The PTEN gene is involved in 10q23 deletions in several types of cancer, in
cluding glioma, melanoma, endometrial and prostate carcinomas. The PTEN gen
e product is a dual-specificity phosphatase with putative tumor suppressor
function. Deletions and rearrangements of 10q22-25 have been reported in si
milar to 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 sub
types for mutations and homozygous deletions of PTEN. We report somatic cod
ing/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 cytogene
tically characterized NHL cases (n = 6) with 10q22-q25 abnormalities displa
yed neither biallelic deletions nor mutations of PTEN. These results sugges
t that a tumor suppressor gene distinct from PTEN may be involved in 10q de
letions in this subgroup of NHL cases. Genes Chromosomes Cancer 24:322-327,
1999. (C) 1999 Wiley-Liss, Inc.