Sentences with phrase «receptor tyrosine kinases»

First - line combination therapy with the programmed death ligand 1 (PD - L1) inhibitor avelumab and the vascular endothelial growth factor receptor tyrosine kinase inhibitor axitinib resulted in encouraging antitumor activity in patients with previously untreated renal cell carcinoma (RCC) and had a manageable toxicity profile, according to the results of the JAVELIN Renal 100 study published in Lancet Oncology.

To further assess the effect of Tie2 in pericytes on EC - pericyte intercellular signalling, we performed a phospho - receptor tyrosine kinase array of BP and HUVEC co-cultures.

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.

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

They also compared the DFT cancer with a human cancer and found that anti-cancer drugs for people, intended to stop the growth of molecules called receptor tyrosine kinases, worked well and stopped the growth of devil cancer cells growing in the lab.

In addition, the tumor was positive for estrogen receptor alpha (ER alpha) and cell proliferation marker Ki67, and negative for receptor tyrosine kinase HER2 / ErbB2, suggesting that it has features like luminal B type breast cancer in humans.

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).

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.

These events occur when specific extracellular molecules bind to receptor proteins in the plasma membrane known as receptor tyrosine kinases and heterotrimeric G - protein - coupled receptors.

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

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.

Sina Koch (Ehninger, TUD)-- «Aberrant subcellular localization as a potential mechanism contributing to the abnormal signaling of the mutant Flt3 - ITd receptor tyrosine kinase in acute myeloid leukemia» (2007)

[42 - 46] KIT, a type III transmembrane receptor tyrosine kinase that sits upstream of NRAS and BRAF, feeds into several signaling pathways, including both the RAS / RAF / MEK / ERK cascade and the PI3K / Akt / mTOR pathway.

The largest expansions are in the tyrosine kinase and tyrosine - kinase - like groups, and include over 150 likely receptor tyrosine kinases (RTKs).

In addition, at least some Eph receptors can also signal through non-canonical mechanisms that are independent of ligand binding and kinase activity, for example through interplay with other receptor tyrosine kinase families and with serine / threonine kinases.

The oral VEGF receptor tyrosine kinase inhibitor pazopanib in combination with the MEK inhibitor trametinib in advanced cholangiocarcinoma.

They found that certain GBM tumors — particularly those deficient in PTEN — had multiple co-activated receptor tyrosine kinases (RTKs).

(h) Human phospho - receptor tyrosine kinase array for EphA2, EphB2 and EphB4 ephrin receptors from control BP (shCtr) and BP silenced for Tie2 (siTie2 I and siTie2 II).

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

Also, genes that code for receptor tyrosine kinases, a family of receptors on the surface of cells, may rearrange to form multiple distinct gene fusion partners, as evidenced in an article by Kulkarni, et al, on a translational study involving a patient who developed a BRAF fusion following treatment with a BRAF inhibitor1.

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.

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.

Note that PKC can also be activated by receptor tyrosine kinases that activate PLC - gamma.

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.

The scientists determined that the key to this process was the receptor tyrosine kinase Tie.

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.

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.

We are focusing on a few key molecular pathways including; 1) Polycomb - mediated epigenetic gene silencing in the tumor initiation, maintenance, and invasion, 2) c - Met (receptor tyrosine kinase) signal transduction pathways in stemness and migration of these tumor cells, 3) Novel mitogenic signaling pathways that are specific to GSCs, and 4) Identification of radio - and chemo - sensitizing pathway to maximize therapeutic efficacy.

Mouse angiogenesis and phospho - receptor tyrosine kinase array were performed according to the manufacturer's instructions (R&D, #ARY015 and #ARY014).

Several different genetic defects have been described, including translocations involving genes of the CBF family as well activating mutations in signal transduction proteins, e.g. members of the Ras family of small G - proteins (N - RAS, K - RAS) and receptor tyrosine kinases (RTKs).

AXL encodes a receptor tyrosine kinase that promotes breast cancer bone metastasis in mouse models (41).

Further, we identified a role for ABL kinases in promoting the expression of multiple pro — bone metastasis genes such as AXL (which encodes a receptor tyrosine kinase), IL6 (which encodes interleukin - 6), MMP1 (which encodes matrix metalloproteinase 1), and TNC (which encodes tenascin - C) through TAZ - and signal transducer and activator of transcription 5 (STAT5)-- mediated signaling.

Receptor tyrosine kinases of the Eph family and their ligands, the ephrins, represent an important cell communication system that controls a vast array physiological and disease processes.

FLT3 is a receptor tyrosine kinase that is normally expressed on many cell types including hematologic stem cells.

[1] DIM was found to have «lung cancer preventive effects» mediated via modulation of the receptor tyrosine kinase / PI3K / Akt - signaling pathway.

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.