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Jansson, Agneta
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Publications (10 of 32) Show all publications
Hilborn, E., Gacic, J., Fornander, T., Nordenskjöld, B., Stål, O. & Jansson, A. (2016). Androgen receptor expression predicts beneficial tamoxifen response in oestrogen receptor-alpha-negative breast cancer. British Journal of Cancer, 114(3), 248-255
Open this publication in new window or tab >>Androgen receptor expression predicts beneficial tamoxifen response in oestrogen receptor-alpha-negative breast cancer
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2016 (English)In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 114, no 3, p. 248-255Article in journal (Refereed) Published
Abstract [en]

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

Place, publisher, year, edition, pages
NATURE PUBLISHING GROUP, 2016
Keywords
Androgen receptor; breast cancer; tamoxifen; oestrogen receptor; triple-negative breast cancer
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:liu:diva-125675 (URN)10.1038/bjc.2015.464 (DOI)000369223600003 ()26742006 (PubMedID)
Note

Funding Agencies|Swedish research council [A0346701]; Swedish cancer foundation [13 0435]

Available from: 2016-03-02 Created: 2016-02-29 Last updated: 2017-05-03
Hilborn, E., Sivik, T., Fornander, T., Stål, O., Nordenskjöld, B. & Jansson, A. (2014). C-X-C ligand 10 and C-X-C receptor 3 status can predict tamoxifen treatment response in breast cancer patients. Breast Cancer Research and Treatment, 145(1), 73-82
Open this publication in new window or tab >>C-X-C ligand 10 and C-X-C receptor 3 status can predict tamoxifen treatment response in breast cancer patients
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2014 (English)In: Breast Cancer Research and Treatment, ISSN 0167-6806, E-ISSN 1573-7217, Vol. 145, no 1, p. 73-82Article in journal (Refereed) Published
Abstract [en]

To investigate the expression levels of CXCL10 and CXCR3 in tumors from breast cancer patients randomized to adjuvant tamoxifen treatment or no endocrine treatment, in order to further study the connection to prognosis and prediction of tamoxifen treatment outcome. Immunohistochemistry on tissue microarrays from 912 breast cancer patients randomized to tamoxifen or no endocrine treatment. CXCR3 status was found to be a prognostic tool in predicting distant recurrence, as well as reduced breast cancer-specific survival. In patients with estrogen receptor (ER)-positive tumors, tumors with strong CXCL10 levels had improved effect of tamoxifen treatment in terms of local recurrence-free survival [risk ratio (RR) 0.46 (95 % CI 0.25-0.85, P = 0.01)] compared with patients with tumors expressing weak CXCL10 expression. Further, patients with ER-positive tumors with strong CXCR3 expression had an improved effect of tamoxifen in terms of breast cancer-specific survival [RR 0.34 (95 % CI 0.19-0.62, P less than 0.001)] compared with the group with weak CXCR3 levels [RR 1.33 (95 % CI 0.38-4.79, P = 0.65)]. We show here for the first time that CXCL10 and CXCR3 expression are both predictors of favorable outcome in patients treated with tamoxifen.

Place, publisher, year, edition, pages
Springer Verlag (Germany), 2014
Keywords
CXCL10; CXCR3; Endocrine treatment; Prognosis; Tamoxifen
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-106833 (URN)10.1007/s10549-014-2933-7 (DOI)000334519400007 ()
Available from: 2014-05-28 Created: 2014-05-23 Last updated: 2017-12-05Bibliographically approved
Jerhammar, F., Johansson, A.-C., Ceder, R., Welander, J., Jansson, A., Grafstrom, R. C., . . . Roberg, K. (2014). YAP1 is a potential biomarker for cetuximab resistance in head and neck cancer. Oral Oncology, 50(9), 832-839
Open this publication in new window or tab >>YAP1 is a potential biomarker for cetuximab resistance in head and neck cancer
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2014 (English)In: Oral Oncology, ISSN 1368-8375, E-ISSN 1879-0593, Vol. 50, no 9, p. 832-839Article in journal (Refereed) Published
Abstract [en]

Objectives: Targeted therapy against the epidermal growth factor receptor (EGFR) only variably represents a therapeutic advance in head and neck squamous cell carcinoma (HNSCC). This study addresses the need of biomarkers of treatment response to the EGFR-targeting antibody cetuximab (Erbitux (R)). Materials and Methods: The intrinsic cetuximab sensitivity of HNSCC cell lines was assessed by a crystal violet assay. Gene copy number analysis of five resistant and five sensitive cell lines was performed using the Affymetrix SNP 6.0 platform. Quantitative real-time PCR was used for verification of selected copy number alterations and assessment of mRNA expression. The functional importance of the findings on the gene and mRNA level was investigated employing siRNA technology. The data was statistically evaluated using Mann-Whitney U-test and Spearmans correlation test. Results: Analysis of the intrinsic cetuximab sensitivity of 32 HNSCC cell lines characterized five and nine lines as cetuximab sensitive or resistant, respectively. Gene copy number analysis of five resistant versus five sensitive cell lines identified 39 amplified protein-coding genes, including YAP1, in the genomic regions 11q22.1 or 5p13-15. Assessment using qPCR verified that YAP1 amplification associated with cetuximab resistance. Amplification of YAP1 correlated to higher mRNA levels, and RNA knockdown resulted in increased cetuximab sensitivity. Assessment of several independent clinical data sets in the public domain confirmed YAP1 amplifications in multiple tumor types including HNSCC, along with highly differential expression in a subset of HNSCC patients. Conclusion: Taken together, we provide evidence that YAP1 could represent a novel biomarker gene of cetuximab resistance in HNSCC cell lines.

Place, publisher, year, edition, pages
Elsevier, 2014
Keywords
Head and neck cancer; SCCHN; YAP1; Predictive marker; Treatment response; Gene copy number; Drug resistance
National Category
Clinical Medicine
Identifiers
urn:nbn:se:liu:diva-110268 (URN)10.1016/j.oraloncology.2014.06.003 (DOI)000340267300011 ()24993889 (PubMedID)
Note

Funding Agencies|Swedish Cancer Society [2008/552, 2010/545]; Ake Wiberg foundation; National board of health and welfare; Ostergotland county council; Foundation of Olle Engkvist; Swedish Cancer and Allergy Fund; Swedish Research Council; Swedish Fund for Research

Available from: 2014-09-05 Created: 2014-09-05 Last updated: 2017-12-05
Olsson, H., Jansson, A., Holmlund, B. & Gunnarsson, C. (2013). Methods for evaluating HER2 status in breast cancer: comparison of IHC, FISH, and real-time PCR analysis of formalin-fixed paraffin-embedded tissue. Pathology and Laboratory Medicine International, 5, 31-37
Open this publication in new window or tab >>Methods for evaluating HER2 status in breast cancer: comparison of IHC, FISH, and real-time PCR analysis of formalin-fixed paraffin-embedded tissue
2013 (English)In: Pathology and Laboratory Medicine International, ISSN 1179-2698, Vol. 5, p. 31-37Article in journal (Refereed) Published
Abstract [en]

The human epidermal growth factor receptor 2 gene (HER2) is amplified in approximately 15%–20% of all breast cancers. This results in overexpression of the HER2 protein, which is associated with worse clinical outcomes in breast cancer patients. Several studies have shown that trastuzumab, a monoclonal antibody that interferes with the HER2/neu receptor, can improve overall survival in patients with HER2-positive breast cancer. Immunohistochemistry (IHC), combined with different methods for in situ hybridization, is currently used for routine assessment of HER2 status. The aim of the present study was to determine whether real-time polymerase chain reaction (PCR) can serve as a supplementary method for evaluation of HER2 status in primary breast cancer. For this purpose, 145 formalin-fixed paraffin-embedded primary breast cancer samples were tested by real-time PCR amplification of HER2, using amyloid precursor protein as a reference. The results were compared with HER2 status determined by fluorescence in situ hybridization (FISH) and IHC. The specificity, sensitivity, and reproducibility of real-time PCR were evaluated, and a comparison of formalin-fixed and fresh-frozen samples was performed. This showed concordance of 93% between real-time PCR and FISH, and 86% between real-time PCR and IHC. Therefore, we suggest that real-time PCR can be a useful supplementary method for assessment of HER2 status.

Place, publisher, year, edition, pages
Dove Medical Press, 2013
Keywords
17q, breast cancer, HER2, real-time PCR
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-105270 (URN)10.2147/PLMI.S44976 (DOI)
Available from: 2014-03-14 Created: 2014-03-14 Last updated: 2017-12-05Bibliographically approved
Sivik, T., Gunnarsson, C., Fornander, T., Nordenskjöld, B., Skoog, L., Stål, O. & Jansson, A. (2012). 17β-hydroxysteroid dehydrogenase type 14 is a predictive marker for tamoxifen response in oestrogen receptor positive breast cancer. PLoS ONE, 7(7), e40568
Open this publication in new window or tab >>17β-hydroxysteroid dehydrogenase type 14 is a predictive marker for tamoxifen response in oestrogen receptor positive breast cancer
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2012 (English)In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 7, no 7, p. e40568-Article in journal (Refereed) Published
Abstract [en]

Introduction: 17β-hydroxysteroid dehydrogenases (17βHSDs) are important enzymes regulating the pool of bioactive steroids in the breast. The current study was undertaken in order to evaluate implications of 17βHSD14 in breast cancer, measuring 17βHSD14 protein expression in breast tumours.

Methods: An antibody targeting the 17βHSD14 antigen was generated and validated using HSD17B14-transfected cells and a peptide-neutralising assay. Tissue microarrays with tumours from 912 post-menopausal women diagnosed with lymph node-negative breast cancer, and randomised to adjuvant tamoxifen or no endocrine treatment, were analysed for 17βHSD14 protein expression with immunohistochemistry.

Results: Results were obtained from 847 tumours. Patients with oestrogen positive tumours with high 17βHSD14 expression had fewer local recurrences when treated with tamoxifen (HR 0.38; 95% C.I. 0.19–0.77, p = 0.007) compared to patients with lower tumoural 17βHSD14 expression, for whom tamoxifen did not reduce the number of local recurrences (HR 1.19; 95% C.I. 0.54–2.59; p = 0.66). No prognostic importance of 17βHSD14 was seen for systemically untreated patients.

Conclusions: Using a highly specific validated antibody for immunohistochemical analysis of a large number of breast tumours, we have shown that tumoural expression levels of 17βHSD14 can predict the outcome of adjuvant tamoxifen treatment in terms of local recurrence-free survival in patients with lymph node-negative ER+ breast cancer. The results need be verified to confirm any clinical relevance.

Place, publisher, year, edition, pages
Plos ONE, 2012
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-80247 (URN)10.1371/journal.pone.0040568 (DOI)
Available from: 2012-08-23 Created: 2012-08-23 Last updated: 2017-12-07
Sivik, T., Vikingsson, S., Gréen, H. & Jansson, A. (2012). Expression Patterns of 17β-Hydroxysteroid Dehydrogenase 14 in Human Tissues. Hormone and Metabolic Research, 44(13), 949-956
Open this publication in new window or tab >>Expression Patterns of 17β-Hydroxysteroid Dehydrogenase 14 in Human Tissues
2012 (English)In: Hormone and Metabolic Research, ISSN 0018-5043, E-ISSN 1439-4286, Vol. 44, no 13, p. 949-956Article in journal (Refereed) Published
Abstract [en]

17βHSD enzymes catalyze the stereospecific oxidation/reduction at carbon 17β of androgens and estrogens, and are important players in intracrine sex hormone synthesis. The biological relevance of 17βHSD14, first named retSDR3, is largely unknown. We generated and validated an antibody targeting the 17βHSD14 antigen and used this for immunohistochemical evaluation of expression patterns in 33 healthy human tissues. Furthermore, sex steroid conversional activity in HSD17B14 overexpressing HEK293 and MCF10A cells was investigated by assessing interconversion products of estrone, estradiol, androstenedione, testosterone, and dehydroepiandrosterone. Immunohistochemical staining patterns of 17βHSD14 with the enzyme being primarily expressed in glandular epithelial tissue reveal an enzyme with possible implications in the secretion or conversion of externally derived compounds. A role for 17βHSD14 in sex steroid metabolism is supported by the finding that 17HSD14 oxidizes both estradiol and testosterone into less bioactive steroid metabolites estrone and androstenedione, respectively.

Place, publisher, year, edition, pages
Georg Thieme Verlag KG, 2012
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-84681 (URN)10.1055/s-0032-1321815 (DOI)000312501800004 ()22864907 (PubMedID)
Available from: 2012-10-17 Created: 2012-10-17 Last updated: 2017-12-07Bibliographically approved
Sivik, T. & Jansson, A. (2012). Progesterone and levonorgestrel regulate expression of 17 beta HSD-enzymes in progesterone receptor positive breast cancer cell line T47D. Biochemical and Biophysical Research Communications - BBRC, 422(1), 109-113
Open this publication in new window or tab >>Progesterone and levonorgestrel regulate expression of 17 beta HSD-enzymes in progesterone receptor positive breast cancer cell line T47D
2012 (English)In: Biochemical and Biophysical Research Communications - BBRC, ISSN 0006-291X, E-ISSN 1090-2104, Vol. 422, no 1, p. 109-113Article in journal (Refereed) Published
Abstract [en]

The use of combined hormone replacement therapy (HAT) with oestrogens and progestins in postmenopausal women has been associated with an increased risk for developing breast cancer. The reasons are not fully understood, but influence of HRT on endogenous conversion of female sex hormones may be involved. The expression of 17 beta hydroxysteroid dehydrogenases (17 beta HSD), which are enzymes catalysing the conversion between more or less potent oestrogens, may partly be regulated by progestins. The breast cancer cell lines T47D, MCF7 and ZR75-1 were treated with progesterone, medroxyprogesterone acetate (MPA) or levonorgestrel for 48 and 72 h at 10(-7) and 10(-9) M to investigate influence on 17 beta HSD1, 17 beta HSD2 and 17 beta HSD5 mRNA expression measured by real time PCR. The expression of 17 beta HSD1 increased in progesterone and levonorgestrel treated T47D cells (48 h 10(-7) M P = 0.002; P andlt; 0.001) and 17 beta HSD5 increased after progesterone treatment (48 h 10(-7) M P = 0.003), whereas the expression of 17 beta HSD2 decreased after the (48 h 10(-7) M P = 0.003; P andlt; 0.001). Similar, but less prominent effects were seen in MCF7 and ZR75-1. The progestin effects on 17 beta HSD-expression were lost when T47D cells were co-treated with progestins and the progesterone receptor (PgR) inhibitor mifprestone. We show that both reductive (17 beta HSD1 and 17 beta HSD5) and oxidative (17 beta HSD2) members of the 17 beta HSD-family are under control of progesterone and progestins in breast cancer cell lines. This is most clear in T47D cells which have high PgR expression. 17 beta HSD-enzymes are important players in the regulation of sex steroids locally in breast tumours and tumoural expression of various 17 beta HSD-enzymes have prognostic and treatment predictive relevance. We propose a mechanism for increased breast cancer risk after HRT in which hormone replacement affects the expression of 17 beta HSD-enzymes, favouring the expression of reductive enzymes, which in turn could increase levels of bioactive and mitogenic estrogens in local tissue, e.g. breast tissue.

Place, publisher, year, edition, pages
Elsevier, 2012
Keywords
Breast cancer, Progestin, Progesterone, 17 beta HSD1, 17 beta HSD2
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-79104 (URN)10.1016/j.bbrc.2012.04.116 (DOI)000305046200020 ()
Note

Funding Agencies|Cancer and allergy foundation||Hedlunds foundation||Gosta Miltons foundation||Olle Engkvist Byggmastare foundation||Percy Falks Foundation||Cancer Foundation of Ostergotland||

Available from: 2012-06-29 Created: 2012-06-29 Last updated: 2017-12-07
Sivik, T., Vikingsson, S., Greén, H. & Jansson, A. (2010). A validated and rapid high-performance liquidchromatography method for the quantification ofconversion of radio-labelled sex steroids. Hormone Molecular Biology and Clinical Investigation, 3(1), 375-381
Open this publication in new window or tab >>A validated and rapid high-performance liquidchromatography method for the quantification ofconversion of radio-labelled sex steroids
2010 (English)In: Hormone Molecular Biology and Clinical Investigation, ISSN 1868-1891, Vol. 3, no 1, p. 375-381Article in journal (Refereed) Published
Abstract [en]

The 17b -hydroxysteroid dehydrogenase enzymes modify the availability of potent sex steroids and have thus attracted interest in the study of several steroid-dependent pathologies including breast, endometrial and prostate cancers. An increased awareness of the importance of steroidogenic enzymes has brought forth a demand for efficient assays to study the effects of individual enzymes on steroid levels. Methods used for assessing steroid conversion are often laborious and frequently involve hazardous sample preparation steps. We developed and validated an optimised simple method for sample preparation of sex steroids using protein precipitation by the addition of zinc sulphate/sodium hydroxide. The interconversion of radio-labelled oestrogens and androgens was quantified using high-performance liquid chromatography separation of oestrone, oestradiol, androstenedione and testosterone followed by online radiometric flow scintillation analysis. The method, which can be applied for assessing, e.g., the efficacy of inhibitors of steroidogenic enzymes, was successfully used for evaluating oestrogenic interconversion in breast cancer cell lines MCF7 and T-47D.

Place, publisher, year, edition, pages
de Gruyter, 2010
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-65628 (URN)10.1515/HMBCI.2010.038 (DOI)
Available from: 2011-02-14 Created: 2011-02-14 Last updated: 2011-02-18
Jerevall, P.-L., Jansson, A., Fornander, T., Skoog, L., Nordenskjöld, B. & Stål, O. (2010). Predictive relevance of HOXB13 protein expression for tamoxifen benefit in breast cancer. Breast Cancer Research, 12(4)
Open this publication in new window or tab >>Predictive relevance of HOXB13 protein expression for tamoxifen benefit in breast cancer
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2010 (English)In: Breast Cancer Research, ISSN 1465-5411, E-ISSN 1465-542X, Vol. 12, no 4Article in journal (Refereed) Published
Abstract [en]

ABSTRACT: INTRODUCTION: The HOXB13:IL17BR index has been identified to predict clinical outcome in the setting of adjuvant tamoxifen monotherapy of breast cancer. Further studies have shown that HOXB13 in particular can indicate benefit of prolonged tamoxifen treatment. Patients with high-expressing tumors did not benefit from prolonged treatment, suggesting that HOXB13 might be involved in tamoxifen resistance. No studies have been made regarding the HOXB13 protein levels in breast cancer. The aim of our study was to investigate whether tamoxifen benefit can be correlated to different levels of HOXB13 protein expression. METHODS: We used immunohistochemistry to analyze protein levels of HOXB13 in tumor samples from 912 postmenopausal node-negative breast cancer patients randomized to adjuvant tamoxifen therapy or no endocrine treatment. RESULTS: Tamoxifen-treated patients with estrogen receptor-positive tumors expressing none or low levels of HOXB13 had a clear benefit from tamoxifen in terms of longer distant recurrence-free survival (DRFS) (hazard ratio = 0.38, 95% confidence interval = 0.23 to 0.60, P = 0.000048). However, for patients with a high or intermediate HOXB13 tumor expression, tamoxifen did not prolong the DRFS compared with the untreated patients (hazard ratio = 0.88, 95% confidence interval = 0.47 to 1.65, P = 0.69). Interaction between HOXB13 expression and benefit from tamoxifen was statistically significant for DRFS (P = 0.035). No prognostic value could be ascribed to HOXB13 among systemically untreated patients. CONCLUSIONS: A high HOXB13 expression was associated with decreased benefit from tamoxifen, which indicates that HOXB13 protein level may be used as a predictive marker for tamoxifen treatment.

National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-58819 (URN)10.1186/bcr2612 (DOI)
Available from: 2010-08-27 Created: 2010-08-27 Last updated: 2017-12-12Bibliographically approved
Jansson , A. (2009). 17Beta-hydroxysteroid dehydrogenase enzymes and breast cancer. JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY, 114(1-2), 64-67
Open this publication in new window or tab >>17Beta-hydroxysteroid dehydrogenase enzymes and breast cancer
2009 (English)In: JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY, ISSN 0960-0760 , Vol. 114, no 1-2, p. 64-67Article in journal (Refereed) Published
Abstract [en]

Sex steroids play an important role in the development and differentiation in several tissues. Biologically active hormones that are locally converted in endocrine organs in the tissue where they exert their effects without release into extracellular space is a field of endocrinology that has been called intracrinology. In pre-menopausal women the ovary is the main source of estrogens, but in post-menopausal women the estrogen production as main site of synthesis moves to peripheral tissues and almost all of the sex steroids are synthesised from precursors of adrenal origin. In breast cancer 60-80% of the tumors express high levels of oestrogen receptor (ER) alpha which gives estrogen a proliferative effect. Breast tumors tend to have a higher intratumoral estrogen concentration than normal breast tissue and plasma, and in situ synthesis and the metabolism of estrogens is believed to be of great importance for the development and progression of the disease. The activity of estrogen metabolizing enzymes in breast are mainly aromatase, estrone sulfatases and 17HSD enzymes. 17HSD1 and 17HSD2 are the family members known to be of main importance in breast cancer. High expression of 17HSD1 has been associated to poor prognosis in breast cancer and late relapse among patients with ER-positive tumors. One of the mechanisms behind high 17HSD1 expression is gene amplification. Low or absent expression of 17HSD2 is associated to decreased survival in ER-positive breast cancer. 17HSD14 is one of the latest discovered 17HSD enzymes, transfection of 17HSD14 in human breast cancer cells significantly decreased the levels of estradiol in the culture medium. Low expression of 17HSD14 mRNA expression in breast cancer was correlated to decreased survival.

The understanding of intratumoral synthesis of sex steroids in breast cancer is crucial to understand the disease both in pre- and post-menopausal women. Further studies are desirable to state the direct role of these enzymes in breast cancer and which patients that may benefit from new therapeutic strategies targeting 17HSD enzymes. The new inhibitors targeting 17HSD1 have shown promising results in preclinical studies to have clinical potential in the future.

Keywords
Breast cancer, 17Beta-hydroxysteroid dehydrogenase enzymes, Sex hormones, Estradiol
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-18145 (URN)10.1016/j.jsbmb.2008.12.012 (DOI)
Available from: 2009-05-09 Created: 2009-05-08 Last updated: 2009-05-09
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