Proto-Oncogene Proteins p21(ras)

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  Subject Areas on Research

  • A Landscape of Therapeutic Cooperativity in KRAS Mutant Cancers Reveals Principles for Controlling Tumor Evolution. 
  • A comprehensive survey of genomic alterations in gastric cancer reveals systematic patterns of molecular exclusivity and co-occurrence among distinct therapeutic targets. 
  • A conserved alternative splice in the von Recklinghausen neurofibromatosis (NF1) gene produces two neurofibromin isoforms, both of which have GTPase-activating protein activity. 
  • A high-throughput CRISPR interference screen for dissecting functional regulators of GPCR/cAMP signaling. 
  • A model for RAS mutation patterns in cancers: finding the sweet spot. 
  • A murine lung cancer co-clinical trial identifies genetic modifiers of therapeutic response. 
  • A next-generation dual-recombinase system for time- and host-specific targeting of pancreatic cancer. 
  • A phase II study of capecitabine, oxaliplatin, bevacizumab and cetuximab in the treatment of metastatic colorectal cancer. 
  • A proteomic approach for dissecting H-Ras signaling networks in NIH/3T3 mouse embryonic fibroblast cells. 
  • ADAP1 promotes latent HIV-1 reactivation by selectively tuning KRAS-ERK-AP-1 T cell signaling-transcriptional axis. 
  • Activation of RalA is critical for Ras-induced tumorigenesis of human cells. 
  • Acute DNA damage activates the tumour suppressor p53 to promote radiation-induced lymphoma. 
  • Addressing Resistance to Targeted Therapies in Metastatic Colorectal Cancer. 
  • Adenoma-like adenocarcinoma: a subtype of colorectal carcinoma with good prognosis, deceptive appearance on biopsy and frequent KRAS mutation. 
  • Adjuvant Hepatic Artery Infusion Chemotherapy is Associated With Improved Survival Regardless of KRAS Mutation Status in Patients With Resected Colorectal Liver Metastases: A Retrospective Analysis of 674 Patients. 
  • Alterations in driver genes are predictive of survival in patients with resected pancreatic ductal adenocarcinoma. 
  • An ultra-sensitive method to detect mutations in human RAS templates. 
  • Analysis of the neurofibromatosis type 1 (NF1) GAP-related domain by site-directed mutagenesis. 
  • Association between KRAS rs61764370 and triple-negative breast cancer--a false positive? 
  • Association of k-ras, b-raf, and p53 status with the treatment effect of bevacizumab. 
  • Autophagic activity dictates the cellular response to oncogenic RAS. 
  • Beryllium fluoride-induced cell proliferation: a process requiring P21(ras)-dependent activated signal transduction and NF-kappaB-dependent gene regulation. 
  • CHK1 protects oncogenic KRAS-expressing cells from DNA damage and is a target for pancreatic cancer treatment. 
  • Cabozantinib and Panitumumab for RAS Wild-Type Metastatic Colorectal Cancer. 
  • Cancer-Associated Fibroblasts Induce a Collagen Cross-link Switch in Tumor Stroma. 
  • Capturing the primordial Kras mutation initiating urethane carcinogenesis. 
  • Cetuximab Alone or With Irinotecan for Resistant KRAS-, NRAS-, BRAF- and PIK3CA-wild-type Metastatic Colorectal Cancer: The AGITG Randomized Phase II ICECREAM Study. 
  • Characterization of the cytotoxic activities of novel analogues of the antitumor agent, lavendamycin. 
  • Chemoradiotherapy and gefitinib in stage III non-small cell lung cancer with epidermal growth factor receptor and KRAS mutation analysis: cancer and leukemia group B (CALEB) 30106, a CALGB-stratified phase II trial. 
  • Clinical significance and prognostic relevance of KRAS, BRAF, PI3K and TP53 genetic mutation analysis for resectable and unresectable colorectal liver metastases: A systematic review of the current evidence. 
  • Codon bias imposes a targetable limitation on KRAS-driven therapeutic resistance. 
  • Codon usage regulates human KRAS expression at both transcriptional and translational levels. 
  • Colon cancer, version 3.2014. 
  • Combination Therapies with CDK4/6 Inhibitors to Treat KRAS-Mutant Pancreatic Cancer. 
  • Combination of ERK and autophagy inhibition as a treatment approach for pancreatic cancer. 
  • Combined circulating tumor DNA and protein biomarker-based liquid biopsy for the earlier detection of pancreatic cancers. 
  • Comparative Molecular Analysis of Gastrointestinal Adenocarcinomas. 
  • Computed tomography imaging of primary lung cancer in mice using a liposomal-iodinated contrast agent. 
  • Concurrent Inhibition of ERK and Farnesyltransferase Suppresses the Growth of HRAS Mutant Head and Neck Squamous Cell Carcinoma. 
  • Concurrent PEDF deficiency and Kras mutation induce invasive pancreatic cancer and adipose-rich stroma in mice. 
  • Concurrent molecular alterations in tumors with germ line epidermal growth factor receptor T790M mutations. 
  • Data analysis: evaluation of nanoscale contrast agent enhanced CT scan to differentiate between benign and malignant lung cancer in mouse model. 
  • Decreased tumorigenesis in mice with a Kras point mutation at C118. 
  • Development and validation of a scalable next-generation sequencing system for assessing relevant somatic variants in solid tumors. 
  • Development of Aggressive Pancreatic Ductal Adenocarcinomas Depends on Granulocyte Colony Stimulating Factor Secretion in Carcinoma Cells. 
  • Differential Cell Susceptibilities to KrasG12D in the Setting of Obstructive Chronic Pancreatitis. 
  • Differential Expression of KRAS and SIRT1 in Ovarian Cancers with and Without Endometriosis. 
  • Direct evidence that Gi-coupled receptor stimulation of mitogen-activated protein kinase is mediated by G beta gamma activation of p21ras. 
  • Distinct and overlapping sarcoma subtypes initiated from muscle stem and progenitor cells. 
  • Distinct pathways of Gi- and Gq-mediated mitogen-activated protein kinase activation. 
  • EJ-Ras inhibits phospholipase C gamma 1 but not actin polymerization induced by platelet-derived growth factor-BB via phosphatidylinositol 3-kinase. 
  • Effect of cyclical intermittent hypoxia on Ad5CMVCre induced solitary lung cancer progression and spontaneous metastases in the KrasG12D+; p53fl/fl; myristolated p110fl/fl ROSA-gfp mouse. 
  • Efficacy of BET bromodomain inhibition in Kras-mutant non-small cell lung cancer. 
  • Efficient CD4Cre-Mediated Conditional KRas Expression in Alveolar Macrophages and Alveolar Epithelial Cells Causes Fatal Hyperproliferative Pneumonitis. 
  • Endocervical-like (Müllerian) mucinous borderline tumours of the ovary are frequently associated with the KRAS mutation. 
  • Enzymatic modification of proteins with a geranylgeranyl isoprenoid. 
  • Epigenetic basis of oncogenic-Kras-mediated epithelial-cellular proliferation and plasticity. 
  • Epithelial NOTCH Signaling Rewires the Tumor Microenvironment of Colorectal Cancer to Drive Poor-Prognosis Subtypes and Metastasis. 
  • Evaluation of KRAS mutations, angiogenic biomarkers, and DCE-MRI in patients with advanced non-small-cell lung cancer receiving sorafenib. 
  • Evidence for type II cells as cells of origin of K-Ras-induced distal lung adenocarcinoma. 
  • Exome sequencing identifies recurrent somatic RAC1 mutations in melanoma. 
  • Exome-wide Sequencing Shows Low Mutation Rates and Identifies Novel Mutated Genes in Seminomas. 
  • Expression of oncogenic HRAS in human Rh28 and RMS-YM rhabdomyosarcoma cells leads to oncogene-induced senescence. 
  • G protein beta gamma subunits stimulate phosphorylation of Shc adapter protein. 
  • GNAS and KRAS Mutations Define Separate Progression Pathways in Intraductal Papillary Mucinous Neoplasm-Associated Carcinoma. 
  • Gene expression markers of efficacy and resistance to cetuximab treatment in metastatic colorectal cancer: results from CALGB 80203 (Alliance). 
  • Genetic And Morphological Evaluation (GAME) score for patients with colorectal liver metastases. 
  • Genetic Determinants of Outcome in Intrahepatic Cholangiocarcinoma. 
  • Genetically manipulating endogenous Kras levels and oncogenic mutations in vivo influences tissue patterning of murine tumorigenesis. 
  • Genome-wide CRISPR Screen to Identify Genes that Suppress Transformation in the Presence of Endogenous KrasG12D. 
  • Gli Transcription Factors Mediate the Oncogenic Transformation of Prostate Basal Cells Induced by a Kras-Androgen Receptor Axis. 
  • H-Ras peptide and protein substrates bind protein farnesyltransferase as an ionized thiolate. 
  • High affinity for farnesyltransferase and alternative prenylation contribute individually to K-Ras4B resistance to farnesyltransferase inhibitors. 
  • High early death rates, treatment resistance, and short survival of Black adolescents and young adults with AML. 
  • High level expression of mammalian protein farnesyltransferase in a baculovirus system. The purified protein contains zinc. 
  • Histological and molecular evaluation of patient-derived colorectal cancer explants. 
  • Human homologue of Drosophila CNK interacts with Ras effector proteins Raf and Rlf. 
  • ICECREAM: randomised phase II study of cetuximab alone or in combination with irinotecan in patients with metastatic colorectal cancer with either KRAS, NRAS, BRAF and PI3KCA wild type, or G13D mutated tumours. 
  • Increased expression of Drosophila tetraspanin, Tsp68C, suppresses the abnormal proliferation of ytr-deficient and Ras/Raf-activated hemocytes. 
  • Induction of cyclooxygenase-2 synthesis by ligation of the macrophage alpha(2)-macroglobulin signalling receptor. 
  • Inhibiting the palmitoylation/depalmitoylation cycle selectively reduces the growth of hematopoietic cells expressing oncogenic Nras. 
  • Inhibition of purified p21ras farnesyl:protein transferase by Cys-AAX tetrapeptides. 
  • Injury promotes sarcoma development in a genetically and temporally restricted manner. 
  • Interrogating the protein interactomes of RAS isoforms identifies PIP5K1A as a KRAS-specific vulnerability. 
  • Inverse Correlation of STAT3 and MEK Signaling Mediates Resistance to RAS Pathway Inhibition in Pancreatic Cancer. 
  • Isoform-Specific Effects of Wild-Type Ras Genes on Carcinogen-Induced Lung Tumorigenesis in Mice. 
  • Isoprenylcysteine carboxylmethyltransferase is required for the impact of mutant KRAS on TAZ protein level and cancer cell self-renewal. 
  • KRAS Activation and over-expression of SIRT1/BCL6 Contributes to the Pathogenesis of Endometriosis and Progesterone Resistance. 
  • KRAS Allelic Imbalance Enhances Fitness and Modulates MAP Kinase Dependence in Cancer. 
  • KRAS mutation influences recurrence patterns in patients undergoing hepatic resection of colorectal metastases. 
  • KRAS2 mutations in human pancreatic acinar-ductal metaplastic lesions are limited to those with PanIN: implications for the human pancreatic cancer cell of origin. 
  • KRASG12C Inhibition with Sotorasib in Advanced Solid Tumors. 
  • LigAmp for sensitive detection of single-nucleotide differences. 
  • Ligation of the alpha2M signalling receptor elevates the levels of p21Ras-GTP in macrophages. 
  • Ligation of the alpha2M* signaling receptor regulates synthesis of cytosolic phospholipase A2. 
  • Loss of EGFR signaling regulated miR-203 promotes prostate cancer bone metastasis and tyrosine kinase inhibitors resistance. 
  • Loss of microRNA-21 leads to profound stromal remodeling and short survival in K-Ras-driven mouse models of pancreatic cancer. 
  • Low-Dose Vertical Inhibition of the RAF-MEK-ERK Cascade Causes Apoptotic Death of KRAS Mutant Cancers. 
  • Mapping Effector-Phenotype Landscapes in KRAS-Driven Cancers. 
  • Measurement of Reactive Oxygen Species by Fluorescent Probes in Pancreatic Cancer Cells. 
  • Methods to generate genetically engineered mouse models of soft tissue sarcoma. 
  • Modeling RAS phenotype in colorectal cancer uncovers novel molecular traits of RAS dependency and improves prediction of response to targeted agents in patients. 
  • Molecular diagnosis of pancreatic and biliary cancer: ready for broad implementation? 
  • Mutant forms of growth factor-binding protein-2 reverse BCR-ABL-induced transformation. 
  • Mutation location on the RAS oncogene affects pathologic features and survival after resection of colorectal liver metastases. 
  • Mutational landscape in genetically engineered, carcinogen-induced, and radiation-induced mouse sarcoma. 
  • Mutually exclusive recurrent KRAS and MAP2K1 mutations in Rosai-Dorfman disease. 
  • N-cadherin functions as a growth suppressor in a model of K-ras-induced PanIN. 
  • Nicotine does not enhance tumorigenesis in mutant K-ras-driven mouse models of lung cancer. 
  • No clinical utility of KRAS variant rs61764370 for ovarian or breast cancer. 
  • Non-canonical genomic driver mutations of urethane carcinogenesis. 
  • Notch-Induced Myeloid Reprogramming in Spontaneous Pancreatic Ductal Adenocarcinoma by Dual Genetic Targeting. 
  • Obesogenic high-fat diet heightens aerobic glycolysis through hyperactivation of oncogenic KRAS. 
  • Oncogene-dependent control of miRNA biogenesis and metastatic progression in a model of undifferentiated pleomorphic sarcoma. 
  • Oncogenic KRAS Reduces Expression of FGF21 in Acinar Cells to Promote Pancreatic Tumorigenesis in Mice on a High-Fat Diet. 
  • Oncogenic KRAS is dependent upon an EFR3A-PI4KA signaling axis for potent tumorigenic activity. 
  • Oncogenic Kras maintains pancreatic tumors through regulation of anabolic glucose metabolism. 
  • Oncogenic Kras-induced leukemogeneis: hematopoietic stem cells as the initial target and lineage-specific progenitors as the potential targets for final leukemic transformation. 
  • Oncogenic RAS-induced CK1α drives nuclear FOXO proteolysis. 
  • Oncogenic Ras induces inflammatory cytokine production by upregulating the squamous cell carcinoma antigens SerpinB3/B4. 
  • Ovarian cancer progression is controlled by phenotypic changes in dendritic cells. 
  • PI3K regulation of RAC1 is required for KRAS-induced pancreatic tumorigenesis in mice. 
  • PPDPF Promotes the Development of Mutant KRAS-Driven Pancreatic Ductal Adenocarcinoma by Regulating the GEF Activity of SOS1. 
  • Pancreatic ductal adenocarcinoma with autoimmune pancreatitis-like histologic and immunohistochemical features. 
  • Phase III trial of cetuximab, bevacizumab, and 5-fluorouracil/leucovorin vs. FOLFOX-bevacizumab in colorectal cancer. 
  • Preclinical and clinical pharmacodynamic assessment of L-778,123, a dual inhibitor of farnesyl:protein transferase and geranylgeranyl:protein transferase type-I. 
  • Predictive and prognostic analysis of PIK3CA mutation in stage III colon cancer intergroup trial. 
  • Prenylation-dependent association of Ki-Ras with microtubules. Evidence for a role in subcellular trafficking. 
  • Proliferative nodules arising within congenital melanocytic nevi: a histologic, immunohistochemical, and molecular analyses of 43 cases. 
  • Prostate-specific expression of p53(R172L) differentially regulates p21, Bax, and mdm2 to inhibit prostate cancer progression and prolong survival. 
  • Pten-null tumors cohabiting the same lung display differential AKT activation and sensitivity to dietary restriction. 
  • Rare codons capacitate Kras-driven de novo tumorigenesis. 
  • Rare codons regulate KRas oncogenesis. 
  • Ras induces p21Cip1/Waf1 cyclin kinase inhibitor transcriptionally through Sp1-binding sites. 
  • Ras-dependent mitogen-activated protein kinase activation by G protein-coupled receptors. Convergence of Gi- and Gq-mediated pathways on calcium/calmodulin, Pyk2, and Src kinase. 
  • Recurrent GNAS mutations define an unexpected pathway for pancreatic cyst development. 
  • Reduction in the requirement of oncogenic Ras signaling to activation of PI3K/AKT pathway during tumor maintenance. 
  • Regulated spindle orientation buffers tissue growth in the epidermis. 
  • Relationship between statin use and colon cancer recurrence and survival: results from CALGB 89803. 
  • Response to Cetuximab With or Without Irinotecan in Patients With Refractory Metastatic Colorectal Cancer Harboring the KRAS G13D Mutation: Australasian Gastro-Intestinal Trials Group ICECREAM Study. 
  • Roles of genetic variants in the PI3K and RAS/RAF pathways in susceptibility to endometrial cancer and clinical outcomes. 
  • Sensitive and quantitative detection of KRAS2 gene mutations in pancreatic duct juice differentiates patients with pancreatic cancer from chronic pancreatitis, potential for early detection. 
  • Serial EUS-Guided FNA for the Surveillance of Pancreatic Cysts: A Study of Long-Term Performance of Tumor Markers. 
  • Signal Transducer and Activator of Transcription 3, Mediated Remodeling of the Tumor Microenvironment Results in Enhanced Tumor Drug Delivery in a Mouse Model of Pancreatic Cancer. 
  • Sotorasib for previously treated colorectal cancers with KRAS^G12C mutation (CodeBreaK100): a prespecified analysis of a single-arm, phase 2 trial. 
  • Sotorasib in KRAS p.G12C-Mutated Advanced Pancreatic Cancer. 
  • Suppression of Rev3, the catalytic subunit of Pol{zeta}, sensitizes drug-resistant lung tumors to chemotherapy. 
  • Synthesis of isomeric 3-piperidinyl and 3-pyrrolidinyl benzo[5,6]cyclohepta[1,2-b]pyridines: sulfonamido derivatives as inhibitors of Ras prenylation. 
  • Synthetic lethal interaction between oncogenic KRAS dependency and STK33 suppression in human cancer cells. 
  • Synthetic lethal interaction of combined BCL-XL and MEK inhibition promotes tumor regressions in KRAS mutant cancer models. 
  • Targeted inactivation of the isoprenylcysteine carboxyl methyltransferase gene causes mislocalization of K-Ras in mammalian cells. 
  • Targeted therapy for non-small cell lung cancer. 
  • The COOH-terminal domain of the Rap1A (Krev-1) protein is isoprenylated and supports transformation by an H-Ras:Rap1A chimeric protein. 
  • The Current Molecular Treatment Landscape of Advanced Colorectal Cancer and Need for the COLOMATE Platform. 
  • The Genetic Basis of Hepatosplenic T-cell Lymphoma. 
  • The oncocytic subtype is genetically distinct from other pancreatic intraductal papillary mucinous neoplasm subtypes. 
  • The role of KRAS rs61764370 in invasive epithelial ovarian cancer: implications for clinical testing. 
  • To oxidize or not to oxidize? 
  • Trametinib Drives T-cell-Dependent Control of KRAS-Mutated Tumors by Inhibiting Pathological Myelopoiesis. 
  • Ubiquitination of K-Ras enhances activation and facilitates binding to select downstream effectors. 
  • Ultrasensitive detection of KRAS2 mutations in bile and serum from patients with biliary tract carcinoma using LigAmp technology. 
  • Uptake of KRAS Testing and Anti-EGFR Antibody Use for Colorectal Cancer in the VA. 
  • Utility of DNA Profiling From Main Pancreatic Duct Fluid by Endoscopic Ultrasound and Endoscopic Retrograde Cholangiopancreatography to Screen for Malignant Potential. 
  • Ventricular expression of a MLC-2v-ras fusion gene induces cardiac hypertrophy and selective diastolic dysfunction in transgenic mice. 
  • Vitamin C selectively kills KRAS and BRAF mutant colorectal cancer cells by targeting GAPDH. 
  • Wild-Type Hras Suppresses the Earliest Stages of Tumorigenesis in a Genetically Engineered Mouse Model of Pancreatic Cancer. 
  • Wild-type Kras expands and exhausts hematopoietic stem cells. 
  • Yield of Malignant Pleural Effusion for Detection of Oncogenic Driver Mutations in Lung Adenocarcinoma. 
  • mTOR inhibition specifically sensitizes colorectal cancers with KRAS or BRAF mutations to BCL-2/BCL-XL inhibition by suppressing MCL-1. 
  • rac, a novel ras-related family of proteins that are botulinum toxin substrates. 
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  Keywords of People

  • Badea, Cristian Tudorel, Professor in Radiology, Biomedical Engineering
  • Hogan, Brigid L. M., Research Professor of Cell Biology, Cell Biology