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Frequent mutations in the p53 gene in human myeloid leukemia cell lines
K Sugimoto, H Toyoshima, R Sakai, K Miyagawa, K Hagiwara, F Ishikawa, F Takaku, Y Yazaki and H Hirai
Third Department of Internal Medicine, Faculty of Medicine, University of
Tokyo, Japan.
The p53 gene is currently considered to function as a tumor-suppressor gene
in various human malignancies. In hematologic malignancies, alterations in
the p53 gene have been shown in some human leukemias and lymphomas.
Although mutations in the p53 gene are infrequent in acute myelogenous
leukemia (AML) patients, we show in this report that alterations in the p53
gene are frequent in myeloid leukemia cell lines. We studied alterations of
the p53 gene in nine human myeloid leukemia cell lines by reverse
transcriptase-polymerase chain reaction (RT-PCR), single-strand
conformation polymorphism (SSCP) analysis, and direct sequencing.
Expression of the p53 gene was not detected at all by RT-PCR in two of the
nine cell lines. In these two cell lines, Southern blot analysis showed
gross rearrangements and deletions in both of the p53 alleles. Six of the
nine cell lines were found to express only mutant p53 mRNA by RT-PCR/SSCP
analysis and direct sequencing, and wild-type p53 mRNA was not detected.
Two of the mutant p53 mRNAs were shown to be products of abnormal splicing
events induced by intronic point mutations. Taken together, eight of nine
human myeloid leukemia cell lines expressed no or an undetectable amount of
wild-type p53 mRNA. Three of the eight cell lines were growth factor-
dependent. Our results suggest that inactivation of the p53 gene may be a
common feature in myeloid leukemia cell lines and may play an important
role in the establishment of these cell lines.
Volume 79,
Issue 9,
pp. 2378-2383,
05/01/1992
Copyright © 1992 by The American Society of Hematology
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