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p16 INK4 /p15 INK4B gene inactivation is a frequent event in malignant T‐cell lines
Author(s) -
Brandter Laura Borgonovo,
Heyman Mats,
Rasool Omid,
Liu Yie,
Grandér Dan,
Einhorn Stefan
Publication year - 1996
Publication title -
european journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.904
H-Index - 84
eISSN - 1600-0609
pISSN - 0902-4441
DOI - 10.1111/j.1600-0609.1996.tb00721.x
Subject(s) - gene , event (particle physics) , cell culture , cancer research , biology , physics , microbiology and biotechnology , genetics , astrophysics
The cell cycle regulators p16 INK4 and p15 INK4B have been mapped to the minimal region of overlap for chromosome 9p21 deletions, observed in a number of malignancies, suggesting that they could be tumor suppressor genes (TSGs). In the case of pl6 INK4 this has been further substantiated by the finding of small intragenic mutations. In this study we have investigated the p16 INK4 and p15 INK4B genes in 16 malignant T‐cell lines by means of Southern blot, PCR and sequence analysis. p16 INK4 allelic deletions occurred in 15 of 16 cell lines; 12 of which were homozygous and 3 hemizygous. In 1 cell line (DND 41) the remaining p16 INK4 allele carried a microdeletion of 29 bp of exon 2, supporting the concept that p16 INK4 is a target TSG for deletions on 9p21. Most p16 INK4 deletions also included the p15 INK4B gene. However, 4 of the cell lines deleted for p16 INK4 showed no evidence of p15 INK4B loss, indicating that p15 INK4B is not the target in these cell lines.