نتایج جستجو برای: bcrabl
تعداد نتایج: 84 فیلتر نتایج به سال:
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/AIMS The treatment of chronic myeloid leukemia (CML) has achieved impressive success since the development of the Bcr-Abl tyrosine kinase inhibitor, imatinib mesylate. Nevertheless, resistance to imatinib has been observed, and a substantial number of patients need alternative treatment strategies. METHODS We have evaluated the effects of deferasirox, an orally active iron chelator...
The receptor-associated protein tyrosine kinase janus-kinase 2 (JAK2) is essential for normal red cell development and for erythropoietin receptor (EpoR) signaling. JAK22/2 embryos are severely deficient in erythropoiesis and die at an early stage of development from fetal anemia. The binding of erythropoietin (Epo) to the EpoR triggers the activation of JAK2, the phosphorylation of the EpoR, a...
The introduction in 1998 of imatinib mesylate (IM) revolutionized management of patients with chronic myeloid leukemia (CML) and the second generation of tyrosine kinase inhibitors may prove superior to IM. Real-time quantitative polymerase chain reaction (RQ-PCR) provides an accurate measure of the total leukemiacell mass and the degree to which BCRABL transcripts are reduced by therapy correl...
The characterization and targeting of Philadelphia chromosome positive (Ph ) acute lymphoblastic leukemia (ALL)– initiating cells remains unresolved. Expression of the polycomb protein Bmi1 is up-regulated in patients with advanced stages of chronic myelogenous leukemia (CML). We report that Bmi1 transforms and reprograms CML B-lymphoid progenitors into stem cell leukemia (Scl) promoter-driven,...
Chronic myelogenous leukemia is a malignant disease of the hematopoietic stem cell compartment, which is characterized by expression of the BCR-ABL fusion protein. Expression of BCR-ABL allows myeloid cells to grow in the absence of the growth factors interleukin-3 and granulocyte-macrophage colony-stimulating factor. The tyrosine kinase activity of BCR-ABL constitutively activates signaling pa...
Bcr-abl antisense oligodeoxynucleotides (AS-ODNs) have provided evidence of an antileukemia effect when tested in vitro against Philadelphia-positive cells. In order to investigate the efficacy of AS-ODNs as purging agents in chronic myeloid leukemia (CML) patients, K562 cells, a human CML cell line, were treated in vitro with various types of AS-ODNs and interferon-alpha. Cells were treated in...
Purpose:Chronic myelogenous leukemia (CML) is characterized by the constitutive activation of BcrAbl tyrosine kinase. Bcr-Abl-T315I is the predominant mutation that causes resistance to imatinib, cytotoxic drugs, and the second-generation tyrosine kinase inhibitors. The emergence of imatinib resistance in patients with CML leads to searching for novel approaches to the treatment of CML. Gambogi...
Kumari and colleagues have recently reported a detailed analysis of BCR-ABL expression in CFU-Cs (colony forming units in culture) of patients with chronic myeloid leukemia (CML).1 Using quantitative reverse-transcription PCR on individual Ph1 hematopoietic colonies, they demonstrated that CFU-Cs from patients in major molecular response (MMR) displayed lower BCR-ABL mRNA expression than CFU-Cs...
In this issue of Clinical Cancer Research , Desai et al. (1) present evidence that new modules appearing in preexisting lesions can represent clonally resistant populations. Imatinib mesylate, the prototypic oral tyrosine kinase inhibitor that has activity against ABL, KIT, and platelet-derived growth factor receptor kinases arguably represents the most important oncologic advance of the past 3...
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