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Blood, Vol. 95 No. 6 (March 15), 2000:
pp. 2138-2143
Deletions of chromosome 5q13.3 and 17p loci cooperate in myeloid
neoplasms
Patricia D. Castro,
Jan C. Liang, and
Lalitha Nagarajan
From the Department of Molecular Genetics, Division of Pathology and
Laboratory Medicine, University of Texas M. D. Anderson Cancer Center,
Houston, TX.
Nonrandom interstitial deletions and monosomy of chromosomes 5, 7, and 17 in refractory myelodysplasia (MDS) and acute myelogenous leukemia (AML) suggest a multistep pathway that culminates in aggressive clinical course. Because cytogenetic studies frequently identify chromosome 5 and 17 deletions within a single clone, we
searched for allele loss for 5q loci and TP53 gene mutations in the
same leukemic samples. Cosegregating deletions of chromosomes 5 and 17 were found to specifically include the 5q13.3 interval between the loci
D5S672 and D5S620/D5S626, a locus hypothesized to
harbor a tumor suppressor gene1 and the TP53 gene
on 17p. A rare patient with secondary refractory MDS and an unbalanced
translocation [der(5;17)], which resulted in deletions of the
5q13.3-qter and 17p loci, provided clues on the sequence of genetic
alterations. Serial molecular analysis of this patient revealed a
dysplastic clone with der(5;17), which gave rise to a leukemic clone on
acquiring an inactivating mutation of TP53. Our findings are
consistent with functional cooperation between a putative tumor
suppressor gene at 5q13.3 that contributes toward the progression of
early stages of MDS, and the TP53 gene when mutated, causes
transformation to AML.
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