Sentences with phrase «tyrosine kinase inhibitors in»

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.

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.

Not exact matches

An approach often used in treating CML is to block the Bcr - Abl activity using tyrosine kinase inhibitors (TKIs).

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.

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.

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.

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).

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, 2005In 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, 2005in 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 Caninhibitor) and Erdafitinib (JNJ - 42756493, pan-FGFR Tyrosine Kinase Inhibitor) in ER + / HER2 - / FGFR - amplified Metastatic Breast CanInhibitor) in ER + / HER2 - / FGFR - amplified Metastatic Breast Cancer (MBC)

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 inhibitorIn 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 inhibitorin high - throughput screens for tyrosine kinase inhibitors.

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.

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.

Currently, 31 tyrosine kinase inhibitors are FDA approved for human therapy, with many more in clinical trials.

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).

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 unknowin 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 unknowin 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 unknowIn 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 unknowin 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 unknowin 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 unknowin 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 unknowin 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 unknowin a subset of MPD and AML, in many cases the genetic events that contribute to the molecular pathogenesis of these diseases remain unknowin 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.

One of the main mechanisms of secondary resistance in patients treated with tyrosine kinase inhibitors is acquisition of new inhibitor - resistant mutations.

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 canceIn particular, he is focused on studying therapeutic resistance to lapatinib, a tyrosine kinase inhibitor of HER2, in breast cancein breast cancer.

33) Gandhi J, Zhang J, Xie Y, Shigematsu H, Soh J, Zhang W, Yamamoto H, Peyton M, Girard L, Lockwood WW, Lam WL, Garcia M, Minna JD, Gazdar AF (2009) Alterations in genes of the EGFR signaling pathway and their relationship to EGFR tyrosine kinase inhibitor sensitivity in lung cancer cell lines.

Erlotinib, an EGFR tyrosine kinase inhibitor, has proven to be an effective agent in patients with mutations in the EGFR gene, but its efficacy in wild - type EGFR patients was unclear.

Genistein Inhibits Both Estrogen and Growth Factor — stimulated Proliferation of Human Breast Cancer Cells Cell Growth & Differentiation 1996 (Oct); 7 (10): 1345 — 1351 Genistein is a naturally occurring dietary protein tyrosine kinase (PTK) inhibitor that is hypothesized to be responsible for the lower rate of breast cancer observed in Asian women consuming soy.

«In the near future, we'll likely see more medications specifically targeting receptors on cells involved in allergic reactions, such as tyrosine kinase inhibitors (mast cells), for dermatologic use.&raquIn the near future, we'll likely see more medications specifically targeting receptors on cells involved in allergic reactions, such as tyrosine kinase inhibitors (mast cells), for dermatologic use.&raquin allergic reactions, such as tyrosine kinase inhibitors (mast cells), for dermatologic use.»

Investigated TAM family receptor tyrosine kinase gene expression in response to small molecule inhibitors in glioblastoma multiforme