Not exact matches
An approach often used in treating CML is to block the Bcr - Abl activity using
tyrosine kinase inhibitors (TKIs).
The estimation of EGFR mutation status is essential for the identification of non-small cell lung carcinoma (NSCLC) patients who may benefit from treatment with EGFR
tyrosine kinase inhibitors (TKIs), and hence for improving therapeutic efficacy.
Imatinib is an
inhibitor that blocks the ATP - binding site of the
tyrosine kinase Abl in affected blood cells, thereby suppressing their overactivity.
For example, epidermal growth factor (EGFR) mutations may result in sensitivity to drugs that are EGFR
tyrosine kinase inhibitors (TKIs), such as erlotinib or gefitinib, whereas individuals with the EGFR T790M mutation are more resistant to these drugs.
EGFR
tyrosine kinase inhibitor (TKI) therapy is approved for EGFR activating mutation positive patients with advanced NSCLC, but the standard for determining mutation status is with DNA derived directly from tumor tissue, which can be limited or not available.
Among patients with advanced non-small cell lung cancer without a mutation of a certain gene (EGFR), conventional chemotherapy, compared with treatment using epidermal growth factor receptor
tyrosine kinase inhibitors, was associated with improvement in survival without progression of the cancer, but not with overall survival, according to a study in the April 9 issue of JAMA.
Epidermal growth factor receptor (EGFR)
tyrosine kinase inhibitors (TKIs) are the preferred treatment option for patients with advanced non-small cell lung cancer (NSCLC) who have mutations in the EGFR gene.
Pazopanib is a known
tyrosine kinase inhibitor.
(Moussa is listed as an inventor on a patent application that Georgetown University filed related to nilotinib and the use of other
tyrosine kinase inhibitors for the treatment of neurodegenerative diseases.)
This finding is the latest from Georgetown University Medical Center's Translational Neurotherapeutics Program (TNP) examining
tyrosine kinase inhibitors in the treatment of neurodegenerative diseases.
DDRs inhibition with a
tyrosine kinase inhibitor appears to insulate the brain via blood - brain barrier repair, which prevents harmful immune cells that circulate in the body from getting into the brain where they can indiscriminately attack and kill healthy and sick neurons, like those that have been unable to perform autophagy to «take out their trash,» says Moussa.
Pao was involved in studies of EGFR
tyrosine -
kinase inhibitors while at MSKCC, where he trained in medical oncology.
Approximately 10 - 15 % of Caucasian and 30 - 35 % of Asian patients with NSCLC have a mutation in the epidermal growth factor receptor (EGFR), which can be successfully targeted with EGFR
inhibitors called
tyrosine kinase inhibitors (TKI), such as erlotinib, gefitinib and afatinib.
If this is true, then immunocheckpoint blockade combination with EGFR
tyrosine kinase inhibitors is a major path towards improving outcome of patients who have EGFR - mutant non-small-cell lung cancer.»
The presence of a germline EGFR T790M mutation also predicts for resistance to standard
tyrosine kinase inhibitors (TKIs), which adds complexity to treatment.
Drugs called
tyrosine kinase inhibitors (TKIs) are generally successful at controlling the cancer.
The researchers, including scientists from pharmaceutical company AstraZeneca, report in an advanced online publication in Nature Medicine on May 4, that their findings indicate «an underappreciated genomic heterogeneity» in mechanisms of resistance to
tyrosine kinase inhibitor (TKI) drugs that target the Epidermal Growth Factor Receptor (EGFR) mutation that drive some cases of non-small cell lung cancer (NSCLC).
These therapies, the first an antibody and the second of a class called
tyrosine kinase inhibitors (TKIs), reduce the ability of a target gene to manufacture the protein it encodes.
A class of oral specialty drugs,
tyrosine kinase inhibitors (TKIs), has revolutionized the treatment of CML, largely transforming it into a chronic condition and enabling many patients to have a near - normal lifespan, particularly when compared to a median survival of less than three years with prior therapies.
In 2005, Cagan's team created a general fly model of a human thyroid tumor caused by mutations in the Ret receptor
tyrosine kinase gene, then screened a panel of drugs including a
kinase inhibitor called vandetanib that suppressed the tumor (Cancer Res, 65:3538 - 41, 2005).
PHIb Trial of Fulvestrant, Palbociclib (CDK4 / 6
inhibitor) and Erdafitinib (JNJ - 42756493, pan-FGFR Tyrosine Kinase Inhibitor) in ER + / HER2 - / FGFR - amplified Metastatic Breast Can
inhibitor) and Erdafitinib (JNJ - 42756493, pan-FGFR
Tyrosine Kinase Inhibitor) in ER + / HER2 - / FGFR - amplified Metastatic Breast Can
Inhibitor) in ER + / HER2 - / FGFR - amplified Metastatic Breast Cancer (MBC)
Scanning electron micrograph of the coronary microvasculature of a mouse that has been treated with a small molecule
tyrosine kinase inhibitor of platelet - derived growth factor receptor beta.
In the late 1990s, STI - 571 (imatinib, Gleevec / Glivec) was identified by the pharmaceutical company Novartis (then known as Ciba Geigy) in high - throughput screens for
tyrosine kinase inhibitors.
We have specifically studied the potential of endothelial differentiation of MSC and the impact of a
tyrosine kinase inhibitor (Imatinib mesylate) on this type of stem cells.
Abrogation of the cell death response to oxidative stress by the c - Abl
tyrosine kinase inhibitor STI571.
Oral administration of Bruton's
Tyrosine Kinase (Btk)
inhibitors impairs GPVI - mediated platelet function.
Another focus was the differential sensitivity of different mutations towards inhibition with specific
tyrosine kinase inhibitors (5).
Oral administration of Bruton's
tyrosine kinase inhibitors impairs GPVI - mediated platelet function.
The study tested a lower dose of the oral multi-targeted
tyrosine kinase inhibitor sunitinib than in previous trials, where toxicity proved too much of a problem.
The statement also makes recommendations for clinical guidance and research priorities, such as optimal choice of EGFR
tyrosine kinase inhibitors (TKIs), management of brain metastasis, role of re-biopsies, and use of circulating free DNA (cfDNA) for molecular studies.
Patients receiving
tyrosine kinase inhibitors (TKIs) targeting EGFR mutations had a longer overall survival (OS) than those who did not receive TKIs, demonstrating the effectiveness of TKIs for LM therapy.
BETHESDA, MD. — June 28, 2016 — The College of American Pathologists (CAP), the International Association for the Study of Lung Cancer (IASLC), and the Association for Molecular Pathology (AMP) announced today the open comment period for the revised evidence - based guideline, «Molecular Testing Guideline for Selection of Lung Cancer Patients for EGFR and ALK
Tyrosine Kinase Inhibitors.»
Patients with chronic myeloid leukemia in the blast phase pose a significant therapeutic challenge and have poor survival, even in the
tyrosine kinase inhibitor era, according to a new study.
The researchers also screened more than 100 anticancer compounds to see whether they killed lab - grown cancer cells from the devils and found that both strains responded to
inhibitors of proteins known as receptor
tyrosine kinases.
The US Food and Drug Administration (FDA) recently approved the oral Bruton
tyrosine kinase (BTK)
inhibitor ibrutinib for the treatment of patients with relapsed or refractory marginal zone lymphoma who require systemic therapy and have had at least one prior anti-CD20 therapy.
Currently, 31
tyrosine kinase inhibitors are FDA approved for human therapy, with many more in clinical trials.
The breakthrough led to a new type of cancer pharmaceutical, the
tyrosine kinase inhibitor.
The adenosine triphosphate (ATP)-- competitive
kinase inhibitors imatinib (STI571; trade name: Gleevec), dasatinib, and nilotinib inhibit multiple
tyrosine kinases in addition to ABL1 and ABL2 (5).
The major drawback of
tyrosine kinase inhibitor therapy is the development of secondary resistance caused by the acquisition of new mutations.
These mutant
kinases are attractive therapeutic targets, as demonstrated by the efficacy of imatinib in BCR - ABL — positive chronic myelogenous leukemia (CML), 5 as well as in MPD associated with activating alleles involving PDGFRA or PDGFRB.2, 6,7 In addition, activating mutations in the FLT3 receptor
tyrosine kinase are the most common genetic event in acute myeloid leukemia (AML), and specific
inhibitors of the FMS - like
tyrosine kinase 3 (FLT3) have entered late - stage clinical trials.8 Although mutations in
tyrosine kinases and in other genes have been identified in a subset of MPD and AML, in many cases the genetic events that contribute to the molecular pathogenesis of these diseases remain unknown.
However, as proposed for the T790M mutation in the EGFR, 31 the significant gain - of - function property conferred by the mutations that we describe here may favor their initial presence before drug selection, and rapid selection during
tyrosine kinase inhibitor - based therapy.
Novel drug therapies and novel indications of drug therapy, e.g.
tyrosine kinase inhibitors in lung disease other than lung cancer, biological treatments for asthma, COPD, cystic fibrosis and interstitial lung disease.
Similar results were obtained for the protein
tyrosine kinase inhibitor regorafenib (data not shown).
One of the main mechanisms of secondary resistance in patients treated with
tyrosine kinase inhibitors is acquisition of new
inhibitor - resistant mutations.
RIPK2
inhibitor 2 appears to inhibit 38 % of the activity of SNARK and 27 % of the activity of FGFR2, GSK3 - β, JNK1, CSNK1G2 (casein
kinase 1), and MET
tyrosine kinase.
We can clearly observe RIPK2
inhibitor 1 and 2 inhibition of MDP - dependent activation of RIPK2 autophosphorylation (on
tyrosine 474) using an in vitro
kinase assay in HCT116 cells (Fig. 3B).
Acquired resistance to anti-angiogenic
tyrosine kinase inhibitors is an important clinical problem in treating various cancers.
32) Kubo T, Yamamoto H, Lockwood WW, Fujii T, Ouchida M, Soh J, Takigawa J, Kiura K, Shimizu K, Date H, Minna JD, Lam WL, Gazdar AF, Toyooka S (2009) MET gene amplification or EGFR mutation activate MET in lung cancers untreated with EGFR
tyrosine kinase inhibitors.
244/2: 30 Functional correction of dwarfism in a mouse model of achondroplasia using the
tyrosine kinase inhibitor NVP - BGJ398.
In particular, he is focused on studying therapeutic resistance to lapatinib, a
tyrosine kinase inhibitor of HER2, in breast cancer.