J. Schutte et al., ANALYSIS OF THE P53 GENE IN PATIENTS WITH ISOCHROMOSOME-17Q AND PH(1)-POSITIVE OR PH1-NEGATIVE MYELOID-LEUKEMIA, Leukemia research, 17(6), 1993, pp. 533-539
Increased incidence of p53 gene aberrations or chromosome 17p monosomy
resulting from an isochromosome 17q [i(17q)] has been observed with t
ransition of chronic myelogenous leukemia (CML) to myeloid blast crisi
s (BC), and in some patients with poor risk acute myeloid leukemia (AM
L) progressing from myelodysplastic syndrome (MDS). These data suggest
ed that disease progression may be linked to bi-allelic inactivation o
f p53. Here, we report on p53 gene analyses of nine patients with CML-
BC and AML who showed an i(17q) as characteristic cytogenetic anomaly.
Using Southern blots, agarose gel electrophoresis and single-strand c
onformation polymorphism analyses of PCR products from genomic DNA and
cDNA, spanning exons 4 through 9, we did not detect any structural ab
normalities of the remaining p53 allele. These findings question the h
ypothesis that p53 gene alterations are the principal molecular event
responsible for progression of CML chronic phase or MDS to i(17q)-posi
tive CML-BC or AML, respectively.