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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:
Stacy L. Littlechild, James J. Moresco, Thomas McFall, Ed Stites, Meron Mengistu, Andrey S. Shaw, Jolene K. Diedrich, Laura Sisk-Hackworth
Publikováno v:
Molecular Cancer Research. 18:B43-B43
Standard protocol to treat colorectal cancer (CRC) includes surgery, chemotherapy and radiotherapy as first-line treatment options. When applicable, targeting agents such as anti-EGFR therapies (i.e., cetuximab and panitumumab) have become important
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
Autor:
Kelly S. Oliner, Meinholf Karthaus, Salvatore Siena, Jean-Yves Douillard, J. Randolph Hecht, Scott Jung, Will Go, Fernando Rivera, Ying Tian, Josep Tabernero, Lee S. Schwartzberg, Hua Yu
Publikováno v:
Molecular Cancer Research. 12:A57-A57
Background: PRIME was a randomized phase 3 study of panitumumab (pmab)+FOLFOX4 vs FOLFOX4 in the 1st-line treatment (tx) of pts with mCRC by KRAS exon 2 status. PEAK was a randomized phase 2 study of pmab+mFOLFOX6 or bevacizumab (bev)+mFOLFOX6 in the
Autor:
Josep M. Llovet, Ho Yeong Lim, Michael Teufel, Florian Puehler, Joachim Reischl, Barrett H. Childs, Frank Diehl, Heiko Krissel
Publikováno v:
Molecular Cancer Research. 12:B42-B42
Background: Per COSMIC database, RAS mutations are uncommon events in hepatocellular carcinoma (HCC). Refametinib (BAY 86-9766) is a potent (IC50=17-60 nM) allosteric dual MEK 1/2 inhibitor, which exhibits high selectivity for MEK as compared to othe
Autor:
Ahmed A. Samatar
Publikováno v:
Molecular Cancer Research. 12:IA06-IA06
The RAS /RAF /MEK / ERK signal transduction pathway is frequently activated in several human cancers, due to a gain of function mutations in KRAS, NRAS, or BRAF. Because of the high frequency of activating mutations, this pathway has become a focus f
Autor:
Solit David, Hanrahan Aphrothiti, Rosen Neal, Abdel-Wahab Omar, Wei Min, Torres N Merna, Zhan Yao, Luo Lusong, Poulikakos Poulikos
Publikováno v:
Molecular Cancer Research. 12:A41-A41
Dysregulation of ERK signaling is a common event in malignancy. Receptor activation of RAS leads to dimerization and activation of RAF kinase, which in turn activates ERK. Physiologic activation of the pathway is limited by ERK dependent feedback inh