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John W M Martens - One of the best experts on this subject based on the ideXlab platform.

  • characterizing Steroid Hormone Receptor chromatin binding landscapes in male and female breast cancer
    Nature Communications, 2018
    Co-Authors: Tesa M Severson, Yongsoo Kim, Stacey E P Joosten, Karianne Schuurman, Petra Van Der Groep, Cathy B Moelans, Natalie D Ter Hoeve, Quirine F Manson, John W M Martens
    Abstract:

    Male breast cancer (MBC) is rare and largely hormonally driven. Here, the authors examine the action of Steroid Hormone Receptors in male and female breast cancers and find gender selective Hormone Receptor action that associates with the survival of MBC patients.

  • association of dna methylation of phosphoserine aminotransferase with response to endocrine therapy in patients with recurrent breast cancer
    Cancer Research, 2005
    Co-Authors: John W M Martens, Inko Nimmrich, Thomas Koenig, Maxime P Look, N Harbeck, Fabian Model, Antje Kluth, Joan Boltde Vries, Anieta M Sieuwerts, Henk Portengen
    Abstract:

    To understand the biological basis of resistance to endocrine therapy is of utmost importance in patients with Steroid Hormone Receptor-positive breast cancer. Not only will this allow us prediction of therapy success, it may also lead to novel therapies for patients resistant to current endocrine therapy. DNA methylation in the promoter regions of genes is a prominent epigenetic gene silencing mechanism that contributes to breast cancer biology. In the current study, we investigated whether promoter DNA methylation could be associated with resistance to endocrine therapy in patients with recurrent breast cancer. Using a microarray-based technology, the promoter DNA methylation status of 117 candidate genes was studied in a cohort of 200 Steroid Hormone Receptor-positive tumors of patients who received the antiestrogen tamoxifen as first-line treatment for recurrent breast cancer. Of the genes analyzed, the promoter DNA methylation status of 10 genes was significantly associated with clinical outcome of tamoxifen therapy. The association of the promoter hypermethylation of the strongest marker, phosphoserine aminotransferase (PSAT1) with favorable clinical outcome was confirmed by an independent quantitative DNA methylation detection method. Furthermore, the extent of DNA methylation of PSAT1 was inversely associated with its expression at the mRNA level. Finally, also at the mRNA level, PSAT1 was a predictor of tamoxifen therapy response. Concluding, our work indicates that promoter hypermethylation and mRNA expression of PSAT1 are indicators of response to tamoxifen-based endocrine therapy in Steroid Hormone Receptor-positive patients with recurrent breast cancer.

Laure Dossus - One of the best experts on this subject based on the ideXlab platform.

  • vegetable and fruit consumption and the risk of Hormone Receptor defined breast cancer in the epic cohort
    The American Journal of Clinical Nutrition, 2016
    Co-Authors: Marleen J Emaus, Petra H M Peeters, Marije F Bakker, Kim Overvad, Anne Tjonneland, Anja Olsen, Isabelle Romieu, Pietro Ferrari, Laure Dossus
    Abstract:

    Background: The recent literature indicates that a high vegetable intake and not a high fruit intake could be associated with decreased Steroid Hormone Receptor–negative breast cancer risk.Objective: This study aimed to investigate the association between vegetable and fruit intake and Steroid Hormone Receptor–defined breast cancer risk.Design: A total of 335,054 female participants in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort were included in this study (mean ± SD age: 50.8 ± 9.8 y). Vegetable and fruit intake was measured by country-specific questionnaires filled out at recruitment between 1992 and 2000 with the use of standardized procedures. Cox proportional hazards models were stratified by age at recruitment and study center and were adjusted for breast cancer risk factors.Results: After a median follow-up of 11.5 y (IQR: 10.1–12.3 y), 10,197 incident invasive breast cancers were diagnosed [3479 estrogen and progesterone Receptor positive (ER+PR+); 1021 ER and PR negative (ER−PR−)]. Compared with the lowest quintile, the highest quintile of vegetable intake was associated with a lower risk of overall breast cancer (HRquintile 5–quintile 1: 0.87; 95% CI: 0.80, 0.94). Although the inverse association was most apparent for ER−PR− breast cancer (ER−PR−: HRquintile 5–quintile 1: 0.74; 95% CI: 0.57, 0.96; P-trend = 0.03; ER+PR+: HRquintile 5–quintile 1: 0.91; 95% CI: 0.79, 1.05; P-trend = 0.14), the test for heterogeneity by Hormone Receptor status was not significant (P-heterogeneity = 0.09). Fruit intake was not significantly associated with total and Hormone Receptor–defined breast cancer risk.Conclusion: This study supports evidence that a high vegetable intake is associated with lower (mainly Hormone Receptor–negative) breast cancer risk.

  • vegetable and fruit consumption and the risk of Hormone Receptor defined breast cancer in the epic cohort
    The American Journal of Clinical Nutrition, 2016
    Co-Authors: Marleen J Emaus, Petra H M Peeters, Marije F Bakker, Kim Overvad, Anne Tjonneland, Anja Olsen, Isabelle Romieu, Pietro Ferrari, Laure Dossus
    Abstract:

    Background: The recent literature indicates that a high vegetable intake and not a high fruit intake could be associated with decreased Steroid Hormone Receptor–negative breast cancer risk.Objectiv ...

Petra H M Peeters - One of the best experts on this subject based on the ideXlab platform.

  • vegetable and fruit consumption and the risk of Hormone Receptor defined breast cancer in the epic cohort
    The American Journal of Clinical Nutrition, 2016
    Co-Authors: Marleen J Emaus, Petra H M Peeters, Marije F Bakker, Kim Overvad, Anne Tjonneland, Anja Olsen, Isabelle Romieu, Pietro Ferrari, Laure Dossus
    Abstract:

    Background: The recent literature indicates that a high vegetable intake and not a high fruit intake could be associated with decreased Steroid Hormone Receptor–negative breast cancer risk.Objective: This study aimed to investigate the association between vegetable and fruit intake and Steroid Hormone Receptor–defined breast cancer risk.Design: A total of 335,054 female participants in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort were included in this study (mean ± SD age: 50.8 ± 9.8 y). Vegetable and fruit intake was measured by country-specific questionnaires filled out at recruitment between 1992 and 2000 with the use of standardized procedures. Cox proportional hazards models were stratified by age at recruitment and study center and were adjusted for breast cancer risk factors.Results: After a median follow-up of 11.5 y (IQR: 10.1–12.3 y), 10,197 incident invasive breast cancers were diagnosed [3479 estrogen and progesterone Receptor positive (ER+PR+); 1021 ER and PR negative (ER−PR−)]. Compared with the lowest quintile, the highest quintile of vegetable intake was associated with a lower risk of overall breast cancer (HRquintile 5–quintile 1: 0.87; 95% CI: 0.80, 0.94). Although the inverse association was most apparent for ER−PR− breast cancer (ER−PR−: HRquintile 5–quintile 1: 0.74; 95% CI: 0.57, 0.96; P-trend = 0.03; ER+PR+: HRquintile 5–quintile 1: 0.91; 95% CI: 0.79, 1.05; P-trend = 0.14), the test for heterogeneity by Hormone Receptor status was not significant (P-heterogeneity = 0.09). Fruit intake was not significantly associated with total and Hormone Receptor–defined breast cancer risk.Conclusion: This study supports evidence that a high vegetable intake is associated with lower (mainly Hormone Receptor–negative) breast cancer risk.

  • vegetable and fruit consumption and the risk of Hormone Receptor defined breast cancer in the epic cohort
    The American Journal of Clinical Nutrition, 2016
    Co-Authors: Marleen J Emaus, Petra H M Peeters, Marije F Bakker, Kim Overvad, Anne Tjonneland, Anja Olsen, Isabelle Romieu, Pietro Ferrari, Laure Dossus
    Abstract:

    Background: The recent literature indicates that a high vegetable intake and not a high fruit intake could be associated with decreased Steroid Hormone Receptor–negative breast cancer risk.Objectiv ...

Bert W Omalley - One of the best experts on this subject based on the ideXlab platform.

  • dual functions of the Steroid Hormone Receptor coactivator 3 in modulating resistance to thyroid Hormone
    Molecular and Cellular Biology, 2005
    Co-Authors: Hao Ying, Bert W Omalley, Fumihiko Furuya, Mark C Willingham, Sheueyann Cheng
    Abstract:

    Mutations of the thyroid Hormone Receptor β (TRβ) gene cause resistance to thyroid Hormone (RTH). RTH is characterized by increased serum thyroid Hormone associated with nonsuppressible thyroid-stimulating Hormone (TSH) and impaired growth. It is unclear how the actions of TRβ mutants are modulated in vivo to affect the manifestation of RTH. Using a mouse model of RTH that harbors a knockin mutation of the TRβ gene (TRβPV mouse), we investigated the effect of the Steroid Hormone Receptor coactivator 3 (SRC-3) on RTH. In TRβPV mice deficient in SRC-3, dysfunction of the pituitary-thyroid axis and hypercholesterolemia was lessened, but growth impairment of RTH was worsened. The lessened dysfunction of the pituitary-thyroid axis was attributed to a significant decrease in growth of the thyroid and pituitary. Serum insulin-like growth factor 1 (IGF-1) was further reduced in TRβPV mice deficient in SRC-3. This effect led to reduced signaling of the IGF-1/phosphatidylinositol 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) pathway that is known to mediate cell growth and proliferation. Thus, SRC-3 modulates RTH by at least two mechanisms, one via its role as a Receptor coregulator and the other via its growth regulatory role through the IGF-1/PI3K/AKT/mTOR signaling.

  • Steroid Hormone Receptor coactivation and alternative rna splicing by u2af65 related proteins caperα and caperβ
    Molecular Cell, 2005
    Co-Authors: Dennis H Dowhan, Eugene P Hong, Didier Auboeuf, Andrew P Dennis, Michelle M Wilson, Sissel Marie Berget, Bert W Omalley
    Abstract:

    Abstract Increasing evidence indicates that transcription and pre-mRNA processing are functionally coupled to modulate gene expression. Here, we report that two members of the U2AF 65 family of proteins, hCC1.3, which we call CAPERα, and a related protein, CAPERβ, regulate both Steroid Hormone Receptor-mediated transcription and alternative splicing. The CAPER proteins coactivate the progesterone Receptor in luciferase transcription reporter assays and alter alternative splicing of a calcitonin/calcitonin gene-related peptide minigene in a Hormone-dependent manner. The importance of CAPER coactivators in the regulation of alternative RNA splicing of an endogenous cellular gene (VEGF) was substantiated by siRNA knockdown of CAPERα. Mutational analysis of CAPERβ indicates that the transcriptional and splicing functions are located in distinct and separable domains of the protein. These results indicate that Steroid Hormone Receptor-regulated transcription and pre-mRNA splicing can be directly linked through dual function coactivator molecules such as CAPERα and CAPERβ.

  • sequence and characterization of a coactivator for the Steroid Hormone Receptor superfamily
    Science, 1995
    Co-Authors: Sergio A Onate, Sophia Y. Tsai, Ming Jer Tsai, Bert W Omalley
    Abstract:

    A yeast two-hybrid system was used to identify a protein that interacts with and enhances the human progesterone Receptor (hPR) transcriptional activity without altering the basal activity of the promoter. Because the protein stimulated transactivation of all the Steroid Receptors tested, it has been termed Steroid Receptor coactivator-1 (SRC-1). Coexpression of SRC-1 reversed the ability of the estrogen Receptor to squelch activation by hPR. Also, the amino terminal truncated form of SRC-1 acted as a dominant-negative repressor. Together, these results indicate that SRC-1 encodes a coactivator that is required for full transcriptional activity of the Steroid Receptor superfamily.

  • members of the Steroid Hormone Receptor superfamily interact with tfiib s300 ii
    Journal of Biological Chemistry, 1992
    Co-Authors: Nancy H Ing, Sophia Y. Tsai, Ming Jer Tsai, J M Beekman, Bert W Omalley
    Abstract:

    The S300-II factor was discovered as an activator of ovalbumin gene transcription with the chicken ovalbumin upstream promoter-transcription factor (COUP-TF, Sagami, I., Tsai, S. Y., Wang, H., Tsai, M.-J., and O'Malley, B. W. (1986) Mol. Cell. Biol. 6, 4259-4267). Although S300-II does not bind DNA selectively, it stabilizes the binding of COUP-TF to its ciselement (Tsai, S. Y., Sagami, I., Wang, H., Tsai, M.-J., and O'Malley, B. W. (1987) Cell 50, 701-709). Purified S300-II is also required for Steroid Receptor-activated transcription. Cloning and sequencing of S300-II showed that it is the general transcription factor TFIIB. Specific protein-protein interactions between recombinant S300-II/TFIIB and three members of the Steroid Hormone Receptor superfamily, COUP-TF, estrogen Receptor, and progesterone Receptor, indicate that S300-II/TFIIB is one of the targets of these transactivators. Interestingly, a truncated estrogen Receptor construct containing only the N-terminal transcription activation function 1 did not interact with S300-II/TFIIB in our assay, revealing that individual transcription activation functions of a single Steroid Hormone Receptor may contact different targets. Demonstration of a direct association of S300-II/TFIIB and COUP-TF, independent of additional "adaptor" proteins, suggests that members of the Steroid hromone Receptor superfamily facilitate the transcription of activated genes at least in part via protein-protein interactions with the general transcription factor TFIIB.

Lena Sahlin - One of the best experts on this subject based on the ideXlab platform.

  • sex Steroid Hormone Receptor expression in the vaginal wall in cervical cancer survivors after radiotherapy
    Acta Oncologica, 2019
    Co-Authors: Alexandra Hofsjö, Karin Bergmark, Britt Masironi, Nina Bohmstarke, Lena Sahlin
    Abstract:

    Background: Sex Steroid Hormones and their Receptors are important in female sexual function. The aim of this study was to investigate the expression and distribution of estrogen Receptor (ER)α, ER...

  • Sex Steroid Hormone Receptor expression in the vaginal wall in cervical cancer survivors after radiotherapy
    2019
    Co-Authors: Alexandra Hofsjö, Nina Bohm-starke, Karin Bergmark, Britt Masironi, Lena Sahlin
    Abstract:

    Background: Sex Steroid Hormones and their Receptors are important in female sexual function. The aim of this study was to investigate the expression and distribution of estrogen Receptor (ER)α, ERβ, G-protein-coupled ER-1 (GPER), androgen Receptor (AR), progesterone Receptor (PR)A, PRB and connective tissue growth factor (CTGF) in the vaginal wall among women who had been treated for cervical cancer with radiotherapy. Material and methods: We included cervical cancer survivors treated with radiotherapy and premenopausal control women of the same age scheduled for benign gynecological surgery. We analyzed the expression and distribution of sex Steroid Hormone Receptors and CTGF in biopsies from the vaginal wall, by real-time PCR and immunohistochemistry (IHC). Serum samples were analyzed for Hormone levels and radiation dose at biopsy site were calculated and correlated to levels of the sex Steroid Hormone Receptors. Results: In the cervical cancer survivors (n = 34), we found a lower expression of ERα at both mRNA and protein levels, compared to the control women (n = 37). In the survivors with high radiation dose at biopsy site, the immunostaining of ERα and AR was lower in the epithelium and the stroma, compared to survivors with minimal radiation dose. The later group showed expression of ERα comparable to the control women. The cancer survivors were sufficiently substituted with systemic estradiol with no difference in the serum estradiol levels compared to control women. Conclusions: We found that external radiation reduces the ERα and AR protein expression in the vaginal mucosa, indicating that the vaginal changes in irradiated cervical cancer survivors and the lack of response to hormonal treatment could be due to the decreases in sex Steroid Hormone Receptor expression.