Proliferation, apoptosis and cell cycle regulation in prostatic carcinogenesis.
Cancer progression occurs because of imbalance in the processes of proliferation, differentiation and programmed cell death. In prostate cells, these processes are regulated at least in part by androgens. Structural alterations occur in a variety of genes regulating such processes. In order to obtain meaningful information on the biologic behavior of prostate cancers, it is important to assess androgen dependence and alterations in key genes regulating cell cycle kinetics as well as the aberrant response in cellular proliferation and death that such genetic events bring about. Most genetic alterations resulting in cancer progression alter normal cell cycle progression. Assessment of cell division cycle alterations by means of quantitative methods may have prognostic value, while interference with cell cycle regulatory proteins may result in powerful therapeutic tools. Here we review the methodologies utilized in the assessment of cell cycle kinetics and the abnormalities in proliferation and apoptosis encountered in prostate cancer. In addition, alterations in novel, important genes likely to have an impact on the behavior of prostate cancer and its precursor lesions are discussed. Molecular assessment of genetic alterations in genes that play a pivotal role in prostate cancer coupled with quantitative cytometry of cell kinetics may be utilized for a more precise evaluation of biologic behavior of prostate neoplasms.
Magi-Galluzzi
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Department of Pathology, Beth Israel-Deaconess Medical Center, Boston, Massachusetts 02215, USA. mloda@bidmc.harvard.edu
Murphy
M
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Cangi
M G
MG
Loda
M
M
D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D002455:Cell Division; D002471:Cell Transformation, Neoplastic / Q000473:pathology*; D018450:Disease Progression; D006801:Humans; D008297:Male; D011471:Prostatic Neoplasms / Q000175:diagnosis / Q000473:pathology*