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https://www.readbyqxmd.com/read/28514740/differential-expression-of-circulating-biomarkers-of-tumor-phenotype-and-outcomes-in-previously-treated-non-small-cell-lung-cancer-patients-receiving-erlotinib-vs-cytotoxic-chemotherapy
#1
Mary Jo Fidler, Casey Frankenberger, Richard Seto, Gabriela C Lobato, Cristina L Fhied, Selina Sayidine, Sanjib Basu, Mark Pool, Reem Karmali, Marta Batus, Wen-Rong Lie, David Hayes, Jehangir Mistry, Philip Bonomi, Jeffrey A Borgia
BACKGROUND: The objective of this study was to identify serum biomarkers capable of predicting clinical outcomes in previously-treated NSCLC patients with wild-type for EGFR activating mutations or insufficient tissue for mutation status determination. METHODS: Sixty-six Luminex immunoassays representative of biological themes that emerged from a re-analysis of transcriptome data from the Cancer Genome Atlas (TCGA) were evaluate against pretreatment serum specimens from previously-treated advanced NSCLC patients received either cytotoxic chemotherapy (n=32) or erlotinib (n=79)...
April 28, 2017: Oncotarget
https://www.readbyqxmd.com/read/28514724/sirna-mediated-inactivation-of-her3-improves-the-antitumour-activity-and-sensitivity-of-gefitinib-in-gastric-cancer-cells
#2
Heng-Heng Yuan, Ying-Nan Yang, Jian-Hua Zhou, Yan-Jing Li, Li-Ying Wang, Jun-Wei Qin, Tao Liu, Zhen-Zhen Li, Qing-Xin Zhou, Xiao-Li Wei, Ting-Ting Zhang, Peng Huang, Wen-Jie Zhang, Lei Liu, Xiao-Xue Du, Yu Han
The human EGFR family consists of four type-1 transmembrane tyrosine kinase receptors: HER1 (EGFR, ErbB1), HER2 (Neu, ErbB2), HER3 (ErbB3), and HER4 (ErbB4). HER3 can dimerize with EGFR, HER2 and even c-Met and likely plays a central role in the response to EGFR-targeted therapy. Because HER3 lacks significant kinase activity and cannot be inhibited by tyrosine kinase inhibitors, neutralizing antibodies and alternative inhibitors of HER3 have been sought as cancer therapeutics. Here, we describe the stable suppression of HER3 mRNA and protein using siRNA...
April 29, 2017: Oncotarget
https://www.readbyqxmd.com/read/28511645/therapeutic-potential-of-tas-115-via-c-met-and-pdgfr%C3%AE-signal-inhibition-for-synovial-sarcoma
#3
Shutaro Yamada, Yoshinori Imura, Takaaki Nakai, Sho Nakai, Naohiro Yasuda, Keiko Kaneko, Hidetatsu Outani, Satoshi Takenaka, Kenichiro Hamada, Akira Myoui, Nobuhito Araki, Takafumi Ueda, Kazuyuki Itoh, Hideki Yoshikawa, Norifumi Naka
BACKGROUND: The prognosis of synovial sarcoma (SS), an aggressive soft tissue sarcoma, remains poor. We previously reported that c-MET or platelet-derived growth factor receptor α (PDGFRα) signalling pathway is related to SS progression based upon the findings of phospho-receptor tyrosine kinase (RTK) arrays. TAS-115 is a novel c-MET/ vascular endothelial growth factor receptor-targeting tyrosine kinase inhibitor that has been shown to inhibit multiple RTKs. Here we aimed to investigate the therapeutic potential of TAS-115 against SS...
May 16, 2017: BMC Cancer
https://www.readbyqxmd.com/read/28508421/subversion-of-host-kinases-a-key-network-in-cellular-signaling-hijacked-by-helicobacter-pylori-caga
#4
REVIEW
Nicole Tegtmeyer, Matthias Neddermann, Carmen Isabell Asche, Steffen Backert
Helicobacter pylori is a paradigm of persistent pathogens and major risk factor for developing severe diseases including adenocarcinoma in the human stomach. An important bacterial factor linked to gastric disease progression is the cag pathogenicity island-encoded type-IV secretion system (T4SS) effector protein CagA. Translocated CagA undergoes tyrosine phosphorylation at EPIYA-motifs and then activates or inactivates multiple host signaling proteins in a phosphorylation-dependent and phosphorylation-independent fashion...
May 15, 2017: Molecular Microbiology
https://www.readbyqxmd.com/read/28488172/clear-cell-renal-cell-carcinoma-a-comparative-study-of-histological-and-chromosomal-characteristics-between-primary-tumors-and-their-corresponding-metastases
#5
Julien Dagher, Solène-Florence Kammerer-Jacquet, Frédéric Dugay, Marion Beaumont, Alexandra Lespagnol, Laurence Cornevin, Grégory Verhoest, Karim Bensalah, Nathalie Rioux-Leclercq, Marc-Antoine Belaud-Rotureau
Clear cell renal cell carcinoma (ccRCC) has a poor prognosis with a 50% risk of metastases. Little is known about the phenotypic and molecular profiles of metastases regarding their corresponding primary tumors. This study aimed to screen phenotypic and genotypic differences between metastases and their corresponding primary tumors. We selected four cases with available frozen material. The histological, immunohistochemical (VEGFA, CD31, SMA, Ki67, p53, PAR-3), FISH (VHL gene), next-generation sequencing (VHL and c-MET genes), multiplex ligation-dependent probe amplification, and array-(comparative genomic hybridization) CGH analyses were realized...
May 10, 2017: Virchows Archiv: An International Journal of Pathology
https://www.readbyqxmd.com/read/28485480/shikonin-inhibited-migration-and-invasion-of-human-lung-cancer-cells-via-suppression-of-c-met-mediated-epithelial-to-mesenchymal-transition
#6
Yei-San Hsieh, Chiung-Ho Liao, Wan-Shen Chen, Jih-Tung Pai, Meng-Shih Weng
Epithelial-to-mesenchymal transition (EMT) is a major process to regulate cell migration and invasion. Inhibition of epidermal growth factor receptor (EGFR)-mediated EMT by tyrosine kinase inhibitors (TKIs) is a strategy to prevent lung cancer invasion. However, drug resistance is emerged and accelerated invasion through other signaling bypassing EGFR after TKIs therapy. c-Met signaling pathway is highly activated in EGFR-mutated lung cancer cells. Targeting c-Met signaling pathway may be a strategy to suppress EGFR-independent migration and invasion for lung cancer therapy...
May 9, 2017: Journal of Cellular Biochemistry
https://www.readbyqxmd.com/read/28485003/analysis-of-progress-and-challenges-for-various-patterns-of-c-met-targeted-molecular-imaging-a-systematic-review
#7
REVIEW
Zhaoguo Han, Yongyi Wu, Kai Wang, Yadi Xiao, Zhen Cheng, Xilin Sun, Baozhong Shen
BACKGROUND: Mesenchymal-epithelial transition factor also named c-MET is a receptor tyrosine kinase for the hepatocyte growth factor that plays a pivotal role in tumorigenesis. c-MET-targeted therapies have been tested in preclinical models and patients, with significant benefits for cancer treatment. In recent years, many studies have shown that the expression level and activation status of c-MET are closely correlated to c-MET-targeted therapy response and clinical prognosis, thus highlighting the importance of evaluating the c-MET status during and prior to targeted therapy...
December 2017: EJNMMI Research
https://www.readbyqxmd.com/read/28477027/efficacy-and-safety-of-different-molecular-targeted-agents-based-on-chemotherapy-for-gastric-cancer-patients-treatment-a-network-meta-analysis
#8
Zheng Ren, Jinping Sun, Xinfang Sun, Hongtao Hou, Ke Li, Quanxing Ge
Increasing numbers of reports have been published to demonstrate that molecular targeted agents are able to improve the efficacy of chemotherapy in gastric cancer. This network meta-analysis aimed to evaluate the efficacy and safety of different molecular targeted agents, which were divided into six groups based on the targets including hepatocyte growth factor receptor (c-MET), vascular endothelial factor and its receptor (VEGF/VEGFR), human epidermal growth factor receptor 2 (HER2), epidermal growth factor receptor (EGFR), mammalian target of rapamycin (mTOR) and tyrosine kinase inhibitor (TKI)...
April 18, 2017: Oncotarget
https://www.readbyqxmd.com/read/28475179/mtorc1-independent-autophagy-regulates-receptor-tyrosine-kinase-phosphorylation-in-colorectal-cancer-cells-via-an-mtorc2-mediated-mechanism
#9
Aikaterini Lampada, James O'Prey, Gyorgy Szabadkai, Kevin M Ryan, Daniel Hochhauser, Paolo Salomoni
The intracellular autophagic degradative pathway can have a tumour suppressive or tumour-promoting role depending on the stage of tumour development. Upon starvation or targeting of oncogenic receptor tyrosine kinases (RTKs), autophagy is activated owing to the inhibition of PI3K/AKT/mTORC1 signalling pathway and promotes survival, suggesting that autophagy is a relevant therapeutic target in these settings. However, the role of autophagy in cancer cells where the PI3K/AKT/mTORC1 pathway is constitutively active remains partially understood...
June 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28471540/-in-vitro-antitumor-effects-of-ahr-ligands-aminoflavone-afp-464-and-benzothiazole-5f-203-in-human-renal-carcinoma-cells
#10
G A Luzzani, M A Callero, A I Kuruppu, V Trapani, C Flumian, L Todaro, T D Bradshaw, A I Loaiza Perez
We investigated activity and mechanism of action of two AhR ligand antitumor agents, AFP 464 and 5F 203 on human renal cancer cells, specifically examining their effects on cell cycle progression, apoptosis and migration. TK-10, SN12C, Caki-1 and ACHN human renal cancer cell lines were treated with AFP 464 and 5F 203. We evaluated cytotoxicity by MTS assays, cell cycle arrest and apoptosis by flow cytometry and corroborated a mechanism of action involving AhR signal transduction activation. Changes in migration properties by wound healing assays were investigated: 5F 203-sensitive cells show decreased migration after treatment, therefore we measured c-Met phosphorylation by Western blot in these cells...
May 4, 2017: Journal of Cellular Biochemistry
https://www.readbyqxmd.com/read/28469968/the-selective-c-met-inhibitor-tepotinib-can-overcome-epidermal-growth-factor-receptor-inhibitor-resistance-mediated-by-aberrant-c-met-activation-in-nsclc-models
#11
Manja Friese-Hamim, Friedhelm Bladt, Giuseppe Locatelli, Uz Stammberger, Andree Blaukat
Non-small cell lung cancer (NSCLC) sensitive to first-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) often acquires resistance through secondary EGFR mutations, including the T790M mutation, aberrant c-Met receptor activity, or both. We assessed the ability of the highly selective c-Met inhibitor tepotinib to overcome EGFR TKI resistance in various xenograft models of NSCLC. In models with EGFR-activating mutations and low c-Met expression (patient explant-derived LU342, cell line PC-9), EGFR TKIs caused tumors to shrink, but growth resumed upon cessation of treatment...
2017: American Journal of Cancer Research
https://www.readbyqxmd.com/read/28469773/crizotinib-synergizes-with-cisplatin-in-preclinical-models-of-ovarian-cancer
#12
Xiao-Xiu Huang, Feng-Feng Xie, Li-Jiao Hou, Xiu-Xiu Chen, Rong-Ying Ou, Jiang-Tao Yu, Jian-Ge Qiu, Wen-Ji Zhang, Qi-Wei Jiang, Yang Yang, Di-Wei Zheng, Yao Chen, Jia-Rong Huang, Kun Wang, Meng-Ning Wei, Wen-Feng Li, Zhi Shi, Xiao-Jian Yan
Crizotinib, a small molecule inhibitor of anaplastic lymphoma kinase (ALK), c-ros oncogene 1 (ROS1) and c-MET (also called MET or hepatocyte growth factor receptor), has been approved by the Food and Drug Administration for the treatment of patients with advanced non-small cell lung cancer whose tumors have rearrangements in the ALK or ROS1 gene. However, the anticancer effect of crizotinib on ovarian cancer is still unclear. In this study, our data show that crizotinib can actively induce cell growth inhibition, cell cycle arrest at G2/M phase and apoptosis with the decreasing phosphorylation of the downstream signaling effectors AKT and ERK in human ovarian cancer cells...
2017: American Journal of Translational Research
https://www.readbyqxmd.com/read/28469401/hepatocyte-growth-factor-c-met-axis-in-thyroid-cancer-from-diagnostic-biomarker-to-therapeutic-target
#13
REVIEW
Maria Trovato, Alfredo Campennì, Salvatore Giovinazzo, Massimiliano Siracusa, Rosaria Maddalena Ruggeri
The hepatocyte growth factor (HGF)/c-met axis plays a crucial role in cancer development by promoting cellular proliferation, motility, and morphogenesis, as well as angiogenesis. Different cellular distributions of both the ligand and the receptor in benign vs malignant lesions indicate this biological system as a candidate for a diagnostic biomarker of malignancy occurring in endocrine glands, such as the thyroid and pituitary. Furthermore, the HGF/c-met expression may help to identify a subset of patients eligible for potential targeted therapies with HGF/c-met inhibitors or antagonists in thyroid tumour, as well as in other malignancies...
2017: Biomarker Insights
https://www.readbyqxmd.com/read/28464908/a-phase-i-study-of-lapatinib-in-combination-with-foretinib-a-c-met-axl-and-vascular-endothelial-growth-factor-receptor-inhibitor-in-human-epidermal-growth-factor-receptor-2-her-2-positive-metastatic-breast-cancer
#14
Stephen K Chia, Susan L Ellard, Mihaela Mates, Stephen Welch, Catalin Mihalcioiu, Wilson H Miller, Karen Gelmon, Caroline Lohrisch, Vikaash Kumar, Sara Taylor, Linda Hagerman, Rachel Goodwin, Tao Wang, Shingo Sakashita, Ming S Tsao, Elizabeth Eisenhauer, Penelope Bradbury
BACKGROUND: The mechanisms of resistance to anti-human epidermal growth factor receptor 2 (HER 2) therapies are unclear but may include the tyrosine-protein kinase Met (c-Met), vascular endothelial growth factor (VEGF) and AXL pathways. Foretinib is an inhibitor of c-Met, VEGF receptor 2 (VEGFR-2), platelet-derived growth factor receptor beta (PDGFRB), AXL, Fms-like tyrosine kinase 3 (FLT3), angiopoiten receptor (TIE-2), RET and RON kinases. This phase Ib study sought to establish the associated toxicities, pharmacokinetics (PK) and recommended phase II doses (RP2D) of foretinib and lapatinib in a cohort of HER-2-positive patients with metastatic breast cancer (MBC)...
May 2, 2017: Breast Cancer Research: BCR
https://www.readbyqxmd.com/read/28461158/pancreatic-stellate-cells-increase-pancreatic-cancer-cells-invasion-through-the-hepatocyte-growth-factor-c-met-survivin-regulated-by-p53-p21
#15
Xiao-Peng Yang, Shang-Long Liu, Jian-Fei Xu, Shou-Gen Cao, Yu Li, Yan-Bing Zhou
Pancreatic stellate cells (PSCs) are a key cellular component of the pancreatic tumor microenvironment and are considered to contribute to tumor invasion and metastasis. Multiple cytokines and growth factors derived from PSCs are involved in malignant cancer progression, including hepatocyte growth factor (HGF). However, the molecular mechanisms by which HGF regulates cancer invasion and metastasis have not been completely elucidated. Here, we report that two pancreatic cancer (PC) cell lines, Panc-1 and SW1990, displayed different invasive and migratory abilities after treatment with HGF secreted by PSCs...
April 29, 2017: Experimental Cell Research
https://www.readbyqxmd.com/read/28459467/ribonucleotide-reductase-represents-a-novel-therapeutic-target-in-primary-effusion-lymphoma
#16
L Dai, Z Lin, J Qiao, Y Chen, E K Flemington, Z Qin
Primary effusion lymphoma (PEL) is a highly aggressive B-cell malignancy that is closely associated with one of oncogenic viruses infection, Kaposi's sarcoma-associated herpesvirus. PEL prognosis is poor and patients barely survive >6 months even following active chemotherapy interventions. There is therefore an urgent need to discover more effective targets for PEL management. We recently found that the ribonucleotide reductase (RR) subunit M2 is potentially regulated by the key oncogenic hepatocyte growth factor/c-MET pathway in PEL...
May 1, 2017: Oncogene
https://www.readbyqxmd.com/read/28459362/the-c-met-receptor-implication-for-targeted-therapies-in-colorectal-cancer
#17
Elmira Safaie Qamsari, Sepideh Safaei Ghaderi, Bahareh Zarei, Ruhollah Dorostkar, Salman Bagheri, Farhad Jadidi-Niaragh, Mohammad Hossein Somi, Mehdi Yousefi
c-Met (mesenchymal-epithelial transition factor) is a tyrosine kinase receptor activated by hepatocyte growth factor and regulates multiple biological processes, such as cell scattering, survival, and proliferation. Aberrant c-Met signaling has been implicated in a variety of cancer types, including colorectal cancer. c-Met is genetically altered through various mechanisms that is associated with colorectal cancer progression and metastasis. Especially, in colorectal cancer, preclinical evidence for the aberrant activation of the c-Met signaling exists...
May 2017: Tumour Biology: the Journal of the International Society for Oncodevelopmental Biology and Medicine
https://www.readbyqxmd.com/read/28449393/a-phase-1-study-of-the-c-met-inhibitor-tivantinib-arq197-in-children-with-relapsed-or-refractory-solid-tumors-a-children-s-oncology-group-study-phase-1-and-pilot-consortium-trial-advl1111
#18
James I Geller, John P Perentesis, Xiaowei Liu, Charles G Minard, Rachel A Kudgus, Joel M Reid, Elizabeth Fox, Susan M Blaney, Brenda J Weigel
BACKGROUND: The c-Met receptor tyrosine kinase is dysregulated in many pediatric cancers. Tivantinib is an oral small molecule that inhibits the c-Met receptor tyrosine kinase. A phase 1 and pharmacokinetic (PK) trial evaluating tivantinib was conducted in children with relapsed/refractory solid tumors. METHODS: Oral tivantinib capsules were administered twice daily with food, continuously in 28-day cycles. Dose levels 170, 200, and 240 mg/m(2) /dose were evaluated using a rolling-six design (Part A)...
April 27, 2017: Pediatric Blood & Cancer
https://www.readbyqxmd.com/read/28445954/a-clinically-feasible-multiplex-proteomic-immunoassay-as-a-novel-functional-diagnostic-for-pancreatic-ductal-adenocarcinoma
#19
Kian-Huat Lim, Emma Langley, Feng Gao, Jingqin Luo, Lin Li, Gary Meyer, Phillip Kim, Sharat Singh, Vladamir M Kushnir, Dayna S Early, Daniel K Mullady, Steven A Edmundowicz, Sachin Wani, Faris M Murad, Dengfeng Cao, Riad R Azar, Andrea Wang-Gillam
To date, targeted therapy for pancreatic ductal adenocarcinoma (PDAC) remains largely unsuccessful in the clinic. Current genomics-based technologies are unable to reflect the quantitative, dynamic signaling changes in the tumor, and require larger tumor samples that are difficult to obtain in PDAC patients. Therefore, a highly sensitive functional tool that can reliably and comprehensively inform intra-tumoral signaling events is direly needed to guide treatment decision. We tested the utility of a highly sensitive proteomics-based functional diagnostic platform, Collaborative Enzyme Enhanced Reactive-immunoassay (CEERTM), on fine-needle aspiration (FNA) samples obtained from 102 patients with radiographically-evident pancreatic tumors...
April 11, 2017: Oncotarget
https://www.readbyqxmd.com/read/28442019/-progress-of-c-met-signaling-pathway-and-tkis-in-non-small-cell-lung-cancer
#20
Xiaoqing Yu, Yanjun Xu, Yun Fan
c-MET is considered a promising oncogenic driver in non-small cell lung cancer (NSCLC) after the discovery of epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK). MET activation including gene mutation, amplification and protein overexpression, all of these are potential therapeutic targets and are associated with poor prognosis. Clinical evidence suggests a role for MET activation as both a primary oncogenic driver in subsets of lung cancer, and as a secondary driver of acquired resistance to EGFR-tyrosine kinase inhibitor (TKI)...
April 20, 2017: Zhongguo Fei Ai za Zhi, Chinese Journal of Lung Cancer
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