作者: Adolfo A. Ferrando , Donna S. Neuberg , Jane Staunton , Mignon L. Loh , Christine Huard
DOI: 10.1016/S1535-6108(02)00018-1
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摘要: Human T cell leukemias can arise from oncogenes activated by specific chromosomal translocations involving the receptor genes. Here we show that five different (HOX11, TAL1, LYL1, LMO1, and LMO2) are often aberrantly expressed in absence of abnormalities. Using oligonucleotide microarrays, identified several gene expression signatures were indicative leukemic arrest at stages normal thymocyte development: LYL1+ signature (pro-T), HOX11+ (early cortical thymocyte), TAL1+ (late thymocyte). Hierarchical clustering analysis grouped samples according to their shared oncogenic pathways HOX11L2 activation as a novel event leukemogenesis. These findings have clinical importance, since HOX11 is significantly associated with favorable prognosis, while or, surprisingly, confers much worse response treatment. Our results illustrate power profiles elucidate transformation relevant human leukemia.