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Deletion of cyclin-dependent kinase 4 inhibitor genes P15 and P16 in
non-Hodgkin's lymphoma
PR Koduru, M Zariwala, M Soni, JZ Gong, Y Xiong and JD Broome
Department of Laboratories, North Shore University Hospital, Manhasset, NY
11030, USA.
B-cell non-Hodgkin's lymphoma (NHL) is a heterogeneous lymphoid malignancy
consisting of several histologic types. Alterations in proto- oncogenes
caused by reciprocal chromosome translocations have been implicated in the
etiology of specific histologic groups. In this study, we examined the
contribution of the cell cycle inhibitor genes P15, P16, and P18 to
pathogenesis in a large panel of 209 cytogenetically characterized B-cell
NHL tumors representing varied histologic groups. We identified the
homozygous deletion of P15 and P16 genes in 13 tumors from 12 patients, all
belonging to diffuse large- cell histology; 10 had this diagnosis made on
presentation, 1 had transformed from small lymphocytic lymphoma, and 1 had
transformed from Hodgkin's disease. Tumor-specific point mutations were not
identified in the coding regions of these genes. Cytogenetically,
chromosome 9p was normal in all but one tumor. On the other hand, eight
tumors hemizygous for 9p by cytogenetic analysis showed wild-type
configuration of these genes. Our study, therefore, indicates that deletion
of P15 and P16 occurs in about 15% of diffuse large-cell NHL and is not
usually detected by cytogenetic analysis. P18 was wild-type in all tumors
including the 13 tumors hemizygous for 1p.
Volume 86,
Issue 8,
pp. 2900-2905,
10/15/1995
Copyright © 1995 by The American Society of Hematology
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