Associated Papers
Phase I/II Study of Combined BCL-xL and MEK Inhibition with Navitoclax and Trametinib in KRAS or NRAS Mutant Advanced Solid Tumors.
Corcoran RB et al.
Clinical Cancer Research : an Official Journal of the American Association for Cancer Research, 2024
The Clinicopathological Correlation of KRAS Mutation and PTEN Expression Status in Primary and Metastatic Colorectal Carcinoma.
Hassan RT et al.
Cureus, 2024
Structural modifications and kinetic effects of KRAS interactions with HRAS and NRAS: an in silico comparative analysis of KRAS mutants.
Silverman I et al.
Frontiers in Molecular Biosciences, 2024
Liquid biopsy detects genomic drivers in NSCLC without EGFR mutations by single-plex testing: WJOG13620L.
Uemura T et al.
Cancer Medicine, 2023
A conserved arginine within the αC-helix of Erk1/2 is a latch of autoactivation and of oncogenic capabilities.
Soudah N et al.
The Journal of Biological Chemistry, 2023
RAF1 contributes to cell proliferation and STAT3 activation in colorectal cancer independently of microsatellite and KRAS status.
Dorard C et al.
Oncogene, 2023
Therapy-induced senescence promotes breast cancer cells plasticity by inducing Lipocalin-2 expression.
Morales-Valencia J et al.
Oncogene, 2022
Interactions between EGFR and EphA2 promote tumorigenesis through the action of Ephexin1.
Kim J et al.
Cell Death & Disease, 2022
KRAS: A Druggable Target in Colon Cancer Patients.
Negri F et al.
International Journal of Molecular Sciences, 2022
Mutational landscape of K-Ras substitutions at 12th position-a systematic molecular dynamics approach.
S UK et al.
Journal of Biomolecular Structure & Dynamics, 2022
Antitumor efficacy of XPO1 inhibitor Selinexor in KRAS-mutant lung adenocarcinoma patient-derived xenografts.
Rosen JC et al.
Translational Oncology, 2021
Diffuse expression of MUC6 defines a distinct clinicopathological subset of pulmonary invasive mucinous adenocarcinoma.
Kishikawa S et al.
Modern Pathology : an Official Journal of the United States and Canadian Academy of Pathology, Inc, 2021
Lysosomal-Associated Protein Transmembrane 5 Functions as a Novel Negative Regulator of Pathological Cardiac Hypertrophy.
Gao L et al.
Frontiers in Cardiovascular Medicine, 2021
Generation of KS-58 as the first K-Ras(G12D)-inhibitory peptide presenting anti-cancer activity in vivo.
Sakamoto K et al.
Scientific Reports, 2020
Metformin selectively inhibits metastatic colorectal cancer with the KRAS mutation by intracellular accumulation through silencing MATE1.
Xie J et al.
Proceedings of the National Academy of Sciences of the United States of America, 2020
An integrative pharmacogenomics analysis identifies therapeutic targets in KRAS-mutant lung cancer.
Wang H et al.
Ebiomedicine, 2019
Cysteine-based regulation of redox-sensitive Ras small GTPases.
Messina S et al.
Redox Biology, 2019
G12V and G12C mutations in the gene KRAS are associated with a poorer prognosis in primary colorectal cancer.
Hayama T et al.
International Journal of Colorectal Disease, 2019
RAC1P29S Induces a Mesenchymal Phenotypic Switch via Serum Response Factor to Promote Melanoma Development and Therapy Resistance.
Lionarons DA et al.
Cancer Cell, 2019
High-throughput screening identifies small molecules that bind to the RAS:SOS:RAS complex and perturb RAS signaling.
Burns MC et al.
Analytical Biochemistry, 2018
A KRAS wild type mutational status confers a survival advantage in pancreatic ductal adenocarcinoma.
Windon AL et al.
Journal of Gastrointestinal Oncology, 2018
Skb5, an SH3 adaptor protein, regulates Pmk1 MAPK signaling by controlling the intracellular localization of the MAPKKK Mkh1.
Kanda Y et al.
Journal of Cell Science, 2016
A Phase I Study of the Safety, Pharmacokinetics, and Pharmacodynamics of Combination Therapy with Refametinib plus Sorafenib in Patients with Advanced Cancer.
Adjei AA et al.
Clinical Cancer Research : an Official Journal of the American Association for Cancer Research, 2016
Intrinsically active variants of Erk oncogenically transform cells and disclose unexpected autophosphorylation capability that is independent of TEY phosphorylation.
Smorodinsky-Atias K et al.
Molecular Biology of the Cell, 2016
The combinatorial activation of the PI3K and Ras/MAPK pathways is sufficient for aggressive tumor formation, while individual pathway activation supports cell persistence.
Thompson KN et al.
Oncotarget, 2015
RASopathies: unraveling mechanisms with animal models.
Jindal GA et al.
Disease Models & Mechanisms, 2015
Clinical and metabolic parameters in non-small cell lung carcinoma and colorectal cancer patients with and without KRAS mutations.
Yilmaz A et al.
International Journal of Environmental Research and Public Health, 2014
Characterization of rare transforming KRAS mutations in sporadic colorectal cancer.
Tong JH et al.
Cancer Biology & Therapy, 2014
Frequencies and prognostic role of KRAS and BRAF mutations in patients with localized pancreatic and ampullary adenocarcinomas.
Schultz NA et al.
Pancreas, 2012
Postzygotic HRAS and KRAS mutations cause nevus sebaceous and Schimmelpenning syndrome.
Groesser L et al.
Nature Genetics, 2012
Allosteric modulation of Ras-GTP is linked to signal transduction through RAF kinase.
Buhrman G et al.
The Journal of Biological Chemistry, 2011
Germline KRAS mutations cause aberrant biochemical and physical properties leading to developmental disorders.
Gremer L et al.
Human Mutation, 2011
Mutation of ERBB2 provides a novel alternative mechanism for the ubiquitous activation of RAS-MAPK in ovarian serous low malignant potential tumors.
Anglesio MS et al.
Molecular Cancer Research : Mcr, 2008
Molecular alterations in tumors and response to combination chemotherapy with gefitinib for advanced colorectal cancer.
Ogino S et al.
Clinical Cancer Research : an Official Journal of the American Association for Cancer Research, 2005
Amino acids interfere with the ERK1/2-dependent control of macroautophagy by controlling the activation of Raf-1 in human colon cancer HT-29 cells.
Pattingre S et al.
The Journal of Biological Chemistry, 2003
Oncogenic insertional mutations in the P-loop of Ras are overactive in MAP kinase signaling.
Klockow B et al.
Oncogene, 2000