Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Tumor suppressor genes in prostatic oncogenesis

R Bookstein1

  • 1Canji, Inc., San Diego, CA 92121.

Journal of Cellular Biochemistry. Supplement
|January 1, 1994
PubMed
Summary

Tumor suppressor gene mutations, like p53 and retinoblastoma (Rb), are key in prostate cancer development. Analyzing these genetic changes and allelic imbalances can offer insights into cancer mechanisms and potential biomarkers.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Evaluation of endostatin antiangiogenesis gene therapy in vitro and in vivo.

Cancer gene therapy·2002
Same author

PTEN expression is maintained in sporadic colorectal tumours.

The Journal of pathology·2001
Same author

The tumor suppressor PTEN negatively regulates insulin signaling in 3T3-L1 adipocytes.

The Journal of biological chemistry·2000
Same author

Adenovirus-mediated gene transfer of MMAC1/PTEN to glioblastoma cells inhibits S phase entry by the recruitment of p27Kip1 into cyclin E/CDK2 complexes.

Cancer research·1999
Same author

Phenotypic analysis of human glioma cells expressing the MMAC1 tumor suppressor phosphatase.

Oncogene·1999
Same author

High-density screen of human tumor cell lines for homozygous deletions of loci on chromosome arm 8p.

Genes, chromosomes & cancer·1999

Area of Science:

  • Oncology
  • Genetics
  • Molecular Biology

Background:

  • Tumor suppressor gene mutations are crucial in cancer development and progression.
  • Retinoblastoma (Rb) and p53 gene mutations are common in advanced prostate cancer but rare in early stages.
  • Understanding these mutations can reveal carcinogenic mechanisms and identify biomarkers.

Purpose of the Study:

  • To investigate the role of tumor suppressor gene mutations in prostate cancer.
  • To explore the potential of genetic alterations as surrogate endpoint biomarkers.
  • To analyze allelic losses in early and advanced prostate cancer stages.

Main Methods:

  • Analysis of retinoblastoma (Rb) and p53 gene mutations in prostate cancer.
  • Immunohistochemistry to detect p53 expression in neoplastic cells.
  • Quantitative measurement of allelic imbalance on chromosome arms 8p and 16q.
  • Assessment of genetic alterations in preneoplastic and neoplastic lesions.

Main Results:

  • Rb and p53 mutations occur in 20-50% of advanced prostate cancers, rarely in early stages.
  • Increased p53 expression may indicate mutation or DNA damage response.
  • Allelic losses on chromosome arms 8p and 16q are frequent, even in early prostate cancers.
  • Quantitative allelic imbalance measurement is feasible in small lesions, though challenging.

Conclusions:

  • Tumor suppressor gene mutations are significant in prostate cancer pathogenesis.
  • Genetic alterations, including allelic imbalances, show potential as biomarkers.
  • Further research is needed to establish the significance of allelic imbalance in prostatic oncogenesis.

Related Experiment Videos