Analysis of PTEN mutations and deletions in B-cell non-Hodgkin's lymphomas

✍ Scribed by Marion P. Butler; Steven I. Wang; R.S.K. Chaganti; Ramon Parsons; Riccardo Dalla-Favera

• Publisher: John Wiley and Sons
• Year: 1999
• Tongue: English
• Weight: 166 KB
• Volume: 24
• Category: Article
• ISSN: 1045-2257
• DOI: 10.1002/(sici)1098-2264(199904)24:4<322::aid-gcc5>3.0.co;2-9

✦ Synopsis

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 ϳ5%-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 ϭ 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 ϭ 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.