PTEN, A PUTATIVE PROTEIN-TYROSINE-PHOSPHATASE GENE MUTATED IN HUMAN BRAIN, BREAST, AND PROSTATE-CANCER

Mapping of homozygous deletions on human chromosome 10q23 has led to t he isolation of a candidate tumor suppressor gene, PTEN, that appears to be mutated at considerable frequency in human cancers. In prelimina ry screens, mutations of PTEN were detected in 31% (13/42) of glioblas toma cell lines and xenografts, 100% (4/4) of prostate cancer cell lin es, 6% (4/65) of breast cancer cell lines and xenografts, and 17% (3/1 8) of primary glioblastomas. The predicted PTEN product has a protein tyrosine phosphatase domain and extensive homology to tensin, a protei n that interacts with actin filaments at focal adhesions. These homolo gies suggest that PTEN may suppress tumor cell growth by antagonizing protein tyrosine kinases and may regulate tumor cell invasion and meta stasis through interactions at focal adhesions.