The Molecular Biology of Prostate Cancer

2008 ◽  
pp. 141-159 ◽  
Author(s):  
J.J. Waxman
Keyword(s):  
Prostate Cancer ◽  
Molecular Biology

Molecular Biology of Androgen Receptors in Prostate Cancer Cells

1991 ◽  
pp. 355-361
Author(s):  
Charles Y.-F. Young ◽  
Shu-Dong Qiu ◽  
James L. Prescott ◽  
Donald J. Tindall
Keyword(s):  
Prostate Cancer ◽  
Molecular Biology ◽  
Cancer Cells ◽  
Androgen Receptors ◽  
Prostate Cancer Cells

Molecular Biology Underlying the Clinical Heterogeneity of Prostate Cancer: An Update

2009 ◽  
Vol 133 (7) ◽  
pp. 1033-1040 ◽  
Author(s):  
A. Craig Mackinnon ◽  
Benjamin C. Yan ◽  
Loren J. Joseph ◽  
Hikmat A. Al-Ahmadie
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Molecular Biology ◽  
Gene Rearrangement ◽  
Molecular Characteristics ◽  
Early Event ◽  
Ablation Therapy ◽  
Androgen Ablation ◽  
Development Of Resistance ◽  
Prostate Cancers

Abstract Context.—Recent studies have uncovered a number of possible mechanisms by which prostate cancers can become resistant to systemic androgen deprivation, most involving androgen-independent reactivation of the androgen receptor. Genome-wide expression analysis with microarrays has identified a wide array of genes that are differentially expressed in metastatic prostate cancers compared to primary nonrecurrent tumors. Recently, recurrent gene fusions between TMPRSS2 and ETS family genes have been identified and extensively studied for their role in prostatic carcinoma. Objective.—To review the recent developments in the molecular biology of prostate cancer, including those pertaining to the androgen receptor and the newly identified TMPRSS2-related translocations. Data Sources.—Literature review and personal experience. Conclusions.—Prostatic adenocarcinoma is a heterogeneous group of neoplasms with a broad spectrum of pathologic and molecular characteristics and clinical behaviors. Numerous mechanisms contribute to the development of resistance to androgen ablation therapy, resulting in ligand-independent reactivation of the androgen receptor, including amplification, mutation, phosphorylation, and activation of coreceptors. Multiple translocations of members of the ETS oncogene family are present in approximately half of clinically localized prostate cancers. TMPRSS2:ERG gene rearrangement appears to be an early event in prostate cancer and is not observed in benign or hyperplastic prostatic epithelium. Duplication of TMPRSS2:ERG appears to predict a worse prognosis. The relationship between TMPRSS2:ERG gene rearrangement and other morphologic and prognostic parameters of prostate cancer is still unclear.

Molecular Biology of Progression of Prostate Cancer

1999 ◽  
Vol 35 (5-6) ◽  
pp. 351-354 ◽  
Author(s):  
Nina Nupponen ◽  
Tapio Visakorpi
Keyword(s):  
Prostate Cancer ◽  
Molecular Biology

Recent advances in the histopathology and molecular biology of prostate cancer

2000 ◽  
Vol 85 (1) ◽  
pp. 87-94 ◽  
Author(s):  
J.L. Burton ◽  
N. Oakley ◽  
J.B. Anderson
Keyword(s):  
Prostate Cancer ◽  
Molecular Biology ◽  
Recent Advances

scholarly journals FTIR spectroscopy reveals the concentration dependence of cellular modifications induced by anticancer drugs

2010 ◽  
Vol 24 (1-2) ◽  
pp. 45-49 ◽  
Author(s):  
Régis Gasper ◽  
Tatjana Mijatovic ◽  
Robert Kiss ◽  
Erik Goormaghtigh
Keyword(s):  
Prostate Cancer ◽  
Molecular Biology ◽  
Anticancer Drugs ◽  
Large Scale ◽  
Proof Of Concept ◽  
Prostate Cancer Cells ◽  
Chemical Libraries ◽  
Anti Cancer ◽  
Cellular Modifications ◽  
Large Scale Screening

Large-scale screening to determine the mechanisms of anti-cancer actions of chemical libraries still presents technical challenges that are beyond the capabilities of conventional methods used in cellular or molecular biology. We recently demonstrated in a proof-of-concept study that infrared (IR) spectrum of cells exposed to anticancer drugs could be used to classify their mechanisms of actions. This study highlighted the fact that molecules inducing unique metabolic modifications could be selected for further pharmacological improvements. We show in this paper that drug concentration is an important parameter to be taken into account when analyzing mechanisms of anti-cancer actions by means of FTIR. The data indeed demonstrated that distinct spectral modifications occur in human PC-3 prostate cancer cells when exposed to ouabain at 10 × IC50versus 1 × IC50. Longer incubation times at 1 × IC50never resulted in spectral modifications fitting with those observed at 10 × IC50.

Prostate cancer: molecular biology of early progression to androgen independence.

1999 ◽  
pp. 487-502 ◽  
Author(s):  
M D Sadar ◽  
M Hussain ◽  
N Bruchovsky
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Molecular Biology ◽  
Tumour Progression ◽  
Specific Antigen ◽  
Signal Transduction Pathway ◽  
Underlying Mechanism ◽  
Amino Terminus ◽  
Androgen Independence ◽  
Androgen Withdrawal

To improve the therapy for prostate cancer, it will be necessary to address the problems of progression to androgen independence and the process of metastatic spread of tumour. The complexity of the latter condition is likely to mitigate against the immediate development of relevant therapeutic approaches. However, the basis of androgen independence appears to be a problem of simpler dimensions and more amenable to treatment with current therapeutic technology. Since early tumour progression can be detected by an incomplete prostate-specific antigen (PSA) response to androgen withdrawal therapy, a study of the molecular biology of PSA gene regulation may well provide insight into new methods for preventing or delaying this problem. Mounting evidence suggests that ligand-independent activation of the androgen receptor may be one underlying mechanism of androgen independence. In the absence of androgen, a compensatory increase in the activity of cAMP-dependent protein kinase (PKA) enhances the ability of the androgen receptor to bind to the response elements regulating PSA gene expression. The activation of the androgen receptor through up-regulation of the PKA signal transduction pathway involves the amino-terminus of the androgen receptor, the function of which may be altered either by modifications such as phosphorylation, or through interactions with co-regulators or other proteins. Of therapeutic interest is the fact that this effect can be counteracted experimentally by the anti-androgen, bicalutamide, and clinically by several other similar agents. We speculate that the inhibition of PKA-activated androgen receptor might also be accomplished by decoy molecules that can bind to the relevant activated site on the amino-terminus or competitively interact with proteins recruited by the PKA pathway that are responsible for activating the receptor in the absence of androgen. Such molecules might include small mimetic substances or agents that can gain access to the nucleus of the cell.

Sign in / Sign up

Export Citation Format

Share Document