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Down regulation of bcl‐2 by p53 in nasopharyngeal carcinoma and lack of detection of its specific t(14;18) chromosomal translocation in fixed tissues
Author(s) -
HARN HJ.,
HO LI.,
LIU CA.,
LIU GC.,
LIN FG.,
LIN JJ.,
CHANG JY.,
LEE WH.
Publication year - 1996
Publication title -
histopathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.626
H-Index - 124
eISSN - 1365-2559
pISSN - 0309-0167
DOI - 10.1046/j.1365-2559.1996.d01-431.x
Subject(s) - chromosomal translocation , nasopharyngeal carcinoma , immunohistochemistry , biology , p53 protein , gene , cancer research , apoptosis , polymerase chain reaction , chromosome , gene expression , carcinoma , microbiology and biotechnology , genetics , medicine , immunology , radiation therapy
High levels of bcl‐2 protein have been found in a wide variety of human cancers. Since p53 gene inactivation occurs in over half of human cancers, it is possible that loss of p53‐mediated repression of bcl‐2 gene expression accounts, at least in part, for the frequent abnormalities in bcl‐2 protein production seen in tumours. By using immunohistochemical methods, we have analysed thirty‐three nasopharyngeal carcinomas for p53 and bcl‐2 expression. We found an inverse correlation between the expression of these two proteins ( P < 0.001). Moreover, we utilized universal oligonucelotide primers of a region 5′ to the bcl‐2 MBR and at the 3′ end of J H segments to initiate a DNA polymerase chain reaction that amplified these bcl‐2‐J H junctures. Of the twelve nasopharyngeal carcinomas expressing bcl‐2, none showed a t(14;18) chromosome translocation. These findings may indicate potential mechanisms by which bcl‐2 regulates apoptosis.