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EVI1 (Ecotropic Viral Integration site I), which was originally identified as a site of viral integration in murine myeloid tumors, encodes a complex protein required for embryogenesis. The gene is known to express inappropriately in many types of human myeloid leukemias and solid tumors. Forced expression of EVI1 in murine hematopoietic precursor cells(More)
Several lines of evidence suggest that specific transcriptional events are involved in cell cycle, proliferation and differentiation processes; however, their deregulation by proto-oncogenes are involved in the development of leukemia and tumors. One such proto-oncogene is ecotropic viral integration site I which can differentially effect cell cycle(More)
BACKGROUND & OBJECTIVES Chronic myeloid leukaemia is (CML) characterized by the presence of a hallmark chromosomal translocation, the Philadelphia chromosome. Although there are many reports available regarding the different variants of BCR-ABL in CML, we studied the co-expression of e13a2 and e14a2 transcripts and a few polymorphisms in CML patients. (More)
Although BCR-ABL is the hallmark genetic abnormality of chronic myeloid leukemia (CML), secondary molecular events responsible for the evolution of the disease to blast crisis are yet to be deciphered. Taking into account the significant association of ecotropic viral integration site I (EVI1) in CML drug resistance, it is necessary to decipher the other(More)
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