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Establishment of a novel human B‐cell line (OZ) with t(14;18)(q32;q21) and aberrant p53 expression was associated with the homozygous deletions of p15 INK4B and p16 INK4A genes
Author(s) -
Nagai M.,
Fujita M.,
Ohmori M.,
Matsubara S.,
Taniwaki M.,
Horiike S.,
Tasaka T.,
Koeffler H. P.,
Takahara J.
Publication year - 1997
Publication title -
hematological oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 44
eISSN - 1099-1069
pISSN - 0278-0232
DOI - 10.1002/(sici)1099-1069(199708)15:3<109::aid-hon604>3.0.co;2-y
Subject(s) - gene , biology , cancer research , genetics , microbiology and biotechnology
The novel human pre‐B cell line OZ was established from a patient with an aggressive form of non‐Hodgkin's lymphoma. Karyotypic analysis of both the primary tumour and OZ cells revealed several marker chromosomes, including the t(14;18)(q32;q21) translocation, which involves the Bcl‐2 gene, and alterations on chromosome 17p. Southern blot analysis found identical rearrangements in the 5′ region of Bcl‐2 gene in the primary tumour and OZ cells. Homozygous deletions of the p15 INK4B and p16 INK4A genes, however, were present only in OZ cells. Western blot analysis detected aberrant small molecular‐weight p53 proteins in both cell types. In addition, OZ cells no longer expressed the CD20 antigen. These findings suggest that Bcl‐2 gene rearrangement and aberrant p53 expression resulted in the original B‐cell tumour. A subsequent transforming event involving the p15 INK4B and p16 INK4A genes may have generated more immature cells with a growth advantage during in vitro culture. The genetic alterations involving p53, p15and p16 INK4A may be implicated in the aggressive form of t(14;18)(q32;q21)‐bearing tumours and their poor prognosis. © 1997 John Wiley & Sons, Ltd.