Results 11 to 20 of about 260,030 (390)
Escaping KRAS: Gaining Autonomy and Resistance to KRAS Inhibition in KRAS Mutant Cancers
Activating mutations in KRAS are present in 25% of human cancers. When mutated, the KRAS protein becomes constitutively active, stimulating various effector pathways and leading to the deregulation of key cellular processes, including the suppression of apoptosis and enhancement of proliferation.
Yuta Adachi +3 more
openaire +4 more sources
Oncogenic Kras are genetic dependencies for the majority of pancreatic and colorectal adenocarcinomas; however, much remains to be understood regarding its tropism to these carcinomas. Recently developed organoid technology presents a more representative model culture system for pancreatic and colon epithelial tissues as well as better fostering the ...
David A. Tuveson, Derek K. Cheng
openaire +3 more sources
Identification of epidermal Pdx1 expression discloses different roles of Notch1 and Notch2 in murine KrasG12D-induced skin carcinogenesis in vivo [PDF]
Background The Ras and Notch signaling pathways are frequently activated during development to control many diverse cellular processes and are often dysregulated during tumorigenesis.
Barbara M. Grüner +9 more
core +15 more sources
Targeting the MAPK Pathway in KRAS-Driven Tumors
Matthias Drosten, Mariano Barbacid
exaly +2 more sources
Chemical remodeling of a cellular chaperone to target the active state of mutant KRAS
The discovery of small-molecule inhibitors requires suitable binding pockets on protein surfaces. Proteins that lack this feature are considered undruggable and require innovative strategies for therapeutic targeting.
C. Schulze +35 more
semanticscholar +1 more source
Mutations in members of the RAS family of small GTPases have been associated with numerous human cancers. However, RAS family members are notoriously difficult to target. In this issue of Structure, Lu et al. (2017) examine the effects of two compounds with distinct chemical scaffolds on the structure and dynamics of an oncogenic KRAS mutant, thus ...
Daniel J, Deredge, Patrick L, Wintrode
openaire +2 more sources
Divarasib plus cetuximab in KRAS G12C-positive colorectal cancer: a phase 1b trial
In an arm of a phase 1b trial, the combination of divarasib, a KRAS G12C inhibitor, and cetuximab, an epidermal growth factor receptor inhibitor, was well tolerated with an encouraging overall response rate of 62.5% in patients with KRA S G12C -positive ...
Jayesh Desai +38 more
semanticscholar +1 more source
Sotorasib in KRAS p.G12C-Mutated Advanced Pancreatic Cancer.
BACKGROUND KRAS p.G12C mutation occurs in approximately 1 to 2% of pancreatic cancers. The safety and efficacy of sotorasib, a KRAS G12C inhibitor, in previously treated patients with KRAS p.G12C-mutated pancreatic cancer are unknown.
J. Strickler +21 more
semanticscholar +1 more source
Co-mutations and KRAS G12C inhibitor efficacy in advanced NSCLC.
Molecular modifiers of KRAS G12C inhibitor (KRAS G12Ci) efficacy in advanced KRAS G12C-mutant NSCLC are poorly defined. In a large unbiased clinico-genomic analysis of 424 NSCLC patients, we identified and validated co-alterations in KEAP1, SMARCA4 and ...
M. Negrão +65 more
semanticscholar +1 more source
Modulation of the proteostasis network promotes tumor resistance to oncogenic KRAS inhibitors
Despite substantial advances in targeting mutant KRAS, tumor resistance to KRAS inhibitors (KRASi) remains a major barrier to progress. Here, we report proteostasis reprogramming as a key convergence point of multiple KRASi-resistance mechanisms ...
Xiangdong Lv +38 more
semanticscholar +1 more source

