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PRLTS gene alterations in human prostate cancer
Japanese Journal of Cancer Research : Gann
|April 1, 1997
Summary
Loss of heterozygosity at the PRLTS gene locus is common in prostate cancer. However, mutations in this candidate tumor suppressor gene are rare, suggesting other mechanisms are involved in prostate cancer development.
Area of Science:
- Oncology
- Genetics
- Molecular Biology
Background:
- Loss of heterozygosity (LOH) on chromosome 8p22-p21.3 is frequently observed in prostate cancer.
- The PRLTS gene, a candidate tumor suppressor, is located in this critical region.
Purpose of the Study:
- To investigate the status of the PRLTS gene in Japanese prostate cancer patients.
- To determine the frequency of LOH and mutations in the PRLTS gene in relation to prostate cancer progression.
Main Methods:
- DNA isolation from 69 Japanese prostate cancer patients (localized and cancer-death cases).
- Analysis of loss of heterozygosity at the PRLTS gene locus.
- Mutation screening of the PRLTS gene.
Main Results:
- LOH at the PRLTS locus was found in 42% of localized and 69% of cancer-death prostate cancer cases.
- A single missense mutation (Thr64Met) was identified in one cancer-death patient with metastatic disease, exhibiting LOH.
- No other mutations were detected in the PRLTS gene across the study cohort, irrespective of LOH status.
Conclusions:
- LOH at the PRLTS gene locus is a common event in prostate cancer, particularly in advanced stages.
- Mutations in the PRLTS gene appear to be infrequent in prostate cancer, suggesting LOH may be the primary mechanism of inactivation or that other genes in the region are involved.