Microsatellite Mutation (Cag24→18) in the Androgen Receptor Gene in Human Prostate Cancer

Schoenberg, Mark; Hakimi, Janette M.; Wang, Suping; Bova, G. Steven; Epstein, Jonathan I.; Fischbeck, Kenneth H.; Isaacs, William B.; Walsh, Patrick C.; Barrack, Evelyn R.

doi:10.1006/bbrc.1994.1011

Cited by 152 publications

(71 citation statements)

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“…The single highest incidence of LOH is found at the AR locus for both borderline and invasive ovarian tumors, thus making AR a likely candidate gene. The only reported role of the androgen receptor in cancer is in the hormonal response of prostate cancer and male breast cancer (Schoenberg et al, 1994;Newmark et al, 1992;Lobaccaro et al, 1993;Tilley et al, 1996;Taplin et al, 1995). Ampli®cation of the androgen receptor gene has been found in recurrent hormone-refractory prostate tumors, but not in primary prostate tumors (Visakorpi et al, 1995).…”

Section: Discussionmentioning

confidence: 99%

A one centimorgan deletion unit on chromosome Xq12 is commonly lost in borderline and invasive epithelial ovarian tumors

et al. 1998

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We have used polymerase chain reaction (PCR) ampli®cation of tandem repeats to study the pattern of allelic loss on chromosome X11.2-q12 in borderline and invasive epithelial ovarian tumors. Using eight microsatellite markers spanning Xq11.2-q12, 41 borderline and 65 invasive ovarian tumors, together with their corresponding normal tissues, were analysed. The highest percentage of loss of heterozygosity (LOH) was observed at the DXS1194 locus in borderline tumors (four of 16 informative cases, 25%) and at the androgen receptor (AR) locus in invasive epithelial ovarian tumors (18 of 47 informative cases, 38%). X chromosome activation studies performed in cases with LOH at the AR locus showed that the allelic loss at the AR locus is not con®ned to the inactive allele. A one centimorgan region including the AR locus and¯anked by the primers DXS1161 and PGK1P1 was identi®ed as the smallest common loss region in both borderline and invasive epithelial ovarian tumors.

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Section: Discussionmentioning

confidence: 99%

A one centimorgan deletion unit on chromosome Xq12 is commonly lost in borderline and invasive epithelial ovarian tumors

et al. 1998

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“…97 Shorter CAG repeat lengths have been associated with a greater risk of developing prostate cancer and prostate cancer progression. 98,99 Clinical trials such as the Prostate Cancer Prevention Trial (PCPT) are drawing to a close and should provide important clinical and molecular data on the role of decreasing the amount of available dehydroxytestosterone (DHT), the most active form of testosterone. Patients on this trial received long-term administration of the 5-hydroxyreductase inhibitor, fenasteride, which lowers levels of circulating DHT.…”

Section: Androgen Receptor and Prostate Cancer Developmentmentioning

confidence: 99%

Molecular genetics of human prostate cancer

Rubin

Marzo

2004

Modern Pathology

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Multiple factors contribute to the high incidence and prevalence of prostate cancer including race, ethnicity, diet, environment, widespread awareness through prostate-specific antigen screening and genetics. Linkage analysis has identified several candidate sites for hereditary prostate cancer gene loci. Molecular studies have also identified genes that are frequently altered in sporadic prostate cancer. It appears that due to the heterogeneity of prostate cancer, multiple genes may be involved in the neoplastic process.

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“…For example mutations in the androgen receptor have been associated with the progression of human prostate cancer to androgen independence. 12 Furthermore, deregulated androgen receptor function, as a consequence of mutation, has been associated with altered response to hormone ligands such as estradiol, 13¯u tamide, 14 progesterone, dehydroepiandrosterone, androstenedione 15 and glucocorticoids. 16,17 Based on these studies it appears that mutated forms of AR may provide a selective growth advantage and implicate these variants in tumor genesis, progression and metastasis.…”

Section: The Androgen Signalling Axismentioning

confidence: 99%

Androgens and growth factors in prostate cancer: a transgenic perspective

Greenberg

2000

Prostate Cancer Prostatic Dis

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With the advent of transgenic technology, novel animal models are being developed to facilitate prostate cancer research. The ability to perform genetic perturbation studies in a temporally and spatially restricted manner has established a new paradigm for investigations of the molecular mechanisms involved in the initiation, progression and metastogenesis of prostate cancer. Using the transgenic adenocarcinoma of the mouse prostate (TRAMP) model we have begun to identify speci®c molecular events related to the emergence of the androgen-insensitive phenotype. In addition, a number of new models have recently been generated to characterize how the deregulation of stromal to epithelial interactions mediated by polypeptide growth factor signaling could facilitate transformation of the prostate. It is anticipated that these models and their successors will ultimately provide new molecular pathway-based strategies for the prevention, detection and treatment of prostate cancer. Prostate Cancer and Prostatic Diseases (2000) 3, 224±228.

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Microsatellite Mutation (Cag24→18) in the Androgen Receptor Gene in Human Prostate Cancer

Cited by 152 publications

References 0 publications

A one centimorgan deletion unit on chromosome Xq12 is commonly lost in borderline and invasive epithelial ovarian tumors

A one centimorgan deletion unit on chromosome Xq12 is commonly lost in borderline and invasive epithelial ovarian tumors

Molecular genetics of human prostate cancer

Androgens and growth factors in prostate cancer: a transgenic perspective

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