Expression profiling reveals fundamental biological differences in acute myeloid leukemia with isolated trisomy 8 and normal cytogenetics
Author(s) -
Kimmo Virtaneva,
Fred A. Wright,
Stephan M. Tanner,
Bo Yuan,
William J. Lemon,
Michael A. Caligiuri,
Clara D. Bloomfield,
Albert de la Chapelle,
Ralf Krahe
Publication year - 2001
Publication title -
proceedings of the national academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.98.3.1124
Subject(s) - myeloid leukemia , biology , trisomy , trisomy 8 , cd34 , cancer research , cytogenetics , leukemia , chromosome abnormality , haematopoiesis , bone marrow , progenitor cell , population , stem cell , myeloid , microbiology and biotechnology , gene , genetics , immunology , karyotype , chromosome , medicine , environmental health
Acute myeloid leukemia (AML) is a heterogeneous group of diseases. Normal cytogenetics (CN) constitutes the single largest group, while trisomy 8 (+8) as a sole abnormality is the most frequent trisomy. How trisomy contributes to tumorigenesis is unknown. We used oligonucleotide-based DNA microarrays to study global gene expression in AML+8 patients with +8 as the sole chromosomal abnormality and AML-CN patients. CD34(+) cells purified from normal bone marrow (BM) were also analyzed as a representative heterogeneous population of stem and progenitor cells. Expression patterns of AML patients were clearly distinct from those of CD34(+) cells of normal individuals. We show that AML+8 blasts overexpress genes on chromosome 8, estimated at 32% on average, suggesting gene-dosage effects underlying AML+8. Systematic analysis by cellular function indicated up-regulation of genes involved in cell adhesion in both groups of AML compared with CD34(+) blasts from normal individuals. Perhaps most interestingly, apoptosis-regulating genes were significantly down-regulated in AML+8 compared with AML-CN. We conclude that the clinical and cytogenetic heterogeneity of AML is due to fundamental biological differences.
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