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Analysis of PTEN mutations and deletions in B‐cell non‐Hodgkin's lymphomas
Author(s) -
Butler Marion P.,
Wang Steven I.,
Chaganti R.S.K.,
Parsons Ramon,
DallaFavera Riccardo
Publication year - 1999
Publication title -
genes, chromosomes and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.754
H-Index - 119
eISSN - 1098-2264
pISSN - 1045-2257
DOI - 10.1002/(sici)1098-2264(199904)24:4<322::aid-gcc5>3.0.co;2-9
Subject(s) - pten , cancer research , biology , tumor suppressor gene , lymphoma , gene , carcinogenesis , genetics , immunology , pi3k/akt/mtor pathway , apoptosis
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. Genes Chromosomes Cancer 24:322–327, 1999. © 1999 Wiley‐Liss, Inc.