AI Article Synopsis
- The PTEN gene regulates the phosphatidylinositol 3-kinase pathway and is often inactive in various cancers, including prostate cancer.
- High loss of heterozygosity rates at the 10q23.3 region containing PTEN are common in prostate cancer, yet true biallelic inactivation rates are lower.
- Research using a mouse model shows that having only one functional PTEN gene (haploinsufficiency) leads to increased prostate cancer progression, explaining the discrepancies in PTEN inactivation rates seen in human cancers.
Article Abstract
The PTEN gene encodes a lipid phosphatase that negatively regulates the phosphatidylinositol 3-kinase pathway and is inactivated in a wide variety of malignant neoplasms. High rates of loss of heterozygosity are observed at the 10q23.3 region containing the human PTEN gene in prostate cancer and other human malignancies, but the demonstrated rate of biallelic inactivation of the PTEN gene by mutation or homozygous deletion is significantly lower than the rate of loss of heterozygosity. The transgenic adenocarcinoma of mouse prostate model is a well characterized animal model of prostate cancer. Analysis of prostate cancer progression in transgenic adenocarcinoma of mouse prostate mice bred to Pten(+/-) heterozygous mice, coupled with analysis of the Pten gene and protein in the resulting tumors, reveals that haploinsufficiency of the Pten gene promotes the progression of prostate cancer in this model system. This observation provides a potential explanation for the discordance in rates of loss of heterozygosity at 10q23 and biallelic PTEN inactivation observed in prostate cancer and many human malignancies.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC58769 | PMC |
| http://dx.doi.org/10.1073/pnas.201167798 | DOI Listing |
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