Sentences with phrase «with tyrosine kinase inhibitors»

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

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.

Not exact matches

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.

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.

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.»

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.

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.

Another focus was the differential sensitivity of different mutations towards inhibition with specific tyrosine kinase inhibitors (5).

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 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.

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.

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.

Inform and educate clinicians as to updates and revisions of their Molecular testing Guideline for the Selection of Lung cancer Patients for Treatment with Targeted Tyrosine Kinase Inhibitors.

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.

Multi-center, placebo - controlled, double - blind, randomized study of oral toceranib phosphate (SU11654), a receptor tyrosine kinase inhibitor, for the treatment of dogs with recurrent (either local or distant) mast cell tumor following surgical excision.