Sentences with phrase «bruton tyrosine kinase»

The Janus tyrosine kinases (Jaks) play a central role in signaling through cytokine receptors.

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.

Although the enzyme itself is inhibited in this state, it can be more easily re-activated through other tyrosine kinases.

The protein, tyrosine kinase 2 or TYK2, helps regulate how strongly the immune system responds to threats.

Therefore, a team led by Vladimir Tesar, MD, PhD (Charles University and General University Hospital, in the Czech Republic) tested the potential of an investigational drug called bosutinib that inhibits a particular tyrosine kinase called Src / Bcr - Abl.

Under physiological conditions, the tyrosine kinase Abl is found in two different spatial structures — an open and a closed state — which exist in a delicate equilibrium.

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.

The target for ibrutinib, an enzyme called Bruton's tyrosine kinase (BTK), is a key component of B - cell receptor signaling.

These receptors, called receptor tyrosine kinases (RTKs), transmit instructions through the cell wall and down through a cascade of reactions to a target gene in the nucleus.

When PDGF arrives at the cell surface, it binds to a protein called PDGF receptor tyrosine kinase (PDGF RTK).

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.

One reason may be that DDRs are protein enzymes known as tyrosine kinases that act as on and off switches of the cell self - cleaning process known as autophagy.

They found higher levels of JAK1 in resistant tumors, which caused increased expression of epidermal growth factor receptor (EGFR)-- a receptor tyrosine kinase that promotes cell proliferation.

The compounds, dubbed OD36 and OD38, specifically appear to curtail inflammation - triggering signals from RIPK2 (serine / threonine / tyrosine kinase 2).

Previous research from the TNP has shown that when tyrosine kinases are inhibited, the garbage disposal system begins working, allowing cells to once again clear toxic proteins.

PDGFRα is a cell surface tyrosine kinase receptor involved in organ development and tumor progression, it is present in multiple cell types such as mesenchymal cells, neurons, astrocytes, megakaryocytes and oligodendrocyte progenitor.

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.

Transmission of signals in a cell is controlled by the coordinated activity of two families of enzymes: protein tyrosine kinases, which add a phosphate group to proteins, and protein tyrosine phosphatases, which remove them.

Regorafenib is one of a new generation of anti-cancer therapies that attack tyrosine kinases — enzymes that activate other proteins.

And, indeed, previous research has shown that receptor tyrosine kinases, e.g. insulin receptors, and cytokine receptors, e.g. growth hormone receptors, exist in dimeric form even in the absence of ligands.

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.»

It inhibits two tyrosine kinase enzymes called Jak1 and Jak2, which rev up production of immune cells.

The presence of a germline EGFR T790M mutation also predicts for resistance to standard tyrosine kinase inhibitors (TKIs), which adds complexity to treatment.

During the early years of my PhD studies, I was very fascinated by the exciting discoveries in the field of signal transduction, in particular how receptor tyrosine kinases are activated to transmit their signals and how protein complexes are formed through defined protein folds (domains) interacting with specific cellular targets.

In 1995, I began graduate studies on signal transduction by growth factors and receptor tyrosine kinases in the laboratory of Graeme Guy at the Institute of Molecular and Cell Biology (IMCB) in Singapore, obtaining my PhD in 2000.

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).

Ari Hashimoto and colleagues found that the MVP promotes the recruitment of Arf6 to the plasma membrane, where it can be activated by receptor tyrosine kinases.

We review progress with the receptor tyrosine kinases (growth factor receptors EGFR, VEGFR, and FGFR) and nonreceptor tyrosine kinases (Bcr - Abl), where advances have been made with cancer therapeutic agents such as Herceptin and Gleevec.

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.

Gene expression in papillary thyroid carcinomas, with special reference to tyrosine kinase receptors and growth factors.

Using immunohistochemistry, we detected basal levels of the tyrosine kinase receptors Flk - 1, FGFR - 1, and Tie - 2.

We also noted constitutive surface expression of the tyrosine kinase receptors Tie - 2, FGFR - 1, and Flk - 1 on proliferating and resting endothelial cells (data not shown).

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.

D'Oro, U., Vacchio, M.S., Weissman, A.M. & Ashwell, J.D. Activation of the Lck tyrosine kinase targets cell surface T cell antigen receptors for lysosomal degradation.

Chan AC, Iwashima M, Trck CW, Weiss A. ZAP - 70: a 70kd protein - tyrosine kinase that associates with the TCRzeta chain.

RET is a type of receptor tyrosine kinase, and mutations that kick its activity into overdrive are linked to certain kinds of cancer.

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 Cancer (MBC)

Aminoglycoside - induced degeneration of adult spiral ganglion neurons involves differential modulation of tyrosine kinase B and p75 neurotrophin receptor signaling.

Tyrosine kinases may regulate choanoflagellate colony formation.

The activity of tyrosine kinases is typically regulated in an auto - inhibitory fashion, but the BCR - Abl fusion gene codes for a protein that is «always on» or continuously activated leading to unregulated cell division (i.e. cancer).