CCR Co NF 1 Mye

recurr moso spann the N tified (10 p gain). each o 2 case sampl reduc hetero of 10 NF1 e numb NF1 e NF protei impor Activa appro cytic leuke mato have marke ing m sine p presen activa his issue of Clinical Cancer Research, Parkin and gues report on the identification of a subset of adult myelogenous leukemia (AML), in which the tumor essor NF1 is functionally inactive, resulting in ind Ras signaling and sensitivity to mammalian target amycin (mTOR) inhibition (1). The authors found ML CD34+/C38− cells with absent NF1 expression nsitive to treatment with rapamycin, thus implicatTOR as a therapeutic target within the leukemiating compartment of a small subgroup of adult atients. L is a highly malignant hematopoietic neoplasm, cterized by a poor prognosis, especially in older ts. In addition to age, the major prognostic marker genetics, and the mutational status of selected genes NPM1, FLT3) strongly influence prognosis in the of AML cases that are cytogenetically normal (2). eatment of AML has changed little in the past several es, and the discovery of additional leukemia-initiating in this disease has the potential to identify novel theric targets. The approach employed by Parkin and gues (1), using high-density single nucleotide polyism (SNP) microarrays to identify chromosomal loci ecurrent somatic copy number abnormalities, has d successful in this regard, and was used to identify and c-CBL as pathogenic genes in myeloid malignan, 4). kin and colleagues report on their detailed investigaf purified leukemic blasts and paired buccal DNA les from 95 adult AML patients, the majority of mary AML and were untreated (1). Using NP microarrays, the authors identified result recent ation show patho Dir As a r ing d exam (ERK) The su n: Division of Hematology, Department of Medicine, en's Hospital, Harvard Medical School, Boston,