Cell-cycle dysregulation and the molecular mechanisms of prostate cancer.
Prostate cancer is the most common cause of non-cutaneous cancer in men and although frequently latent is the second commonest cause of death. Screening for the disease was historically based on symptoms of urethral obstruction, clinical examination of the prostate gland and serum measurements of prostate specific antigen. As prostate cancer growth in the early stages is enhanced by androgens, the mainstay of therapy has been androgen ablation by pharmaco-therapeutic or surgical means. The subsequent development of androgen therapy resistant prostate cancer in many patients, for whom therapeutic options remain limited, has led researchers to focus attention on understanding the molecular genetics of prostate cancer. The array of genetic abnormalities observed in prostate tumors, which include changes in components of the cell cycle, suggest the disease is quite heterogeneous and may require further sub-classification based on genetic markers. Such analyses may lead to identification of relevant new prognostic and therapeutic indicators. The advent of transgenic mouse models of prostate cancer may provide a critical tool for the implementation of rational genetic based therapeutics and alternate drug design.
Amanatullah
D F
DF
The Albert Einstein Cancer Center, Department of Developmental and Molecular Biology, Albert Einstein College of Medicine, 1300 Morris Park Ave., Bronx, NY 10461, USA.
Reutens
A T
AT
Zafonte
B T
BT
Fu
M
M
Mani
S
S
Pestell
R G
RG
D000818:Animals; D015815:Cell Adhesion Molecules / Q000378:metabolism; D002453:Cell Cycle; D016213:Cyclins / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D018734:Genes, erbB-2 / Q000502:physiology; D006801:Humans; D008297:Male; D051379:Mice; D015513:Oncogene Proteins / Q000378:metabolism; D051059:PTEN Phosphohydrolase; D010744:Phosphoric Monoester Hydrolases / Q000378:metabolism; D011471:Prostatic Neoplasms / Q000188:drug therapy / Q000209:etiology / Q000473:pathology*; D018167:Receptors, Calcitriol / Q000378:metabolism; D025521:Tumor Suppressor Proteins
D015815:Cell Adhesion Molecules; D016213:Cyclins; D016207:Cytokines; D015513:Oncogene Proteins; D018167:Receptors, Calcitriol; D025521:Tumor Suppressor Proteins; D010744:Phosphoric Monoester Hydrolases; D051059:PTEN Phosphohydrolase; C494929:PTEN protein, human