| Abstract: |
The PTEN gene is involved in 10q23 deletions in several types of cancer, including glioma, melanoma, endometrial and prostate carcinomas. The PTEN gene product is a dual-specificity phosphatase with putative tumor suppressor function. Deletions and rearrangements of 10q22-25 have been reported in ~5%-10% of non-Hodgkin's lymphomas (NHLs), raising the possibility of PTEN involvement in these tumors. In order to address this question, we analyzed a panel of NHLs (n = 74) representative of the main histologic subtypes for mutations and homozygous deletions of PTEN. We report somatic coding/splice site mutations in 20% (2 of 10) of Burkitt's lymphoma cell lines and in 3% (2 of 64) of primary NHL cases analyzed. No homozygous deletions were found in these tumors. Interestingly, this study showed that cytogenetically characterized NHL cases (n = 6) with 10q22-q25 abnormalities displayed neither biallelic deletions nor mutations of PTEN. These results suggest that a tumor suppressor gene distinct from PTEN may be involved in 10q deletions in this subgroup of NHL cases. |
| Keywords: |
human tissue; gene mutation; major clinical study; sequence analysis; gene deletion; missense mutation; neoplasms; phosphatase; tumor cells, cultured; chromosome aberration; tumor suppressor gene; lymphoma, b-cell; nonhodgkin lymphoma; molecular sequence data; tumor suppressor proteins; pten phosphohydrolase; dna, neoplasm; chromosome breakage; chromosome rearrangement; base sequence; gene inactivation; dna mutational analysis; chromosome deletion; phosphoric monoester hydrolases; genes, tumor suppressor; chromosome mapping; chromosome 10q; lymphoma cell line; chromosome banding pattern; chromosomes, human, pair 10; humans; human; priority journal; article
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