Loss of major molecular response as a trigger for restarting tyrosine kinase inhibitor therapy in patients with chronic-phase chronic myelogenous leukemia who have stopped imatinib after durable undetectable disease.
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Deep molecular responses for treatment-free remission in chronic myeloid leukemiaThe concept of treatment-free remission in chronic myeloid leukemiaCurrent status of ABL tyrosine kinase inhibitors stop studies for chronic myeloid leukemiaCurrent developments in molecular monitoring in chronic myeloid leukemiaPioglitazone together with imatinib in chronic myeloid leukemia: A proof of concept study.Treatment-free remission following frontline nilotinib in patients with chronic myeloid leukemia in chronic phase: results from the ENESTfreedom study.Downregulated microRNA-148b in circulating PBMCs in chronic myeloid leukemia patients with undetectable minimal residual disease: a possible biomarker to discontinue imatinib safely.Is a cure for CML without allogeneic stem cell transplantation around the corner?How we will treat chronic myeloid leukemia in 2016.Asparaginase induces apoptosis and cytoprotective autophagy in chronic myeloid leukemia cells.Phase 3 study of nilotinib vs imatinib in Chinese patients with newly diagnosed chronic myeloid leukemia in chronic phase: ENESTchina.Targeted therapies for advanced Ewing sarcoma family of tumors.Laboratory recommendations for scoring deep molecular responses following treatment for chronic myeloid leukemia.Milestones and monitoring.Frontline nilotinib in patients with chronic myeloid leukemia in chronic phase: results from the European ENEST1st study.Pediatric chronic myeloid leukemia is a unique disease that requires a different approachCost-effectiveness of Tyrosine Kinase Inhibitor Treatment Strategies for Chronic Myeloid Leukemia in Chronic Phase After Generic Entry of Imatinib in the United States.Imatinib withdrawal syndrome and longer duration of imatinib have a close association with a lower molecular relapse after treatment discontinuation: the KID study.Inhibition of interleukin-1 signaling enhances elimination of tyrosine kinase inhibitor-treated CML stem cells.CML cells actively evade host immune surveillance through cytokine-mediated downregulation of MHC-II expression.Molecular techniques for the personalised management of patients with chronic myeloid leukaemia.Definition and treatment of resistance to tyrosine kinase inhibitors in chronic myeloid leukemia.Chronic myeloid leukemia: 2014 update on diagnosis, monitoring, and management.How I determine if and when to recommend stopping tyrosine kinase inhibitor treatment for chronic myeloid leukaemia.The Hepatocyte Growth Factor (HGF)/Met Axis: A Neglected Target in the Treatment of Chronic Myeloproliferative Neoplasms?Analyzing molecular response in chronic myeloid leukemia clinical trials: pitfalls and golden rules.Molecular monitoring to improve outcomes in patients with chronic myeloid leukemia in chronic phase: importance of achieving treatment-free remission.Do we need more drugs for chronic myeloid leukemia?Chronic myeloid leukemia: advances in understanding disease biology and mechanisms of resistance to tyrosine kinase inhibitors.Discontinuation of tyrosine kinase therapy in CML.Transplant to treatment-free remission: the evolving view of 'cure' in chronic myeloid leukemia.Minimal Residual Disease Eradication in CML: Does It Really Matter?Patient perceptions of treatment-free remission in chronic myeloid leukemia.Present and future of molecular monitoring in chronic myeloid leukaemia.Treatment of chronic myeloid leukemia: assessing risk, monitoring response, and optimizing outcome.Cellular and Molecular Networks in Chronic Myeloid Leukemia: The Leukemic Stem, Progenitor and Stromal Cell Interplay.Management of pregnant chronic myeloid leukemia patients.ST1926, an orally active synthetic retinoid, induces apoptosis in chronic myeloid leukemia cells and prolongs survival in a murine model.Rationale and motivating factors for treatment-free remission in chronic myeloid leukemia.Emerging Role of Tyrosine Kinases as Drugable Targets in Cancer.
P2860
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P2860
Loss of major molecular response as a trigger for restarting tyrosine kinase inhibitor therapy in patients with chronic-phase chronic myelogenous leukemia who have stopped imatinib after durable undetectable disease.
description
2013 nî lūn-bûn
@nan
2013年の論文
@ja
2013年学术文章
@wuu
2013年学术文章
@zh-cn
2013年学术文章
@zh-hans
2013年学术文章
@zh-my
2013年学术文章
@zh-sg
2013年學術文章
@yue
2013年學術文章
@zh
2013年學術文章
@zh-hant
name
Loss of major molecular respon ...... durable undetectable disease.
@en
Loss of major molecular respon ...... durable undetectable disease.
@nl
type
label
Loss of major molecular respon ...... durable undetectable disease.
@en
Loss of major molecular respon ...... durable undetectable disease.
@nl
prefLabel
Loss of major molecular respon ...... durable undetectable disease.
@en
Loss of major molecular respon ...... durable undetectable disease.
@nl
P2093
P50
P921
P356
P1476
Loss of major molecular respon ...... durable undetectable disease.
@en
P2093
Agnès Guerci-Bresler
Aude Charbonnier
Bruno Varet
Franck E Nicolini
François-Xavier Mahon
Gabriel Etienne
Jean Claude Chomel
Jean Michel Cayuela
Josy Reiffers
Joëlle Guilhot
P304
P356
10.1200/JCO.2012.48.5797
P407
P577
2013-12-09T00:00:00Z