Targeted CML therapy: controlling drug resistance, seeking cure.
about
Molecular and structural characterization of the SH3 domain of AHI-1 in regulation of cellular resistance of BCR-ABL(+) chronic myeloid leukemia cells to tyrosine kinase inhibitorsKnockout Serum Replacement Promotes Cell Survival by Preventing BIM from Inducing Mitochondrial Cytochrome C ReleaseAHI-1 interacts with BCR-ABL and modulates BCR-ABL transforming activity and imatinib response of CML stem/progenitor cellsAbelson kinase acts as a robust, multifunctional scaffold in regulating embryonic morphogenesis.AHI-1: a novel signaling protein and potential therapeutic target in human leukemia and brain disorders.Targeting RAD51 phosphotyrosine-315 to prevent unfaithful recombination repair in BCR-ABL1 leukemia.Src family kinases phosphorylate the Bcr-Abl SH3-SH2 region and modulate Bcr-Abl transforming activity.Imatinib resistance associated with BCR-ABL upregulation is dependent on HIF-1alpha-induced metabolic reprogramingEvolutionary dynamics of carcinogenesis and why targeted therapy does not work.Hedgehog signalling is essential for maintenance of cancer stem cells in myeloid leukaemia.Properties of CD34+ CML stem/progenitor cells that correlate with different clinical responses to imatinib mesylateTarget enzyme mutations are the molecular basis for resistance towards pharmacological inhibition of nicotinamide phosphoribosyltransferase.Comparison of cancer stem cell antigen expression by tumor cell lines and by tumor biopsies from dogs with melanoma and osteosarcomaInhibition of mutant EGFR in lung cancer cells triggers SOX2-FOXO6-dependent survival pathways.The ABL switch control inhibitor DCC-2036 is active against the chronic myeloid leukemia mutant BCR-ABLT315I and exhibits a narrow resistance profileIdentification of Novel Small Molecule Inhibitors of Oncogenic RET Kinase.The mTOR inhibitor, everolimus (RAD001), overcomes resistance to imatinib in quiescent Ph-positive acute lymphoblastic leukemia cells.Cancer pharmacotherapy: 21st century 'magic bullets' and changing paradigms.Targeting autophagy augments the anticancer activity of the histone deacetylase inhibitor SAHA to overcome Bcr-Abl-mediated drug resistance.The Btk tyrosine kinase is a major target of the Bcr-Abl inhibitor dasatinibChromatin structure determines accessibility of a hairpin polyamide-chlorambucil conjugate at histone H4 genes in pancreatic cancer cellsTargeting the absence: homozygous DNA deletions as immutable signposts for cancer therapy.β-Arrestin2 mediates the initiation and progression of myeloid leukemia.Treatment of human pre-B acute lymphoblastic leukemia with the Aurora kinase inhibitor PHA-739358 (Danusertib)Mechanisms of drug inhibition of signalling molecules.SGX393 inhibits the CML mutant Bcr-AblT315I and preempts in vitro resistance when combined with nilotinib or dasatinib.Optimal drug cocktail design: methods for targeting molecular ensembles and insights from theoretical model systems.Carcinoma of an unknown primary: are EGF receptor, Her-2/neu, and c-Kit tyrosine kinases potential targets for therapy?Small molecules targeting histone H4 as potential therapeutics for chronic myelogenous leukemia.Regulation of c-Myc ubiquitination controls chronic myelogenous leukemia initiation and progression.Chronic Myeloid Leukaemia in The 21st Century.Concomitant inhibition of Mdm2-p53 interaction and Aurora kinases activates the p53-dependent postmitotic checkpoints and synergistically induces p53-mediated mitochondrial apoptosis along with reduced endoreduplication in acute myelogenous leukemiaBCR-ABL-transformed GMP as myeloid leukemic stem cells.Structure and clinical relevance of the epidermal growth factor receptor in human cancerNilotinib: a novel encouraging therapeutic option for chronic myeloid leukemia patients with imatinib resistance or intolerance.The cancer stem cell: premises, promises and challenges.Exploring the biology of cancer of unknown primary: breakthroughs and drawbacks.Chronic inflammation in biomaterial-induced periprosthetic osteolysis: NF-κB as a therapeutic target.Novel biological strategies for treatment of wear particle-induced periprosthetic osteolysis of orthopaedic implants for joint replacement.Significance of OCT1 Expression in Acute Myeloid Leukemia.
P2860
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P2860
Targeted CML therapy: controlling drug resistance, seeking cure.
description
2005 nî lūn-bûn
@nan
2005年の論文
@ja
2005年学术文章
@wuu
2005年学术文章
@zh-cn
2005年学术文章
@zh-hans
2005年学术文章
@zh-my
2005年学术文章
@zh-sg
2005年學術文章
@yue
2005年學術文章
@zh
2005年學術文章
@zh-hant
name
Targeted CML therapy: controlling drug resistance, seeking cure.
@ast
Targeted CML therapy: controlling drug resistance, seeking cure.
@en
type
label
Targeted CML therapy: controlling drug resistance, seeking cure.
@ast
Targeted CML therapy: controlling drug resistance, seeking cure.
@en
prefLabel
Targeted CML therapy: controlling drug resistance, seeking cure.
@ast
Targeted CML therapy: controlling drug resistance, seeking cure.
@en
P1476
Targeted CML therapy: controlling drug resistance, seeking cure.
@en
P2093
Amie S Corbin
Thomas O'Hare
P356
10.1016/J.GDE.2005.11.002
P577
2005-12-15T00:00:00Z