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Am J Translational Res 1(3):235-248,2009
Review Article
Molecular mechanisms involving prostate cancer racial disparity
David Hatcher, Garrett Daniels, Iman Osman, Peng Lee
Department of Pathology and Urology, New York University School of Medicine, New York, NY
Received March 31, 2009; accepted April 15, 2009; available online April 25, 2009
Abstract: African American (AA) men with prostate cancer (PCa) have worse disease, with a higher incidence,
younger age and more advanced disease at diagnosis, and a worse prognosis, compared to Caucasian (CA)
men. In addition to socioeconomic factors and lifestyle differences, molecular alterations contribute to this
discrepancy. In this review, we summarize molecular genetics research results interrelated with the biology of
PCa racial disparity. Androgen and androgen receptor (AR) pathways have long been associated with prostate
growth. Racial differences have also been found among variants of the genes of the enzymes involved in
androgen biosynthesis and metabolism, such as SRD5A2, CYP17, and CYP3A4. The levels of expression and
CAG repeat length of AR also show racial divergence and may be critical molecular alterations for racial disparity.
Growth factors and their receptors, which promote cancer cell growth, are another potential cause of the disparity;
both EGFR and EPHB2, two of the most studied receptors, show interethnic differences. Differences have also
been found among genes regulating cell apoptosis, such as BCL2, which is increased in PCa in the AA
population. Recent developments in genetics, proteomics, and genomics, among other molecular
biotechnologies, will greatly aid the advancement of translational research on PCa racial disparity, hopefully
culminating in the discovery of novel mechanisms of disease, in addition to prognostic markers and novel
therapeutic approaches. (AJTR904002).
Key Words: Prostate cancer, disparity, incidence, prognosis, molecular genetics, SRD5A2, CYP17, CYP3A4
Full Text PDF
Address all correspondence to:
Peng Lee, M.D., Ph.D.
Department of Pathology
New York University School of Medicine
New York Harbor Healthcare System
423 E. 23rd Street, 6139N
New York, NY 10010
Tel: (212)951-3418, Fax: (212)951-6341
E-mail: Peng.Lee@nyumc.org
Review Article
Molecular mechanisms involving prostate cancer racial disparity
David Hatcher, Garrett Daniels, Iman Osman, Peng Lee
Department of Pathology and Urology, New York University School of Medicine, New York, NY
Received March 31, 2009; accepted April 15, 2009; available online April 25, 2009
Abstract: African American (AA) men with prostate cancer (PCa) have worse disease, with a higher incidence,
younger age and more advanced disease at diagnosis, and a worse prognosis, compared to Caucasian (CA)
men. In addition to socioeconomic factors and lifestyle differences, molecular alterations contribute to this
discrepancy. In this review, we summarize molecular genetics research results interrelated with the biology of
PCa racial disparity. Androgen and androgen receptor (AR) pathways have long been associated with prostate
growth. Racial differences have also been found among variants of the genes of the enzymes involved in
androgen biosynthesis and metabolism, such as SRD5A2, CYP17, and CYP3A4. The levels of expression and
CAG repeat length of AR also show racial divergence and may be critical molecular alterations for racial disparity.
Growth factors and their receptors, which promote cancer cell growth, are another potential cause of the disparity;
both EGFR and EPHB2, two of the most studied receptors, show interethnic differences. Differences have also
been found among genes regulating cell apoptosis, such as BCL2, which is increased in PCa in the AA
population. Recent developments in genetics, proteomics, and genomics, among other molecular
biotechnologies, will greatly aid the advancement of translational research on PCa racial disparity, hopefully
culminating in the discovery of novel mechanisms of disease, in addition to prognostic markers and novel
therapeutic approaches. (AJTR904002).
Key Words: Prostate cancer, disparity, incidence, prognosis, molecular genetics, SRD5A2, CYP17, CYP3A4
Full Text PDF
Address all correspondence to:
Peng Lee, M.D., Ph.D.
Department of Pathology
New York University School of Medicine
New York Harbor Healthcare System
423 E. 23rd Street, 6139N
New York, NY 10010
Tel: (212)951-3418, Fax: (212)951-6341
E-mail: Peng.Lee@nyumc.org
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