Effect of cellular quiescence on the success of targeted CML therapy
about
Tyrosine kinase inhibitors and mesenchymal stromal cells: effects on self-renewal, commitment and functionsOptimizing combination therapies with existing and future CML drugsA simple mathematical model based on the cancer stem cell hypothesis suggests kinetic commonalities in solid tumor growthStochastic Tunneling of Two Mutations in a Population of Cancer CellsSpatial heterogeneity in drug concentrations can facilitate the emergence of resistance to cancer therapyDose-Dependent Mutation Rates Determine Optimum Erlotinib Dosing Strategies for EGFR Mutant Non-Small Cell Lung Cancer PatientsEradication of chronic myeloid leukemia stem cells: a novel mathematical model predicts no therapeutic benefit of adding G-CSF to imatinibEstimation of cell proliferation dynamics using CFSE data.A review of mixed-effects models of tumor growth and effects of anticancer drug treatment used in population analysis.p53 regulates hematopoietic stem cell quiescence.Evolution of acquired resistance to anti-cancer therapy.Mechanisms of primary and secondary resistance to imatinib in chronic myeloid leukemia.Rapid initial decline in BCR-ABL1 is associated with superior responses to second-line nilotinib in patients with chronic-phase chronic myeloid leukemiaThe controversial role of the Hedgehog pathway in normal and malignant hematopoiesis.Chronic myeloid leukemia stem cells in the era of targeted therapies: resistance, persistence and long-term dormancy.Cell killing and resistance in pre-operative breast cancer chemotherapyCharacterization and quantification of clonal heterogeneity among hematopoietic stem cells: a model-based approachAn elementary approach to modeling drug resistance in cancer.The p53 tumor suppressor protein is a critical regulator of hematopoietic stem cell behavior.Mathematical modeling as a tool for planning anticancer therapy.The p53 tumor suppressor protein regulates hematopoietic stem cell fate.Roles of p53 in various biological aspects of hematopoietic stem cells.Dynamical models of mutated chronic myelogenous leukemia cells for a post-imatinib treatment scenario: Response to dasatinib or nilotinib therapy.The impact of molecular targets in cancer drug development: major hurdles and future strategies.Selection pressure exerted by imatinib therapy leads to disparate outcomes of imatinib discontinuation trials.Therapy of chronic myeloid leukaemia can benefit from the activation of stem cells: simulation studies of different treatment combinations.Necdin modulates leukemia-initiating cell quiescence and chemotherapy response.Stability Analysis of a Model of Interaction Between the Immune System and Cancer Cells in Chronic Myelogenous Leukemia.Long-term treatment effects in chronic myeloid leukemia.Heterogeneity in chronic myeloid leukaemia dynamics during imatinib treatment: role of immune responses.Quantitative prediction of long-term molecular response in TKI-treated CML - Lessons from an imatinib versus dasatinib comparison
P2860
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P2860
Effect of cellular quiescence on the success of targeted CML therapy
description
2007 nî lūn-bûn
@nan
2007 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած
@hyw
2007 թվականի հոտեմբերին հրատարակված գիտական հոդված
@hy
2007年の論文
@ja
2007年論文
@yue
2007年論文
@zh-hant
2007年論文
@zh-hk
2007年論文
@zh-mo
2007年論文
@zh-tw
2007年论文
@wuu
name
Effect of cellular quiescence on the success of targeted CML therapy
@ast
Effect of cellular quiescence on the success of targeted CML therapy
@en
Effect of cellular quiescence on the success of targeted CML therapy
@nl
type
label
Effect of cellular quiescence on the success of targeted CML therapy
@ast
Effect of cellular quiescence on the success of targeted CML therapy
@en
Effect of cellular quiescence on the success of targeted CML therapy
@nl
prefLabel
Effect of cellular quiescence on the success of targeted CML therapy
@ast
Effect of cellular quiescence on the success of targeted CML therapy
@en
Effect of cellular quiescence on the success of targeted CML therapy
@nl
P2860
P1433
P1476
Effect of cellular quiescence on the success of targeted CML therapy
@en
P2093
Dominik Wodarz
Natalia L Komarova
P2860
P356
10.1371/JOURNAL.PONE.0000990
P407
P577
2007-10-03T00:00:00Z