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CGA gene (coding for the alpha subunit of glycoprotein hormones) overexpression in ER alpha-positive prostate tumors.

Authors: Bieche, I  Latil, A  Parfait, B  Vidaud, D  Laurendeau, I  Lidereau, R  Cussenot, O  Vidaud, M 
Citation: Bieche I, etal., Eur Urol. 2002 Mar;41(3):335-41.
Pubmed: (View Article at PubMed) PMID:12180238

OBJECTIVE: The precise role of estrogen, estrogen receptor (ER) and ER-responsive genes in prostate carcinogenesis is unclear. Paradoxically, estrogens and antiestrogens are used in the treatment of advanced metastatic prostate cancers. Recently, we identified CGA gene coding for the alpha subunit of glycoprotein hormones as a new ER alpha-responsive gene in human breast cancer cells. The aim of this study was to explore the role of CGA in the second major hormone-related cancer, i.e. prostate cancer. PATIENTS AND METHODS: We quantified CGA mRNA in nine cases of benign prostatic hyperplasia (BPH) and 23 sporadic prostate tumors (TP) by using a real-time quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) assay. RESULTS: CGA overexpression (> 10 S.D. above the mean in normal prostate tissues (NP)) was observed in 39% of the TP (ranging from 4.4 to 174.5 times the level in NP) and in none of the BPH samples. CGA overexpression was not accompanied by overexpression of the CGB, LHB, TSHB or FSHB genes to produce ectopic glycoprotein hormones. CGA gene overexpression correlated with ER alpha normal expression (P = 0.016), but not with ER beta or androgen receptor (AR) expression status. CONCLUSION: These results point to CGA gene as a member of a novel dysregulated pathway in prostate cancer. CGA should therefore be considered for investigation as possible novel molecular marker in clinical applications and as possible new potential therapeutic target.

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RGD Object Information
RGD ID: 2293634
Created: 2008-06-10
Species: All species
Last Modified: 2008-06-10
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.