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Neoplasma Vol.52, p.318-324, 2005 |
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Title: Abnormalities of the P53, MDM2, BCL2 and BAX genes in acute leukemias | ||
Author: I., WOJCIK ; M., SZYBKA ; E., GOLANSKA ; P., RIESKE ; J.Z., BLONSKI ; T., ROBAK ; J., BARTKOWIAK ; | ||
Abstract: Abnormalities of the P53 network have been implicated in the
pathogenesis of acute lymphoblastic leukemia (ALL) and
acute myeloblastic leukemia (AML). The purpose of this study was
to define P53 gene mutations, to detect MDM2 gene amplification
and to estimate mRNA expression of P53, MDM2, BCL2 and BAX genes
in patients with ALL and AML.
Twenty-five patients with ALL and 65 patients with AML, both
recently diagnosed, were included into this study. Exons
5-8 of the P53 gene with flanking intronic sequence were amplified
by the polymerase chain reaction (PCR) method and
subjected to mutation screening by single-strand conformation
polymorphism analysis (SSCP). Mutation of the P53 gene
was found in one patient of the 25 with ALL and in five patients
of the 65 with AML. Sequence analysis was subsequently
performed. One mutation in intronic sequence in ALL and four
missense mutations and one silent nucleotide substitution in
AML were identified. Amplification of MDM2 gene was detected by
multiplex-PCR analysis in only one sample from patient
with ALL, but was not observed in any case of AML. To gain further
insight into the role of P53 network in the evolution
of acute leukemias, the P53, MDM2, BCL2 and BAX mRNAexpressions in
portion samples from patients with ALL and
AML were analyzed using multiplex RT-PCR. Although a low frequency
of molecular disturbances of the P53 and the
MDM2 genes was detected in this study, there was a high percentage
of cases with increased mRNA level of P53 and
MDM2. A high frequency of BCL2 mRNA overexpression and a
relatively low frequency of BAX mRNA overexpression
detected in both analyzed leukemias in this study, indicate that
altered transcription of these genes may be involved in
leukemogenesis.
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Keywords: P53, MDM2, BCL2, BAX, ALL, AML | ||
Year: 2005, Volume: 52, Issue: | Page From: 318, Page To: 324 | |
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