نتایج جستجو برای: abl positive
تعداد نتایج: 663991 فیلتر نتایج به سال:
We have developed a competitive polymerase chain reaction (PCR) titration assay that estimates the number of BCR-ABL transcripts in chronic myeloid leukemia patients to monitor minimal residual disease after bone marrow transplantation (BMT). The assay gave reproducible results and allowed differences in BCR-ABL message levels of half an order of magnitude to be distinguished. Of 91 patients st...
PURPOSE Review the state-of-art knowledge of the biology and therapy of chronic myelogenous leukemia (CML). EXPERIMENTAL DESIGN A review of the literature was undertaken to summarize current information on the pathophysiology of CML and to update data of imatinib mesylate therapy, mechanisms of resistance, and in vitro and clinical data with the new tyrosine kinase inhibitors. RESULTS Imati...
Chronic myelogenous leukemia(CML)is characterized by the presence of the abnormal chromosome 22, which is termed the Philadelphia chromosome(Ph). The Ph is derived from a translocation between chromosomes 9 and 22, t (9; 22)(q 34; q 11). The c-abl oncogene on the long arm of chromosome 9 fused to the bcr gene on the long arm of chromosome 22 and leads to the formation of a chimeric bcr abl gene...
SHP-2 phosphatase forms a stable protein complex with and is heavily tyrosine-phosphorylated by the oncogenic tyrosine kinase Bcr-Abl. However, the role of SHP-2 in Bcr-Abl-mediated leukemogenesis is unclear. In the present report, we provide evidence that SHP-2 is required for hematopoietic cell transformation by Bcr-Abl. In vitro biological effects of Bcr-Abl transduction were diminished in S...
BCR-ABL overexpression and stem cell quiescence supposedly contribute to the failure of imatinib mesylate (IM) to eradicate chronic myeloid leukemia (CML). However, BCR-ABL expression levels of persisting precursors and the impact of long-term IM therapy on the clearance of CML from primitive and mature bone marrow compartments are unclear. Here, we have shown that the number of BCR-ABL– positi...
BACKGROUND AND OBJECTIVE We further characterized a novel type of chimeric BCR-ABL mRNA transcript detected in a patient with Philadelphia chromosome positive (Ph+) chronic myeloid leukemia (CML). DESIGN AND METHODS We used reverse-transcription polymerase chain reaction (RT-PCR) and sequence analysis of the fusion region of the amplified cDNA fragment. Western analysis was performed on total...
BCR/ABL-transformed chronic myeloid leukemia (CML) cells accumulate numerous DNA double-strand breaks (DSB) induced by reactive oxygen species (ROS) and genotoxic agents. To repair these lesions BCR/ABL stimulate unfaithful DSB repair pathways, homologous recombination repair (HRR), nonhomologous endjoining (NHEJ), and single-strand annealing (SSA). Here, we show that BCR/ABL enhances the expre...
In Philadelphia chromosome-positive human leukemias, the c-abl proto-oncogene on chromosome 9 becomes fused to the bcr gene on chromosome 22, and chimeric Bcr-Abl proteins are produced. The fused Bcr sequences activate the tyrosine kinase, actin-binding, and transforming functions of Abl. Activation of the Abl transforming function has been shown to require two distinct domains of Bcr: domain 1...
Cellular identity in metazoan organisms is frequently established through lineage-specifying transcription factors, which control their own expression through transcriptional positive feedback, while antagonizing the developmental networks of competing lineages. Here, we have uncovered a distinct positive feedback loop that arises from the reciprocal stabilization of the tyrosine kinase ABL and...
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