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Autor:
Christine A. Pratilas, Sharmeen Uddin, Amy Allen, Zhan Yao, Jiawan Wang, Ira J. Dunkel, Barry S. Taylor, Neal Rosen, Philip Jonsson, Alice Can Ran Qin, Katia Manova, Sofia Haque, David J. Pisapia, Mary Petriccione, Marc K. Rosenblum
Publikováno v:
Cancer Discovery. 8:1130-1141
BRAFV600E hyperactivates ERK and signals as a RAF inhibitor–sensitive monomer. Although RAF inhibitors can produce impressive clinical responses in patients with mutant BRAF tumors, the mechanisms of resistance to these drugs are incompletely chara
Autor:
Vishnu C. Damalanka, James W. Janetka, Lidija Klampfer, Robert J. Coffey, Galina Bogatcheva, Ramona Graves-Deal, Bhuminder Singh
Publikováno v:
Cancer Research. 81:1084-1084
Using a novel 3D culture system, we previously showed that activation of receptor tyrosine kinases (RTKs) MET and RON contributed to cetuximab resistance in colorectal cancer (CRC) cells. CC derived from HCA-7 cells were sensitive to cetuximab, where
Autor:
Scott Kopetz, Oluwadara Coker, Melanie Nicole Woods, Lawrence N. Kwong, Oscar Villareal, Kelly Gale, Alexey V. Sorokin, Fengqin Gao, Ji Wu, John Paul Shen, Hey Min Lee
Publikováno v:
Cancer Research. 81:LB264-LB264
Background: Oncogenic KRAS mutations occur in 50% of colorectal cancer (CRC) patients and have long been considered undruggable. Novel covalent inhibitors targeting the KRASG12C mutation have been developed, presenting a unique opportunity to directl
Autor:
Vishnu C. Damalanka, James W. Janetka, Robert J. Coffey, Lidija Klampfer, Bhuminder Singh, Galina Bogatcheva, Ramona Graves-Deal
Publikováno v:
Cancer Research. 80:3451-3451
Using 3D type I collagen cultures of human colorectal cancer (CRC) cell line HCA-7 derivatives (CC, SC, CC-CR), we previously identified that activation of receptor tyrosine kinases (RTKs) MET and RON contributed to resistance to anti-EGFR monoclonal
Autor:
Lars D. Engstrom, Peter Olson, James G. Christensen, Lauren Hargis, Andrew Calinisan, David Briere, Matthew A. Marx, Ruth Aranda, Jill Hallin
Publikováno v:
Cancer Research. 80:LB-098
The ability to develop effective therapies for KRAS mutant cancers has remained elusive despite decades of research. MRTX849 was identified as a potent, selective, and covalent KRASG12C inhibitor presently under evaluation in clinical trials. MRTX849
Autor:
Maria Luana Poeta, Emanuela Signori, Jesus Garcia-Foncillas, Caterina Fusilli, Luisa Loiacono, Tommaso Mazza, Giuseppe Lamorte, Vito Michele Fazio, Mariangela De Robertis, Massimo Sanchez, Angelo L. Vescovi, Luigi Marchionni
Publikováno v:
Cancer Research. 80:4296-4296
Tumor heterogeneity and the presence of stem-like cells have been identified as key features for resistance to anticancer treatments including targeted therapy. The Eph receptors comprise a large family of receptor tyrosine kinases that marks stem-li
Autor:
Huaixiang Hao, Peter S. Hammerman, Hongyun Wang, Chen Liu, Scott Delach, Jeffrey A. Engelman, Morvarid Mohseni, Susan Moody, Hengyu Lu, Matthew J. LaMarche, Giordano Caponigro
Publikováno v:
Cancer Research. 80:LB-122
Introduction: The RTK-RAS-MAPK pathway is frequently activated in cancers due to a variety of mechanisms including mutations or amplifications in RTK, KRAS or BRAF. The effectiveness of inhibitors targeting those oncogenic drivers is often limited by
Autor:
Peter Olson, David Briere, Matthew A. Marx, Andrew Calinisan, Michael R. Burkhard, Niranjan Sudhakar, Jill Hallin, Lauren Hargis, Fell Jay Bradford, Guy Vigers, Ruth Aranda, Lars D. Engstrom, John P. Fischer, James G. Christensen, James F. Blake, Brian R. Baer, Josh Ballard, Vickie Bowcut
Publikováno v:
Molecular Cancer Therapeutics. 18:C069-C069
The ability to effectively target mutated KRAS has remained elusive despite decades of research. MRTX849 was identified via structure-based drug design as a potent, selective, and covalent KRASG12C inhibitor that exhibits favorable drug-like properti
Publikováno v:
Molecular Cancer Therapeutics. 13:3049-3061
Glioblastoma multiforme (GBM) is an extremely aggressive brain cancer with a median survival of less than 2 years. GBM is characterized by abnormal activation of receptor tyrosine kinase and constitutively activated STAT3. Although EGFR phosphorylati
Autor:
Fawn Qian, Justin Lesch, Yu-Chien Chou, Frauke Bentzien, Jenny Tan, A. Douglas Laird, Stefan Engst, Felix Chu, Kyoko Yamaguchi, F. Michael Yakes, Andrew You, Belinda Cancilla, Yongchang Shi, Jason Chen, Peiwen Yu, Lillian Lee, Jessica Orf, Alison Joly
Publikováno v:
Molecular Cancer Therapeutics. 10:2298-2308
The signaling pathway of the receptor tyrosine kinase MET and its ligand hepatocyte growth factor (HGF) is important for cell growth, survival, and motility and is functionally linked to the signaling pathway of VEGF, which is widely recognized as a