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Absence of WAF1 mutations in a variety of human malignancies
M Shiohara, WS el-Deiry, M Wada, T Nakamaki, S Takeuchi, R Yang, DL Chen, B Vogelstein and HP Koeffler
Division of Hematology/Oncology, Cedars-Sinai Medical Center, UCLA School
of Medicine 90048.
A newly cloned gene named wild-type p53-activated fragment 1 (WAF1; also
known as p21, Pic-1, Cip-1, or SDI1) is directly regulated by p53 and can
itself suppress tumor cell growth in culture. Induction of expression of
WAF1 may be an important means by which cells with DNA injury arrest their
growth to repair DNA or undergo apoptosis. Based on the hypothesis that
mutations of this gene may play a role in carcinogenesis, we have studied
351 DNAs from 14 kinds of malignancies, as well as 36 human transformed
cell lines, for alterations of WAF1 gene by single-strand conformation
polymorphism analysis of polymerase chain reaction amplification of the DNA
coding region of the WAF1 gene. No abnormal band shifts of WAF1 were noted
in any of the samples or cell lines, but three major variants in exons 2
and 3 of the gene were found that are consistent with the existence of two
different DNA polymorphisms. Sequence analysis of the amplified products
producing these three variants in each exon from normal DNAs confirmed the
presence of the polymorphisms in the WAF1 gene. Of 290 selected tumor
samples previously evaluated for p53 mutations by single-strand
conformation polymorphism, 90% had no detectable p53 alterations. In
summary, mutations within the coding portion of the WAF1 gene were
undetectable in a large series of human tumors, many of which had a normal
p53 gene. This suggests that WAF1 alterations are generally caused
indirectly, through p53 mutations rather than through intragenic mutation
of the WAF1 itself.
Volume 84,
Issue 11,
pp. 3781-3784,
12/01/1994
Copyright © 1994 by The American Society of Hematology
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