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by various single mutations(passive) caused bytyrosine kinase inhibitor treatment
T. Another molecular - based drugdesignedas a protein tyrosine kinase inhibitor
the factorsinfluencethe Non - Tyrosine Kinase Inhibitors
by SUGEN as a cancer therapeutic(passive) designed bya tyrosine - kinase inhibitor drug
SUGEN as a cancer therapeutic(passive) designed bya tyrosine - kinase inhibitor drug
by SUGEN(passive) designed bya tyrosine - kinase inhibitor drug
SUGEN as a cancer derapeutic(passive) designed bya tyrosine - kinase inhibitor drug
The epidermal growth factorcontributesEGF)/Src tyrosine kinase pathway
Treatment with MET proto - oncogenecan causereceptor tyrosine kinase inhibitor
by Kyowa Hakko Kirin(passive) discovered byVEGF ) tyrosine kinase inhibitor ( TKI
Exelixis to target VEGF receptors , MET and other kinases related to tumour growth and spread(passive) designed byan oral tyrosine kinase inhibitor
amino acid mutations(passive) caused bykinase inhibitors
e.g.(passive) have been discoveredThe kinase inhibitors
to stop the development of a disease by preventing protein kinases from turning protein activity on or off(passive) are designedKinase inhibitors
has become(passive) discoveredkinase inhibitors
Medicinal chemists knowhow to designkinase inhibitors
inorderto rationally designkinase inhibitors
the design of new drugs ... since it is relatively easierto designkinase inhibitors
to block different cytokine receptor signaling pathways(passive) are designedTyrosine kinase inhibitors
by EGFR gatekeeper T790 M mutation in non - small - cell lung cancer (passive) caused bytyrosine kinase inhibitors
by the In vitro Screening System(passive) Discovered bythe Kinase Inhibitor
to blockade the downstream signaling pathways that promote tumor growth and metastasis when stimulated by angiogenic factors(passive) are designedTyrosine kinase inhibitors ( TKI
by Kyowa Kirin(passive) discovered bytyrosine kinase inhibitor ( TKI
by Kyowa Hakko Kirin(passive) discovered bytyrosine kinase inhibitor ( TKI
the BCR - ABL fusion genecausesthe overproduction of tyrosine kinase
by Eisai(passive) discovered bykinase inhibitor
by fbdd(passive) discovered bya kinase inhibitor
always(passive) be causedkinase inhibitor
by FBDD currently in Phase II clinical trials(passive) discovered bya kinase inhibitor
FBDD currently in Phase II clinical trials(passive) discovered bya kinase inhibitor
of a receptor and a tyrosine kinase(passive) is composedAn EGFR tyrosine kinase
of a receptor and tyrosine kinase(passive) is composedAn EGFR tyrosine kinase
to optimize VEGF blockage while minimizing off - target toxicities(passive) was designedtyrosine kinase inhibitor ( TKI
Therapy with an epidermal growth factormay contributetyrosine kinase inhibitor
by Eisai(passive) discovered bytyrosine kinase inhibitor
by Taiho Pharmaceutical(passive) discovered bytyrosine kinase inhibitor
Taiho Pharmaceutical(passive) discovered bytyrosine kinase inhibitor
by the BCR - ABL gene(passive) caused bythe tyrosine kinase
the BCR - ABL gene(passive) caused byThe tyrosine kinase
by the [ [ BCR / ABL(passive) caused bythe [ [ tyrosine kinase
to inhibit both EGFR sensitizing and EGFR T790 M resistance mutations , with clinical activity against central nervous system ( CNS ) metastasesdesignedto inhibit both EGFR sensitizing and EGFR T790 M resistance mutations , with clinical activity against central nervous system ( CNS ) metastases
the efficacydid ... influencethe efficacy
specifically for the treatment of leukemia associated with the Philadelphia chromosome abnormalitywas designedspecifically for the treatment of leukemia associated with the Philadelphia chromosome abnormality
resistance(passive) caused byresistance
to target and inhibit the ALK mutation in NSCLC.designedto target and inhibit the ALK mutation in NSCLC.
as a targeted therapy for patients with non - small cell lung cancer ( NSCLC ) with specific mutations in EGFR or HER2designedas a targeted therapy for patients with non - small cell lung cancer ( NSCLC ) with specific mutations in EGFR or HER2
growth inhibition of tumors and enhancement of the activity of a number of cytotoxic drugscausegrowth inhibition of tumors and enhancement of the activity of a number of cytotoxic drugs
to responses in most patients with ALK - positive non - small - cell lung cancerleadsto responses in most patients with ALK - positive non - small - cell lung cancer
to target and inhibit the ALK fusion protein in non - small cell lung cancerdesignedto target and inhibit the ALK fusion protein in non - small cell lung cancer
to improved survival in patients positive for EGFR activating mutationshave ledto improved survival in patients positive for EGFR activating mutations
G1 arrestcauseG1 arrest
thrombotic microangiopathy , proteinuria or interstitial diseasecan causethrombotic microangiopathy , proteinuria or interstitial disease
thrombotic microangiopathy , proteinuria or interstitial diseasecan causethrombotic microangiopathy , proteinuria or interstitial disease
to improved survival in patients positive for activating mutationshave ledto improved survival in patients positive for activating mutations
severe side effectscan causesevere side effects
to dramatically improved long - term survival rates since the introduction of the first such agent in 2001have ledto dramatically improved long - term survival rates since the introduction of the first such agent in 2001
to treating the cancerleadingto treating the cancer
systemic therapies for the treatment of renal cell carcinomaare leadingsystemic therapies for the treatment of renal cell carcinoma
to the aberrant activation of the AKT / FOXM1 pathwaycontributeto the aberrant activation of the AKT / FOXM1 pathway
to stop the enzymeare designedto stop the enzyme
cardiotoxicitycan causecardiotoxicity
these as imatinibhave ledthese as imatinib
adverse cardiovascular events(passive) caused byadverse cardiovascular events
to target and inhibit mutated forms of the BRAF protein that is found in various cancer typesspecifically designedto target and inhibit mutated forms of the BRAF protein that is found in various cancer types
to inhibit the same pathwaydesignedto inhibit the same pathway
mitotic arrestcausesmitotic arrest
to inhibit the intracellular domain / downstream signaling pathwaydesignedto inhibit the intracellular domain / downstream signaling pathway
hypertension and proteinuriacan causehypertension and proteinuria
to inhibit BCR - ABLdesignedto inhibit BCR - ABL
to long term durable responsesactually can leadto long term durable responses
hypothyroidismcan causehypothyroidism
to target multiple RTKsdesignedto target multiple RTKs
TNFmight influenceTNF
to a disruption of this networkleadto a disruption of this network
hepatotoxicity(passive) caused byhepatotoxicity
in dramatic cell death and paradoxical enrichment of cells with CSC - like propertiesresultedin dramatic cell death and paradoxical enrichment of cells with CSC - like properties
in a patient on levothyroxinecausingin a patient on levothyroxine
the acne - form rash(passive) caused bythe acne - form rash
hypothyroidism in a patient on levothyroxinecausinghypothyroidism in a patient on levothyroxine
phase 2 and 3 trials with gefitinib in the first line - treatment of EGFR - mutated NSCLCpromptedphase 2 and 3 trials with gefitinib in the first line - treatment of EGFR - mutated NSCLC