Tumor angiogenic switch determines sustained proliferative malignant transformation in tumorigenesis and overlaps with para-inflammatory phenomena

摘要

Contextual BCR-ABL tyrosine kinase over-activity determines in formulated fashion the emergence of udproliferation and anti-apoptosis that arise largely as derived phenomena of otherwise homeostatic mechanisms of udthe c-ABL gene within hematopoietic stem cells and hemangioblasts in the bone marrow. The ability to suppress udalmost completely, both in terms of phenotype and cytogenetically, the myeloid cell line expansion by imatinib udmesylate is indicative of a phenomenon that depends strictly on the transformed status of the cell of origin in the udchronic myeloid leukemia process. It is with relevance to complex participation of the dynamics of the fused BCR- udABL protein product that contextual conditioning of the cells of origin of the gene translocation further motivates the uddimensional expansion of the transformed myeloid cell clones to increasing proliferative rates, thus leading to blast udcrisis as eventual loss of differentiating potential.