Neurofibromatosis 1, and not TP53, seems to be the main target of chromosome 17 deletions in de novo acute myeloid leukemia [15]

Journal of Clinical Oncology

Volumn 25, Issue 9, 2007, Pages 1151-1152

  Suela, Javier ^a   Largo, Cristina ^a   Ferreira, Bibiana ^a   Álvarez, Sara ^a   Robledo, Mercedes ^a   González Neira, Anna ^a   Calasanz, Maria José ^b   Cigudosa, Juan C ^a  

^a Structural Biology and Biocomputing Programme   (Spain)

^b UNIVERSITY OF NAVARRA   (Spain)

Author keywords

[No Author keywords available]

Indexed keywords

NEUROFIBROMIN; PROTEIN P53; TP53 PROTEIN, HUMAN; UNCLASSIFIED DRUG;

ACUTE GRANULOCYTIC LEUKEMIA; ALLELE; CHROMOSOME 17; CHROMOSOME ABERRATION; CHROMOSOME DELETION; DNA FINGERPRINTING; FLUORESCENCE IN SITU HYBRIDIZATION; HETEROZYGOSITY; HUMAN; KARYOTYPE; LETTER; PRIORITY JOURNAL; PROTEIN TARGETING; SINGLE NUCLEOTIDE POLYMORPHISM; ACUTE DISEASE; DNA MICROARRAY; GENE DELETION; GENE EXPRESSION PROFILING; GENE EXPRESSION REGULATION; GENETICS; HETEROZYGOSITY LOSS; MYELOID LEUKEMIA; NEUROFIBROMATOSIS; NOTE; REPRODUCIBILITY;

ACUTE DISEASE; CHROMOSOMES, HUMAN, PAIR 17; GENE DELETION; GENE EXPRESSION PROFILING; GENE EXPRESSION REGULATION, LEUKEMIC; HUMANS; IN SITU HYBRIDIZATION, FLUORESCENCE; LEUKEMIA, MYELOID; LOSS OF HETEROZYGOSITY; NEUROFIBROMATOSIS 1; OLIGONUCLEOTIDE ARRAY SEQUENCE ANALYSIS; REPRODUCIBILITY OF RESULTS; TUMOR SUPPRESSOR PROTEIN P53;

EID: 34047235283     PISSN: 0732183X     EISSN: None     Source Type: Journal    
DOI: 10.1200/JCO.2006.09.3013     Document Type: Letter

References (8)

1. Rücker FG, Bullinger L, Schwaenen C, et al: Disclosure of candidate genes in acute myeloid leukemia with complex karyotypes using microarray-based molecular characterization. J Clin Oncol 24:3887-3894, 2006
2. Barrett MT, Scheffer A, Ben-Dor A, et al: Comparative genomic hybridization using oligonucleotide microarrays and total genomic DNA. Proc Natl Acad Sci U S A 101:17765-17770, 2004
3. Peiffer DA, Le JM, Steemers FJ, et al: High-resolution genomic profiling of chromosomal aberrations using Infinium whole-genome genotyping. Genome Res 16:1136-1148, 2006
4. Raghavan M, Lillington DM, Skoulakis S, et al: Genome-wide single nucleotide polymorphism analysis reveals frequent partial uniparental disomy due to somatic recombination in acute myeloid leukemias. Cancer Res 65:375-378, 2005
5. Christiansen DH, Andersen MK, Pedersen-Bjergaard J: Mutations with loss of heterozygosity of p53 are common in therapy-related myelodysplasia and acute myeloid leukemia after exposure to alkylating agents and significantly associated with deletion or loss of 5q, a complex karyotype, and a poor prognosis. J Clin Oncol 19:1405-1413, 2001
6. Herzog G, Lu-Hesselmann J, Zimmermann Y, et al: Microsatellite instability and p53 mutations are characteristic of subgroups of acute myeloid leukemia but independent events. Haematologica 90:693-695, 2005
7. Stephens K, Weaver M, Leppig KA, et al: Interstitial uniparental isodisomy at clustered breakpoint intervals is a frequent mechanism of NF1 inactivation in myeloid malignancies. Blood 108:1684-1689, 2006
8. Birnbaum RA, O'Marcaigh A, Wardak Z, et al: NF1 and GMCSF interact in myeloid leukemogenesis. Mol Cell 5:189-195, 2000