gene copy number of HSD17B1 in breast cancer. We used real-time PCR and examined 387 postmenopausal breast tumors for amplification of HSD17B1, and if an increased mRNA level of this enzyme is associated with amplification of the gene. We also investigated whether amplification of HSD17B1 has a prognostic value. There was a significant correlation between gene copy number of HSD17B1 and mRNA expression level (P = 0.00002). ER-positive patients with amplification of HSD17B1 showed lower breast cancer survival than patients without amplification (P = 0.025). Among ER-negative patients there was no significant correlation between increased gene copy number of HSD17B1 and prognosis. Furthermore, we found that amplification of the gene had prognostic significance in multivariate analysis adjusting for other clinicopathological variables. © 2007 Springer Science+Business Media, LLC.

Keywords
Breast Neoplasms/*genetics/mortality Disease-Free Survival Estradiol Dehydrogenases/*genetics Female *Gene Amplification Humans Kaplan-Meiers Estimate Middle Aged Postmenopause Prognosis RNA, Messenger/analysis Receptors, Estrogen/metabolism Reverse Trans
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-43344 (URN)10.1007/s10549-007-9579-7 (DOI)73588 (Local ID)73588 (Archive number)73588 (OAI)
Available from: 2009-10-10 Created: 2009-10-10 Last updated: 2017-12-13Bibliographically approved
Perez-Tenorio, G., Karlsson, E., Ahnström Waltersson, M., Olsson, B., Holmlund, B., Nordenskjöld, B., . . . Stål, O. (2008). Clinical Value of RPS6KB1 and RPS6KB2 Gene Amplification in Postmenopausal Breast Cancer.
Open this publication in new window or tab >>Clinical Value of RPS6KB1 and RPS6KB2 Gene Amplification in Postmenopausal Breast Cancer
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2008 (English)Article in journal (Refereed) Submitted
Abstract [en]

The mammalian target of rapamycin (mTOR) and its substrates the ribosomal S6 kinases (S6K)1 and 2 integrate nutrient and hormonal/growth factor mediated signals and are implicated indiabetes, obesity and cancer. The genes encoding S6K1 (RPS6KB1) and S6K2 (RPS6KB2) aresituated close to well known amplicons but information regarding its expression and clinicalvalue is scarce. In this study we quantified RPS6KB1/2 gene copy number, establishedassociations with other clinical factors and explored their clinical value in breast cancer. RPS6KB1/2 copy number was determined by fast real-time PCR in 207 breast tumors.RPS6KB1 was amplified (≥ 4 copies) in 10.7% (22/206) and RPS6KB2 in 4.3% (9/207) of thetumors. Amplification of RPS6KB1 was associated with HER2 gene amplification (P=0.025)and protein expression (P=0.014) while RPS6KB2 correlated with ER+ status (P=0.046) and CCND1 amplification (P<0.00001). In a multivariate analysis, both genes were independentprognostic factors indicating higher risk to develop recurrences. In terms of loco regionalcontrol, amplification of the RPS6KB1 gene predicted less response to radiotherapy (P=0.035) while RPS6KB2 gene copy gain (≥ 3 copies) indicated increased benefit from tamoxifen (P=0.03) among ER+ patients. S6K1/2 gene amplification could be used as an indicator oftherapy response among postmenopausal breast cancer patients.

Keywords
PI3K, AKT, mTOR, CCND1, HER2, ER, Tamoxifen
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:liu:diva-15042 (URN)
Available from: 2008-10-13 Created: 2008-10-13 Last updated: 2009-04-09
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