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Patients with Fanconi anemia and AML have different cytogenetic clones than de novo cases of AML
Author(s) -
Rochowski Andrzej,
Olson Susan B.,
Alonzo Todd A.,
Gerbing Robert B.,
Lange Beverly J.,
Alter Blanche P.
Publication year - 2012
Publication title -
pediatric blood and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.116
H-Index - 105
eISSN - 1545-5017
pISSN - 1545-5009
DOI - 10.1002/pbc.24168
Subject(s) - fanconi anemia , medicine , monosomy , myeloid leukemia , cytogenetics , trisomy 8 , trisomy , leukemia , myeloid , chromosome 7 (human) , oncology , karyotype , cancer research , genetics , biology , chromosome , gene , dna repair
Specific cytogenetic clones might distinguish patients with unrecognized Fanconi anemia (FA) who present with acute myeloid leukemia (AML) from those with sporadic AML. Cytogenetic reports in literature cases of FA and AML were compared with de novo cases enrolled on CCG‐2961. Gain of 1q, gain of 3q, monosomy 7, deleted 7q, gain of 13q, and deleted 20q were more frequent in FA AML; t(8;21), trisomy 8, t(9;11), t(6;9), and inversion 16 were exclusive to de novo AML cases. Observation of the FA AML cytogenetic clonal patterns should raise suspicion of an underlying leukemia predisposition syndrome and influence management. Pediatr Blood Cancer 2012; 59: 922–924. Published 2012. This article is a U.S. Government work and is in the public domain in the USA.