Zobrazeno 1 - 10
of 21
pro vyhledávání: ''
Publikováno v:
Molecular Cancer Research. 18:835-846
Through the use of an unbiased, genome-scale CRISPR modifier screen, we identified NF1 suppression as a mechanism of resistance to EGFR inhibition in NRAS/KRAS/BRAFV600-wild-type colorectal cancer cells. Reduced NF1 expression permitted sustained sig
Autor:
Byung-Gyu Kim, Hye Jin Ham, Jung-Guk Kim, Ji-Hyun Kim, Soo-Young Park, Keun-Gyu Park, Jung Yi Lee, Yeon-Kyung Choi, Se Young Jang, Mi Jin Kim, Hui-Jeon Jeon, Inkyu Lee
Publikováno v:
Molecular Cancer Research. 15:1230-1242
The tyrosine kinase inhibitor sorafenib is the only therapeutic agent approved for the treatment of advanced hepatocellular carcinoma (HCC), but acquired resistance to sorafenib is high. Here, we report metabolic reprogramming in sorafenib-resistant
Autor:
Atsuko Ogino, T. Kosaka, Marzia Capelletti, Jihyun Choi, Hideki Endoh, Junko Tanizaki, Michael J. Eck, Dalia Ercan, Magda Bahcall, Raymond M. Paranal, Geoffrey R. Oxnard, Pasi A. Jänne, Amanda J. Redig, Antonio Calles, Claire E. Repellin, Christine A. Lydon
Publikováno v:
Cancer Research. 77:2712-2721
Insertion mutations in EGFR and HER2 both occur at analogous positions in exon 20. Non–small cell lung cancer (NSCLC) patients with tumors harboring these mutations seldom achieve clinical responses to dacomitinib and afatinib, two covalent quinazo
Autor:
Ilaria Conti, Sheng-Bin Peng, James J. Starling, Igor Mochalkin, Henry James Robert, Sean Buchanan, Robert D. Van Horn, Lysiane Huber, Gregory D. Plowman, Swee Seong Wong, Youyan Zhang, Vipin Yadav, Yong Gang Yue, Shih-Hsun Chen, Tinggui Yin
Publikováno v:
Cancer Discovery. 6:300-315
We have identified previously undiscovered BRAF in-frame deletions near the αC-helix region of the kinase domain in pancreatic, lung, ovarian, and thyroid cancers. These deletions are mutually exclusive with KRAS mutations and occur in 4.21% of KRAS
Autor:
Maria E. Arcila, Efsevia Vakiani, Jaclyn F. Hechtman, Jason T. Huse, Jinru Shia, Laetitia Borsu, Rona Yaeger, Justyna Sadowska, Marc Ladanyi
Publikováno v:
Molecular Cancer Research. 13:1003-1008
The PI3K/AKT/mTOR pathway is activated through multiple mechanisms in colorectal carcinoma. Here, the clinicopathologic and molecular features of AKT1 E17K–mutated colorectal carcinoma in comparison with PIK3CA-mutated colorectal carcinoma are desc
Publikováno v:
Molecular Cancer Research. 13:659-669
KRAS mutations are frequently detected in human colorectal cancer and contribute to de novo apoptosis resistance and ultimately therapeutic failure. To overcome KRAS-mediated apoptosis resistance, the irreversible proteasome inhibitor, carfilzomib, w
Autor:
Ruiyang Tian, Penelope Miron, Gautam Maulik, Scott J. Rodig, Bose Kochupurakkal, Alexander Miron, Debajit K. Biswas, Shannon T. Bailey, Teresa V. Bowman, Kathleen M. Foley, Yoon Jong Choi, J. Dirk Iglehart, Myles Brown
Publikováno v:
Molecular Cancer Research. 12:408-420
Breast cancers with HER2 overexpression are sensitive to drugs targeting the receptor or its kinase activity. HER2-targeting drugs are initially effective against HER2-positive breast cancer, but resistance inevitably occurs. We previously found that
Autor:
Norio Nonomura, Koji Hatano, Mutsumi Tsuchiya, Masashi Nakayama, Souhei Yamaguchi, Akira Nagahara, Kazutoshi Fujita, Yasutomo Nakai, Motohide Uemura, Keisuke Nimura, Yasufumi Kaneda, Kouki Murakami
Publikováno v:
Molecular Cancer Research. 11:1088-1100
Despite an increasing prevalence of patients with docetaxel-refractory prostate cancer, little is known about the tumor biology of the docetaxel-resistant residual tumor cells compared with primary tumor cells. In this study, tumorigenic potential wa
Autor:
Ekkehard Moessner, Pablo Umana, Sylvia Herter, Christian Gerdes, Birgit Bossenmaier, Carola Ries, Michaela Roemmele, Nicolini Valeria G, Hans Joachim Mueller, Thomas Friess, Olivier Freytag, Erwin van Puijenbroek, Sabine Lang
Publikováno v:
Clinical Cancer Research. 19:1126-1138
Purpose: Anti-EGF receptor (EGFR) antibodies and small-molecule tyrosine kinase inhibitors have shown activity in epithelial tumors; however, agents that work by blocking the EGFR growth signal are ineffective when the oncogenic stimulus arises downs
Autor:
Marc Ladanyi, Mark G. Kris, Maria E. Arcila, Gregory J. Riely, Maureen F. Zakowski, Valerie W. Rusch, M. Catherine Pietanza, Camelia S. Sima, Christopher Lau, Paul K. Paik, Jamie E. Chaft
Publikováno v:
Molecular Cancer Therapeutics. 11:485-491
Phosphoinositide-3-kinase catalytic alpha polypeptide (PIK3CA) encodes the p110α subunit of the mitogenic signaling protein phosphoinositide 3-kinase (PI3K). PIK3CA mutations in the helical binding domain and the catalytic subunit of the protein hav