BCR-ABL promotes PTEN downregulation in chronic myeloid leukemia.
Texto
Imagem
Documentos relacionados
the vast majority of CML patients, as well as in 30% of adult acute lymphoblastic leukemia (ALL) and 20% of childhood chromosome Ph positive ALL, the breakpoint in the BCR gene
Multiple BCR-ABL kinase domain mutations confer polyclonal resistance to the tyrosine kinase inhibitor imatinib (STI571) in chronic phase and blast crisis chronic myeloid
Monitoring of BCR-ABL levels in chronic myeloid leukemia patients treated with imatinib in the chronic phase – the importance of a major molecular response1. Medical
Extraordinary scientific progress made in the field of chronic myeloid leukemia (CML) led to the development of orally available tyrosine kinase inhibitors (TKIs), dramatically
The identification of BCR-ABL expression as the defining leu- kemogenic event in chronic myeloid leukemia (CML) and the introduction of BCR-ABL tyrosine kinase inhibitors (TKIs)
Multiple BCR-ABL kinase domain mutations confer polyclonal resis- tance to the tyrosine kinase inhibitor imatinib (STI571) in chronic phase and blast crisis chronic myeloid
Relationship of bcr breakpoint to chronic phase duration, survival, and blast crisis lineage in chronic myelogenous leukemia patients presenting in early chronic phase. Molecu-
Evaluation of the expression of the tumor suppressor gene PTEN, proto-oncogene c-kit, matrilysin (MMP-7), Connexins 32 and 43 and E- caderinas/cateninas complex in mast