Volume 24, Issue 4 pp. 322-327
Research Article

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

Marion P. Butler

Marion P. Butler

Division of Oncology, Departments of Pathology and Medicine, College of Physicians and Surgeons, Columbia University, New York

M.P.B. was supported by the Mater College Hospital, Dublin, and the Vocational Education Committee, Co. Donegal, Ireland, and is a registered Ph.D. student from the University College Dublin, Ireland.

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Steven I. Wang

Steven I. Wang

Division of Oncology, Departments of Pathology and Medicine, College of Physicians and Surgeons, Columbia University, New York

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R.S.K. Chaganti

R.S.K. Chaganti

Cell Biology and Genetics Program, Department of Human Genetics, Memorial Sloan-Kettering Cancer Center, New York

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Ramon Parsons

Ramon Parsons

Division of Oncology, Departments of Pathology and Medicine, College of Physicians and Surgeons, Columbia University, New York

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Riccardo Dalla-Favera

Corresponding Author

Riccardo Dalla-Favera

Division of Oncology, Departments of Pathology and Medicine, College of Physicians and Surgeons, Columbia University, New York

Division of Oncology, Department of Pathology, College of Physicians and Surgeons, Columbia University, 630 West 168th Street, New York, NY 10032.Search for more papers by this author

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. Genes Chromosomes Cancer 24:322–327, 1999. © 1999 Wiley-Liss, Inc.

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