Front-line and salvage therapies with tyrosine kinase inhibitors and other treatments in chronic myeloid leukemia.
about
α-bisabolol is an effective proapoptotic agent against BCR-ABL(+) cells in synergism with Imatinib and NilotinibExosomes released by K562 chronic myeloid leukemia cells promote angiogenesis in a Src-dependent fashion.Trends in chronic myeloid leukemia incidence and survival in the United States from 1975 to 2009.JAK2/STAT5 inhibition by nilotinib with ruxolitinib contributes to the elimination of CML CD34+ cells in vitro and in vivo.Paradoxical MAPK-activation in response to treatment with tyrosine kinase inhibitors in CML: flow cytometry loses track.IL1RAP as a surface marker for leukemia stem cells is related to clinical phase of chronic myeloid leukemia patients.Study protocol of the RAND-study: a multicenter, prospective cohort study investigating response and adherence to nilotinib treatment in chronic myeloid leukemia.shRNA library screening identifies nucleocytoplasmic transport as a mediator of BCR-ABL1 kinase-independent resistance.Altered microenvironmental regulation of leukemic and normal stem cells in chronic myelogenous leukemiaImmunotherapy targets in pediatric cancer.Mutated BCR-ABL generates immunogenic T-cell epitopes in CML patientsSignificance of deeper molecular responses in patients with chronic myeloid leukemia in early chronic phase treated with tyrosine kinase inhibitorsInhibition of interleukin-1 signaling enhances elimination of tyrosine kinase inhibitor-treated CML stem cells.The current role of high-dose imatinib in chronic myeloid leukemia patients, newly diagnosed or resistant to standard dose.Self-renewal related signaling in myeloid leukemia stem cells.Selection of therapy: rational decisions based on molecular events.AMPK in BCR-ABL expressing leukemias. Regulatory effects and therapeutic implications.An overview of the mTOR pathway as a target in cancer therapy.Antileukemic properties of 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors.Molecular genetic evaluation of myeloproliferative neoplasms.OCT1 and imatinib transport in CML: is it clinically relevant?Effective Concentration of a Multikinase Inhibitor within Bone Marrow Correlates with In Vitro Cell Killing in Therapy-Resistant Chronic Myeloid Leukemia.Fas-associated phosphatase 1 mediates Fas resistance in myeloid progenitor cells expressing the Bcr-abl oncogene.The bone marrow microenvironment as niche retreats for hematopoietic and leukemic stem cells.Psychological well-being and social support in chronic myeloid leukemia patients receiving lifelong targeted therapies.Crizotinib: an anaplastic lymphoma kinase inhibitor.Decreased calpain activity in chronic myeloid leukemia impairs apoptosis by increasing survivin in myeloid progenitors and xiap1 in differentiating granulocytes.The role of Fas-associated phosphatase 1 in leukemia stem cell persistence during tyrosine kinase inhibitor treatment of chronic myeloid leukemia.Bcr-abl regulates Stat5 through Shp2, the interferon consensus sequence binding protein (Icsbp/Irf8), growth arrest specific 2 (Gas2) and calpain.Long-term persistence of molecular response after discontinuation of interferon-alpha in two patients with chronic myeloid leukaemia.Early molecular and cytogenetic response is predictive for long-term progression-free and overall survival in chronic myeloid leukemia (CML).What are the challenges in 2016 regarding resistance to tyrosine kinase inhibitors in chronic myeloid leukemia and cancer?International development of an EORTC questionnaire for assessing health-related quality of life in chronic myeloid leukemia patients: the EORTC QLQ-CML24.Non ABL-directed inhibitors as alternative treatment strategies for chronic myeloid leukemia.Real world treatment patterns in chronic myeloid leukemia patients newly initiated on tyrosine kinase inhibitors in an U.S. integrated healthcare system.Omacetaxine mepesuccinate prevents cytokine-dependent resistance to nilotinib in vitro: potential role of the common β-subunit c of cytokine receptors.Velocity of early BCR-ABL transcript elimination as an optimized predictor of outcome in chronic myeloid leukemia (CML) patients in chronic phase on treatment with imatinib.Imatinib and beyond--targeting activated tyrosine kinases in myeloproliferative disorders.Novel AF1q/MLLT11 favorably affects imatinib resistance and cell survival in chronic myeloid leukemia
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Front-line and salvage therapies with tyrosine kinase inhibitors and other treatments in chronic myeloid leukemia.
description
article científic
@ca
article scientifique
@fr
articolo scientifico
@it
artigo científico
@pt
bilimsel makale
@tr
scientific article published on 10 January 2011
@en
vedecký článok
@sk
vetenskaplig artikel
@sv
videnskabelig artikel
@da
vědecký článek
@cs
name
Front-line and salvage therapi ...... s in chronic myeloid leukemia.
@en
Front-line and salvage therapi ...... s in chronic myeloid leukemia.
@nl
type
label
Front-line and salvage therapi ...... s in chronic myeloid leukemia.
@en
Front-line and salvage therapi ...... s in chronic myeloid leukemia.
@nl
prefLabel
Front-line and salvage therapi ...... s in chronic myeloid leukemia.
@en
Front-line and salvage therapi ...... s in chronic myeloid leukemia.
@nl
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P50
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P1476
Front-line and salvage therapi ...... s in chronic myeloid leukemia.
@en
P2093
Timothy Hughes
P2860
P304
P356
10.1200/JCO.2010.31.3619
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P577
2011-01-10T00:00:00Z