PubMed Journals Articles About "Tyrosine Kinase Inhibitors Cancer" RSS

00:57 EDT 25th October 2016 | BioPortfolio

Tyrosine Kinase Inhibitors Cancer PubMed articles on BioPortfolio. Our PubMed references draw on over 21 million records from the medical literature. Here you can see the latest Tyrosine Kinase Inhibitors Cancer articles that have been published worldwide.

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Showing "Tyrosine kinase inhibitors Cancer" PubMed Articles 1–25 of 20,000+

De novo design of new inhibitor of mutated tyrosine-kinase for the myeloid leukemia treatment.

Chronic myelogenous leukemia is associated with hematopoietic stem cells that are manifested primarily with expansion myelopoiesis. It is the first cancer directly associated with a genetic abnormality. Specifically, it is associated to a particular cytogenetic abnormality, known as Philadelphia chromosome (Ph), which results from a fusion between part of the BCR ("breakpoint cluster region") gene from chromosome 22 and the Abelson (ABL) gene on chromosome 9 and leads to the formation a new gene leukemia-sp...

Oncogenic Receptor Tyrosine Kinases Directly Phosphorylate Focal Adhesion Kinase (FAK) as a Resistance Mechanism to FAK-kinase Inhibitors.

Focal adhesion kinase (FAK) is a major drug target in cancer and current inhibitors targeted to the ATP-binding pocket of the kinase domain have entered clinical trials. However, preliminary results have shown limited single-agent efficacy in patients. Despite these unfavorable data, the molecular mechanisms which drive intrinsic and acquired resistance to FAK-kinase inhibitors are largely unknown. We have demonstrated that receptor tyrosine kinases (RTKs) can directly bypass FAK-kinase inhibition in cancer...

The Emerging Role of Tyrosine Kinase Inhibitors in Ovarian Cancer Treatment: A Systematic Review.

The present systematic review summarizes current evidence regarding the mechanisms of action, the efficacy, and the adverse effects of tyrosine kinase inhibitors (TKIs) in ovarian cancer patients. Phase II and III clinical trials were sought in the PubMed database and in the Clinical registry through September 30, 2015. Seventy-five clinical trials regarding TKIs targeting mainly vascular endothelial growth factor receptor, epidermal growth factor receptor, platelet-derived growth factor receptor...

Using Interferon Alfa Before Tyrosine Kinase Inhibitors May Increase Survival in Patients With Metastatic Renal Cell Carcinoma: A Turkish Oncology Group (TOG) Study.

We aimed to investigate the outcomes of interferon alfa and sequencing tyrosine kinase inhibitors (TKIs) in patients with metastatic renal cell carcinoma.

EGFR Exon 19 Deletion is Associated With Favorable Overall Survival After First-line Gefitinib Therapy in Advanced Non-Small Cell Lung Cancer Patients.

Exon 19 deletion and L858R mutation in exon 21 of the epidermal growth factor receptor (EGFR) are both common mutations that predict a good response to EGFR tyrosine kinase inhibitors in non-small cell lung cancer (NSCLC). However, the existence of clinically significant difference in sensitivity to EGFR tyrosine kinase inhibitors among different EGFR mutation subtypes is still a matter of debate.

Efficacy of EGFR tyrosine kinase inhibitors in the adjuvant treatment for operable non-small-cell lung cancer by a meta-analysis.

The role of EGFR tyrosine kinase inhibitors (TKIs) in the adjuvant treatment of non-small-cell lung cancer (NSCLC) has not been well established. Our meta-analysis aimed to determine whether the administration of EGFR-TKIs could improve the outcomes of patients with NSCLC undergoing complete resection.

Macrocytosis as a potential parameter associated with survival after tyrosine kinase inhibitor treatment.

As a rise in mean corpuscular volume (MCV) of the erythrocyte is frequently seen during treatment with imatinib and sunitinib, we investigated whether macrocytosis (MCV > 100 fl) also occurs as a class effect in other tyrosine kinase inhibitors (TKIs) and whether occurrence of macrocytosis is associated with outcome.

Detection of the T790M mutation of EGFR in plasma of advanced non-small cell lung cancer patients with acquired resistance to tyrosine kinase inhibitors (West Japan oncology group 8014LTR study).

Next-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) have been developed to overcome resistance to earlier generations of such drugs mediated by a secondary T790M mutation of EGFR, but the performance of a second tumor biopsy to assess T790M mutation status can be problematic.

Cardiovascular Events Associated With Use of Tyrosine Kinase Inhibitors in Chronic Myeloid Leukemia: A Population-Based Cohort Study.

Tyrosine kinase inhibitors (TKIs) have increased survival dramatically for patients with chronic myeloid leukemia (CML), but continuous administration of these drugs may elicit long-term toxicity.

Effects of epidermal growth factor receptor-tyrosine kinase inhibitors alone on EGFR-mutant non-small cell lung cancer with brain metastasis.

Epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) are remarkably effective for treating EGFR-mutant non-small cell lung cancer (NSCLC). However, the individual role of EGFR-TKIs in patients with brain metastasis (BM) arising from EGFR-mutant NSCLC remains unclear.

Tyrosine kinase inhibitors and mesenchymal stromal cells: effects on self-renewal, commitment and functions.

The hope of selectively targeting cancer cells by therapy and eradicating definitively malignancies is based on the identification of pathways or metabolisms that clearly distinguish "normal" from "transformed" phenotypes. Some tyrosine kinase activities, specifically unregulated and potently activated in malignant cells, might represent important targets of therapy. Consequently, tyrosine kinase inhibitors (TKIs) might be thought as the "vanguard" of molecularly targeted therapy for human neoplasias. Imati...

Pooled Analysis of the Prognostic and Predictive Value of KRAS Mutation Status and Mutation Subtype in Patients with Non-Small Cell Lung Cancer Treated with Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors.

This pooled analysis of four trials of epidermal growth factor receptor tyrosine kinase inhibitors (EGFR TKIs) versus placebo was conducted to clarify the prognostic and predictive roles of Kirsten rat sarcoma viral oncogene homolog (KRAS) mutations (MUTs) and to explore the importance of MUT subtype.

Advanced non-Small cell lung cancer patients at the extremes of age in the era of epidermal growth factor receptor tyrosine kinase inhibitors.

The clinical characteristics and survival of very young (≤40 years) and very old (>80years) patients with advanced non-small cell lung cancer (NSCLC) are distinct. However, the benefits of epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs) to patients at the extremes of age with NSCLC harboring EGFR mutation have not been well studied. We retrospectively studied the effect of extreme age on patients' clinical characteristics and prognosis.

A Decade of Nilotinib and Dasatinib: From In Vitro Studies to First-Line Tyrosine Kinase Inhibitors.

Early Recognition and Management of Posterior Reversible Encephalopathy Syndrome: A Newly Recognized Complication in Patients Receiving Tyrosine Kinase Inhibitors.

Adult patients with cancer receiving antineoplastic, targeted, and other immunosuppressive therapies are at risk for severe side effects. Studies link posterior reversible encephalopathy syndrome (PRES) with immunosuppressants used for patients undergoing transplantation, as well as select tyrosine kinase inhibitors (TKIs) and other targeted therapies used in patients with cancer. PRES is a reversible condition with early recognition and management; however, permanent neurologic toxicities have been reporte...

Sequencing of Tyrosine Kinase Inhibitors in Progressive Differentiated Thyroid Cancer.

Best Use of the Tyrosine Kinase Inhibitors in Progressive Differentiated Thyroid Cancer: Discussion.

Review On EGFR Inhibitors: Critical Updates.

Epidermal Growth Factor Receptor (EGFR) is a transmembrane glycoprotein that constitutes one of four members of the ErbB family of tyrosine kinase receptors. Activation of EGFR to leads to autophosphorylation of receptor tyrosine kinase that initiates a cascade of downstream signaling pathways involved in regulating cellular proliferation, differentiation, and survival. EGFR is abnormally activated by various mechanisms like receptor overexpression, mutation, ligand-dependent receptor dimerization, ligand-i...

Epidermal Growth Factor Receptor (EGFR) co-mutated advanced non-small cell lung cancer (NSCLC) and response to EGFR tyrosine kinase inhibitors (TKIs): A Brief Report.

The evolution of Epidermal Growth Factor Receptor (EGFR) tyrosine kinase inhibitors has changed the landscape of disease for a subset of patients with non-small cell lung cancer (NSCLC). Most patients with an EGFR mutation respond to these drugs, however a proportion show limited or no tumour response. We explored the impact of co-mutation (double or multiple mutation), compared with single mutation, of the EGFR gene on response to TKIs in a series of patients with metastatic NSCLC.

Kinases inhibitors in lung cancer: From benchside to bedside.

Lung cancer still remains one of the major causes of cancer related mortality around the globe. Various different molecular targets have been discovered till date for targeting lung cancer. But not every new molecular target is having successfully designed inhibitor, moreover the conventional chemotherapeutics are having their own limitations such as toxicity, lack of selectivity. Thus, kinases still remain the most effective molecular target in lung cancer therapy. Also, once-shunned kinase inhibitors have...

The discovery of 2-substituted phenol quinazolines as potent RET kinase inhibitors with improved KDR selectivity.

Deregulation of the receptor tyrosine kinase RET has been implicated in medullary thyroid cancer, a small percentage of lung adenocarcinomas, endocrine-resistant breast cancer and pancreatic cancer. There are several clinically approved multi-kinase inhibitors that target RET as a secondary pharmacology but additional activities, most notably inhibition of KDR, lead to dose-limiting toxicities. There is, therefore, a clinical need for more specific RET kinase inhibitors. Herein we report our efforts towards...

Small activating ribonucleic acid reverses tyrosine kinase inhibitor resistance in epidermal growth factor receptor-mutant lung cancer by increasing the expression of phosphatase and tensin homolog.

Epidermal growth factor receptor-tyrosine kinase inhibitors (TKI-EGFRs) present a new prospect for the treatment of lung cancer. However, in clinical application, the majority of patients become TKI resistant within a year. More and more studies have shown that a loss of phosphatase and tensin homolog (PTEN) expression is associated with TKI resistance. An alternative method of upregulating PTEN expression may reverse TKI resistance.

Cost-Effectiveness Analysis of Tyrosine Kinase Inhibitors for Patients with Advanced Gastrointestinal Stromal Tumors.

The management of advanced gastrointestinal stromal tumors (GISTs) has been modified considerably by the availability of costly tyrosine kinase inhibitors (TKIs); however, the best therapeutic sequence in terms of cost and effectiveness remains unknown.

Functional analyses of mutations in receptor tyrosine kinase genes in non-small cell lung cancer: double-edged sword of DDR2.

This study investigated whether mutations of receptor tyrosine kinase (RTK) genes detected using next-generation sequencing (NGS) are suitable therapeutic targets.

miR-26a desensitizes non-small cell lung cancer cells to tyrosine kinase inhibitors by targeting PTPN13.

Epidermal growth factor receptor (EGFR)-targeted tyrosine kinase inhibitors (TKIs) have emerged as first-line drugs for non-small cell lung cancers (NSCLCs). However, the resistance to TKIs represents the key limitation for their therapeutic efficacy. We found that miR-26a was upregulated in gefitinib-refractory NSCLCs; miR-26a is downstream of EGFR signaling and directly targets and silences protein tyrosine phosphatase non-receptor type 13 (PTPN13) to maintain the activation of Src, a dephosphorylation su...

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