Related Experiment Videos

Chromosomal localisation of two putative 11p oncosuppressor genes involved in human ovarian tumours

A Viel1, F Giannini, L Tumiotto

  • 1Division of Experimental Oncology 1, Centro Riferimento Oncologico, Aviano (PN), Italy.

British Journal of Cancer
|December 1, 1992
PubMed

Insights

Loss of heterozygosity (LOH) on chromosome 11p is common in ovarian cancer, suggesting tumor suppressor genes in this region are involved. These findings link 11p deletions to potential hepatic involvement in ovarian carcinomas.

Area of Science:

  • Oncology
  • Human Genetics
  • Molecular Biology

Background:

  • Ovarian carcinomas are a significant cause of cancer-related mortality.
  • The genetic underpinnings of ovarian carcinogenesis are complex and not fully understood.
  • Chromosome 11p is implicated in various cancers, but its role in ovarian cancer requires further investigation.

Purpose of the Study:

  • To investigate allelic deletions on the short arm of chromosome 11 (11p) in human ovarian tumors.
  • To identify potential tumor suppressor genes involved in ovarian carcinogenesis.
  • To explore the association between 11p deletions and clinical parameters in ovarian cancer patients.

Main Methods:

  • Analysis of 44 primary or metastatic human ovarian tumors.
  • Southern blotting to assess loss of heterozygosity (LOH) at 12 polymorphic loci on chromosome 11p.
  • Statistical analysis to correlate 11p LOH with clinical and pathological data.

Main Results:

  • Loss of heterozygosity (LOH) at 11p was detected in 41% of the analyzed ovarian tumors.
  • Two deletion hotspots were tentatively mapped to chromosomal regions 11p13 and 11p15.5.
  • A statistically significant association was observed between 11p deletions and hepatic involvement (P = 0.005).

Conclusions:

  • Loss of heterozygosity at 11p is a frequent event in ovarian carcinomas.
  • The findings suggest the presence of at least two tumor suppressor genes on 11p involved in ovarian cancer development.
  • The observed similarities with 11p allelic losses in Wilms tumors indicate that inactivation of shared growth regulatory genes may contribute to ovarian carcinogenesis.

Related Concept Videos