title: Molecular events in chronic myeloid leukemia progression.
abstract: Chronic myelogenous leukemia presents two distinct clinical phases: the chronic phase is characterised by a marked expansion of the myeloid compartment which still retains a normal differentiative capacity, whereas a differentiation block is the clinical hallmark of the acute transformation. The molecular mechanism underlying the CML progression are still poorly understood. The occurrence of additional molecular lesions, involving the p53, the RAS and the p16 genes may complement and fulfil the BCR/ABL transforming potential, finally leading to an acute leukemic phenotype. However, several lines of evidence suggest that also quantitative changes of the BCR/ABL transcript amounts could explain the progression of the leukemic phenotype in the BCR/ABL-positive hematologic malignancies.
authors.affiliation: Dipartimento Scienze Biomediche e Oncologia Umana Università di Torino, Italy.
authors.forename: A
authors.initials: A
authors.lastname: Guerrasio
authors.forename: A
authors.initials: A
authors.lastname: Serra
authors.forename: E
authors.initials: E
authors.lastname: Gottardi
authors.forename: D
authors.initials: D
authors.lastname: Cilloni
authors.forename: F
authors.initials: F
authors.lastname: Vischia
authors.forename: G
authors.initials: G
authors.lastname: Parvis
authors.forename: V
authors.initials: V
authors.lastname: Cilli
authors.forename: G
authors.initials: G
authors.lastname: Saglio
mesh_terms: D002874:Chromosome Mapping; D002899:Chromosomes, Human, Pair 9; D018450:Disease Progression; D016044:Fusion Proteins, bcr-abl / Q000096:biosynthesis; D017353:Gene Deletion; D016147:Genes, Tumor Suppressor; D016158:Genes, p53; D011905:Genes, ras; D019337:Hematologic Neoplasms / Q000235:genetics / Q000503:physiopathology; D006801:Humans; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000235:genetics* / Q000503:physiopathology*; D010641:Phenotype; D014158:Transcription, Genetic
chemical_list: D016044:Fusion Proteins, bcr-abl