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PTEN, a putative protein tyrosine phosphatase gene mutated in human brain, breast, and prostate cancer
1Department of Pathology, College of Physicians & Surgeons, Columbia University, 630 West 168 Street, New York, NY 10032, USA.
Abstract:
Mapping of homozygous deletions on human chromosome 10q23 has led to the isolation of a candidate tumor suppressor gene, PTEN, that appears to be mutated at considerable frequency in human cancers. In preliminary screens, mutations of PTEN were detected in 31% (13/42) of glioblastoma cell lines and xenografts, 100% (4/4) of prostate cancer cell lines, 6% (4/65) of breast cancer cell lines and xenografts, and 17% (3/18) of primary glioblastomas. The predicted PTEN product has a protein tyrosine phosphatase domain and extensive homology to tensin, a protein that interacts with actin filaments at focal adhesions. These homologies suggest that PTEN may suppress tumor cell growth by antagonizing protein tyrosine kinases and may regulate tumor cell invasion and metastasis through interactions at focal adhesions.
Insights
The tumor suppressor gene PTEN is frequently mutated in various cancers, including glioblastoma and prostate cancer. PTEN
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- The PTEN gene, located on chromosome 10q23, is a candidate tumor suppressor.
- Mutations in tumor suppressor genes are critical in cancer development.
Purpose of the Study:
- To investigate the frequency of PTEN mutations in various human cancers.
- To understand the potential role of PTEN in tumor suppression and metastasis.
Main Methods:
- Screening of glioblastoma, prostate, and breast cancer cell lines and xenografts for PTEN mutations.
- Analysis of primary glioblastoma samples for PTEN alterations.
Main Results:
- PTEN mutations were detected in 31% of glioblastoma, 100% of prostate, and 6% of breast cancer cell lines.
- Mutations were also found in 17% of primary glioblastomas.
- The PTEN protein contains a tyrosine phosphatase domain and homology to tensin.
Conclusions:
- PTEN is frequently mutated in multiple human cancers, suggesting its role as a tumor suppressor.
- PTEN may inhibit tumor growth by antagonizing protein tyrosine kinases.
- PTEN's interaction with focal adhesions may regulate cancer cell invasion and metastasis.