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Isolation of Cancer Stem Cells From Human Prostate Cancer Samples
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Molecular pathways to prostate cancer.

Mark L Gonzalgo1, William B Isaacs

  • 1James Buchanan Brady Urological Institute, The Johns Hopkins Medical Institutions, Baltimore, Maryland, USA. mgonzal@jhmi.edu

The Journal of Urology
|November 25, 2003
PubMed
Summary
This summary is machine-generated.

Understanding prostate cancer progression requires examining genetic predisposition, somatic alterations, and epigenetic changes. New discoveries highlight inflammation

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Prostate cancer is a common malignancy in Western countries.
  • Advances in molecular biology, genetics, and biotechnology enhance understanding of prostate cancer initiation and progression.

Purpose of the Study:

  • To review recent scientific discoveries on genetic predisposition, somatic alterations, and epigenetic phenomena in prostate cancer pathogenesis.
  • To emphasize the role of somatic alterations in prostate cancer development.

Main Methods:

  • Literature search of MEDLINE database for reports on molecular biology, genetics, and epigenetics of prostate cancer.
  • Focus on articles investigating the contribution of somatic alterations.

Main Results:

  • Numerous genes implicated in prostate carcinogenesis have been identified.
  • Inflammation may contribute to preneoplastic or neoplastic lesions.
  • Abnormal methylation, aneuploidy, loss of heterozygosity, and gene mutations represent key pathways in cancer development.

Conclusions:

  • Identifying molecular markers for early and late prostate cancer events is crucial for improved detection and prognostication.
  • The precise mechanisms linking inflammation and prostate cancer require further elucidation.
  • Targeted therapies addressing somatic and epigenetic defects are needed due to their significant role in prostate carcinogenesis.