Expression of the androgen receptor and an androgen-responsive protein, apolipoprotein D, in human breast cancer

Hall, Rosemary E.; Aspinall, James O.; Horsfall, Debbie; Birrell, Stephen N.; Bentel, Jacqueline M.; Sutherland, Robert L.; Tilley, Wayne D.

doi:10.1038/bjc.1996.513

Cited by 64 publications

(43 citation statements)

References 29 publications

(21 reference statements)

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“…AR was detected followinmg microwave retrieval. as reported previously (Hall et al 1996 Figure 1B). Immunoreactive PSA was also localized in the cytoplasm of tumour cells ( Figure IC) and was present extracellularly in ductal luminae.…”

supporting

confidence: 88%

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Prostate-specific antigen and gross cystic disease fluid protein-15 are co-expressed in androgen receptor-positive breast tumours

Hall

Clements²,

Birrell³

et al. 1998

Br J Cancer

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supporting

confidence: 88%

“…Immunohistochemical studies have demonstrated that at least 801% of primary breast cancers contain AR-positive tumour cells (Kuenen-Boumeester et al 1992: Isola. 1993: Hall et al 1996. Moreover.…”

mentioning

confidence: 98%

Prostate-specific antigen and gross cystic disease fluid protein-15 are co-expressed in androgen receptor-positive breast tumours

Hall

Clements²,

Birrell³

et al. 1998

Br J Cancer

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“…Androgen signaling may also activate estrogen-responsive genes (3,(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17). ER-negative and/or PR-negative breast cancers represent f30% of all breast cancers and are known to have a more aggressive clinical course, partly because these tumors are more likely to be poorly differentiated and of higher histologic grade (30,31).…”

Section: Discussionmentioning

confidence: 99%

Androgen Receptor Levels and Association with PIK3CA Mutations and Prognosis in Breast Cancer

González-Angulo¹,

Stemke-Hale²,

Palla

et al. 2009

Clinical Cancer Research

189

167

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Purpose: To examine the androgen receptor (AR) levels in breast cancer and to assess the impact of AR expression on patient outcomes. Experimental Design: Reverse-phase protein arrays were used to measure AR levels and a mass spectroscopy^based approach was used to detect PIK3CA mutations. Means and SDs were generated for AR levels. Linear regression models were used to determine if AR levels differed by tumor subtype and PIK3CA mutation status.Two-sample t tests were used to identify pair-wise differences. Survival probabilities were estimated with the use of the Kaplan-Meier product and log-rank test. Results:The median age was 59 years (23-89 years). Significant differences in AR levels existed among different breast tumor subtypes (highest in estrogen receptor^positive and/or progesterone receptor^positive tumors) as well as by PIK3CA mutation status (P < 0.0001 for both).AR levels were significantly higher in breast tumors with kinase domain PIK3CA mutations versus tumors that are wild type or with PIK3CA helical mutations (P = 0.017 and P < 0.0001, respectively). In 347 patients, dichotomized AR level by the median was a significant prognostic factor of recurrence-free survival (P = 0.0002) and overall survival (P = 0.004). High AR levels were associated with a significantly improved recurrence-free survival in 207 patients with earlystage estrogen/progesterone receptor^positive tumors after adjuvant hormonal therapy. A trend (P = 0.07) was found toward higher AR expression in PIK3CA mutant versus PIK3CA wild-type triple-negative breast tumors. Conclusions: AR levels may represent a prognostic marker in breast cancers and may provide a valuable tool for selecting treatment. There was an association of PIK3CA mutation (kinase domain) with increased AR levels.

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“…Androgen receptor (AR) is expressed in normal mammary epithelial and stromal cells [124;125]. Many pathologic studies have also demonstrated that over 70% of human breast cancer biopsies from untreated women are positive for AR; the ercentages are usually higher than, or equal high to, the percentages of ER and PR positivity [126][127][128][129][130][131][132][133][134][135]. These facts provide the basis for a direct AR-mediated action of androgens in the normal and malignant breast tissues.…”

Section: Uses Of Androgens In Womenmentioning

confidence: 99%

Mechanisms for c-myc Induced Mouse Mammary Gland Carcinogenesis and for the Synergistic Role of TGF(alpha) in the Process

Liao¹

2001

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Public reporting burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructior's, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing this collection of information. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducing this burden to Washington Headquarters Services, Directorate for Information Operations and Reports, 1215 Jefferson Davis Highway, Suite 1204, Arlington, VA 22202-4302, and ABSTRACT (Maximum 200 Words)This project aims to elucidate the cell cycle basis on which c-myc oncogene induces mammary carcinogenesis and transforming growth factor o (tgfcx) promotes the process. Conduction of this training project will help the P.1. to develop his career in breast cancer research. Data obtained so far have shown that c-myc transgenic mammary tumors may develop specific foci that are more aggressive than their adjacent tumor areas and thus represent a second stage of tumor progression. c-Myc may induce E2F1 and cyclin A2 to initiate the tumor development, whereas overexpression of cyclins DI and E may occur as later events to promote tumor progression to a more aggressive phenotype. TGFcc may enhance c-Myc-induced mammary carcinogenesis by inducing cyclin DI and facilitating the loss of pRB expression, resulting in an earlier development of more aggressive tumors in tgfa/c-myc double transgeneic mice, compared to the c-myc tumors. These findings in the transgenic animals may have relevance to human breast cancer. INTRODUCTION:This subject of study aims to elucidate the cell cycle basis on which c-myc oncogene initiates mammary carcinogenesis and transforming growth factor (X (tgfa) promotes the process. Conduction of this training project will help the P.I., Dr. Dezhong Liao, to develop his career in breast cancer research. This research project has four tasks, each of which is consisted of two parts, i.e. in vivo studies with transgenic mice and in vitro studies with cultured cells. The four tasks are: "* Task 1. Study whether expression of E2F1 and cyclin A2 is induced to mediate mammary cancer formation in c-myc mice. (Months 1-15). "* Task 2. Investigate whether c-myc initially suppresses cyclin DI expression, but overexpression of cyclins DI and E occurs as later events to facilitate progression of tumors to faster growing phenotypes. (Months 1-15) "* Task 3. Study the mechanisms and the roles of overexpression of cyclins DI and E in mammary carcinogenesis in TGFc/c-myc mice. . "* Task 4. Investigate the mechanisms for the loss of pRB during mammary carcinogenesis in myc and TGFcu/c-myc mice. BODY:1. In vivo animal experiments on the cell cycle basis of c-myc-induced, tgfu.-enhanced mouse mammary carcinogenesis: We have actually started the project since this proposal was submitted to DOD in June of 1999, about one year earlier than the time when the award was started. During the past two years, ...

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Expression of the androgen receptor and an androgen-responsive protein, apolipoprotein D, in human breast cancer

Cited by 64 publications

References 29 publications

Prostate-specific antigen and gross cystic disease fluid protein-15 are co-expressed in androgen receptor-positive breast tumours

Prostate-specific antigen and gross cystic disease fluid protein-15 are co-expressed in androgen receptor-positive breast tumours

Androgen Receptor Levels and Association with PIK3CA Mutations and Prognosis in Breast Cancer

Mechanisms for c-myc Induced Mouse Mammary Gland Carcinogenesis and for the Synergistic Role of TGF(alpha) in the Process

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