Genes, ras

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  Subject Areas on Research

  • A Genetic Porcine Model of Cancer. 
  • A KRAS-variant in ovarian cancer acts as a genetic marker of cancer risk. 
  • A comparison of interfollicular and hair follicle derived cells as targets for the v-rasHa oncogene in mouse skin carcinogenesis. 
  • A genetically tractable model of human glioma formation. 
  • A model for RAS mutation patterns in cancers: finding the sweet spot. 
  • A novel receptor function for the heat shock protein Grp78: silencing of Grp78 gene expression attenuates alpha2M*-induced signalling. 
  • A synthetic matrix with independently tunable biochemistry and mechanical properties to study epithelial morphogenesis and EMT in a lung adenocarcinoma model. 
  • Absence of the CAAX endoprotease Rce1: effects on cell growth and transformation. 
  • Absent ras gene mutations in human adrenal cortical neoplasms and pheochromocytomas. 
  • An allele of HRAS1 3'variable number of tandem repeats is a frailty allele: implication for an evolutionarily-conserved pathway involved in longevity. 
  • Androgen-induced differentiation and tumorigenicity of human prostate epithelial cells. 
  • Calcitonin driven v-Ha-ras induces multilineage pulmonary epithelial hyperplasias and neoplasms. 
  • Cell type-specific angiotensin II-evoked signal transduction pathways: critical roles of Gbetagamma subunit, Src family, and Ras in cardiac fibroblasts. 
  • Clinical correlates of NRAS and BRAF mutations in primary human melanoma. 
  • Combination PI3K/MEK inhibition promotes tumor apoptosis and regression in PIK3CA wild-type, KRAS mutant colorectal cancer. 
  • Conditional expression of the mutant Ki-rasG12C allele results in formation of benign lung adenomas: development of a novel mouse lung tumor model. 
  • Cooperation of p53 loss of function and v-Ha-ras in transformation of mouse keratinocyte cell lines. 
  • Creation of human tumour cells with defined genetic elements. 
  • Critical aspects of initiation, promotion, and progression in multistage epidermal carcinogenesis. 
  • Cross-species analysis of genetically engineered mouse models of MAPK-driven colorectal cancer identifies hallmarks of the human disease. 
  • Cytogenetic and molecular correlates between rodent and human renal cell carcinoma. 
  • DNA adducts, genetic polymorphisms, and K-ras mutation in human pancreatic cancer. 
  • Deciphering the mechanisms of tumorigenesis in human pancreatic ductal epithelial cells. 
  • Detecting colorectal cancer in stool with the use of multiple genetic targets. 
  • Detection of RAS mutations in archival testicular germ cell tumors by polymerase chain reaction and oligonucleotide hybridization. 
  • Detection of mutated c-Ki-ras in the bile of patients with pancreatic cancer. 
  • Development of an in vitro model to study carcinogen-induced neoplastic progression of initiated mouse epidermal cells. 
  • Differences in K-ras and p53 gene mutations among pancreatic adenocarcinomas associated with regional environmental pollution. 
  • Differential effects of inhibiting chitin and 1,3-{beta}-D-glucan synthesis in ras and calcineurin mutants of Aspergillus fumigatus. 
  • Differing molecular pathology of pancreatic adenocarcinoma in Egyptian and United States patients. 
  • Distinct epidermal growth factor receptor and KRAS mutation patterns in non-small cell lung cancer patients with different tobacco exposure and clinicopathologic features. 
  • E2F4 and E2F5 play an essential role in pocket protein-mediated G1 control. 
  • ELR+ CXC chemokines and oncogenic Ras-mediated tumorigenesis. 
  • Effect of First-Line Chemotherapy Combined With Cetuximab or Bevacizumab on Overall Survival in Patients With KRAS Wild-Type Advanced or Metastatic Colorectal Cancer: A Randomized Clinical Trial. 
  • Effect of a dominant negative ras on myocardial hypertrophy by using adenoviral-mediated gene transfer. 
  • Etiology of the mutational spectrum of ras genes in human carcinomas. 
  • Evaluation of KRAS mutations, angiogenic biomarkers, and DCE-MRI in patients with advanced non-small-cell lung cancer receiving sorafenib. 
  • Expression of v-Ha-ras driven by the calcitonin/calcitonin gene-related peptide promoter: a novel transgenic murine model for medullary thyroid carcinoma. 
  • G-protein-coupled receptor genes as protooncogenes: constitutively activating mutation of the alpha 1B-adrenergic receptor enhances mitogenesis and tumorigenicity. 
  • GM1 expression in H-ras-transformed NIH3T3 results in the suppression of cell proliferation inducing the partial transfer of activated H-ras from non-raft to raft fraction. 
  • Gene expression phenotypic models that predict the activity of oncogenic pathways. 
  • Genetic analysis of second primary lung cancers in patients surviving small cell lung cancer. 
  • Genetic changes in contralateral bronchioloalveolar carcinomas of the lung. 
  • Genetic modeling of human rhabdomyosarcoma. 
  • Ha-ras polymorphisms in epithelial ovarian cancer. 
  • Hdm2 is regulated by K-Ras and mediates p53-independent functions in pancreatic cancer cells. 
  • Heterogeneity in MYC-induced mammary tumors contributes to escape from oncogene dependence. 
  • High-LET Radiation Increases Tumor Progression in a K-Ras-Driven Model of Lung Adenocarcinoma. 
  • Human ovarian cancer of the surface epithelium. 
  • Imaging primary lung cancers in mice to study radiation biology. 
  • Immunization with mutant p53- and K-ras-derived peptides in cancer patients: immune response and clinical outcome. 
  • Immunohistochemical and genetic analysis of non-small cell and small cell gallbladder carcinoma and their precursor lesions. 
  • Inactivation of Icmt inhibits transformation by oncogenic K-Ras and B-Raf. 
  • Infrequent RAS oncogene mutations in human prostate cancer. 
  • K-ras mutation and p16 and preproenkephalin promoter hypermethylation in plasma DNA of pancreatic cancer patients: in relation to cigarette smoking. 
  • K-ras mutations in Müllerian inclusion cysts associated with serous borderline tumors of the ovary. 
  • KRAS mutation in stage III colon cancer and clinical outcome following intergroup trial CALGB 89803. 
  • Keap1 loss promotes Kras-driven lung cancer and results in dependence on glutaminolysis. 
  • Loss of heterozygosity for genes on 11p and the clinical course of patients with lung carcinoma. 
  • Mast cells in tumor microenvironment promotes the in vivo growth of pancreatic ductal adenocarcinoma. 
  • Mitogenic signaling mediated by oxidants in Ras-transformed fibroblasts. 
  • Modulation of oncogene and tumor suppressor gene expression in a hamster model of chronic lung injury with varying degrees of pulmonary neuroendocrine cell hyperplasia. 
  • Modulation of the transformed and neoplastic phenotype of rat fibroblasts by MHC-I gene expression. 
  • Molecular approaches for colorectal cancer screening. 
  • Molecular characterization of adenocarcinoma of the cervix. 
  • Molecular diagnosis of pancreatic and biliary cancer: ready for broad implementation? 
  • Molecular pathologic substaging in 244 stage I non-small-cell lung cancer patients: clinical implications. 
  • Mouse models of human non-small-cell lung cancer: raising the bar. 
  • Mucinous differentiation correlates with absence of EGFR mutation and presence of KRAS mutation in lung adenocarcinomas with bronchioloalveolar features. 
  • Multiple genetic lesions in acquired immunodeficiency syndrome-related non-Hodgkin's lymphoma. 
  • Mutation of the Ki-ras protooncogene in human endometrial hyperplasia and carcinoma. 
  • Mutation-specific RAS oncogenicity explains NRAS codon 61 selection in melanoma. 
  • Mutational analysis defines a minimum level of telomerase activity required for tumourigenic growth of human cells. 
  • Mutations in a member of the Ras superfamily of small GTP-binding proteins causes Bardet-Biedl syndrome. 
  • Mutations of the Ki-ras oncogene in endometrial carcinoma. 
  • NF-kappaB blockade and oncogenic Ras trigger invasive human epidermal neoplasia. 
  • Oncogenic Ras-induced secretion of IL6 is required for tumorigenesis. 
  • Oncogenic capacity of the E2F1 gene. 
  • Ovarian adenocarcinomas in the laying hen and women share similar alterations in p53, ras, and HER-2/neu. 
  • Overview of genetic and molecular events in the pathogenesis of lung cancer. 
  • PTEN expression is consistent in colorectal cancer primaries and metastases and associates with patient survival. 
  • Pancreatic adenocarcinoma cell line, MDAPanc-28, with features of both acinar and ductal cells. 
  • Personalized treatment of lung cancer. 
  • Phase II study of the oral MEK inhibitor selumetinib in advanced acute myelogenous leukemia: a University of Chicago phase II consortium trial. 
  • Preclinical efficacy of MEK inhibition in Nras-mutant AML. 
  • Prognostic importance of mutations in the ras proto-oncogenes in de novo acute myeloid leukemia. 
  • Proliferative nodules arising within congenital melanocytic nevi: a histologic, immunohistochemical, and molecular analyses of 43 cases. 
  • RAS mutations in thyroid FNA specimens are highly predictive of predominantly low-risk follicular-pattern cancers. 
  • Ral activation promotes melanomagenesis. 
  • Rare codons regulate KRas oncogenesis. 
  • Reduction in the requirement of oncogenic Ras signaling to activation of PI3K/AKT pathway during tumor maintenance. 
  • Regression of drug-resistant lung cancer by the combination of rosiglitazone and carboplatin. 
  • Resistance to dual blockade of the kinases PI3K and mTOR in KRAS-mutant colorectal cancer models results in combined sensitivity to inhibition of the receptor tyrosine kinase EGFR. 
  • Serum withdrawal induces apoptotic cell death in Ki-ras transformed but not in normal differentiated thyroid cells. 
  • Statistical analysis of skin tumor data from Tg.AC mouse bioassays. 
  • Systematic RNA interference reveals that oncogenic KRAS-driven cancers require TBK1. 
  • TP53 and RAS mutations in metachronous tumors from patients with cancer of the upper aerodigestive tract. 
  • The Prognostic Value of BRAF, C-KIT, and NRAS Mutations in Melanoma Patients With Brain Metastases. 
  • The cell of origin and subtype of K-Ras-induced lung tumors are modified by Notch and Sox2. 
  • The clinical benefit of bevacizumab in metastatic colorectal cancer is independent of K-ras mutation status: analysis of a phase III study of bevacizumab with chemotherapy in previously untreated metastatic colorectal cancer. 
  • The loss of PIN1 deregulates cyclin E and sensitizes mouse embryo fibroblasts to genomic instability. 
  • The nuclear factor-kappa B RelA transcription factor is constitutively activated in human pancreatic adenocarcinoma cells. 
  • Topical and oral administration of the natural water-soluble antioxidant from spinach reduces the multiplicity of papillomas in the Tg.AC mouse model. 
  • Topotecan, a topoisomerase I inhibitor, is active in the treatment of myelodysplastic syndrome and chronic myelomonocytic leukemia. 
  • Treatment with the nitric oxide synthase inhibitor L-NAME provides a survival advantage in a mouse model of Kras mutation-positive, non-small cell lung cancer. 
  • Tumor multiplicity, DNA adducts and K-ras mutation pattern of 5-methylchrysene in strain A/J mouse lung. 
  • Use of genetically modified mouse models for evaluation of carcinogenic risk: considerations for the laboratory animal scientist. 
  • Use of retrovirus expression of interfering RNA to determine the contribution of activated K-Ras and ras effector expression to human tumor cell growth. 
  • Ventricular expression of a MLC-2v-ras fusion gene induces cardiac hypertrophy and selective diastolic dysfunction in transgenic mice. 
  • p21ras is modified by a farnesyl isoprenoid. 
  • p27 and cyclin D1 abnormalities in uterine papillary serous carcinoma. 
  • rac, a novel ras-related family of proteins that are botulinum toxin substrates. 
  • ras mutations and expression in head and neck squamous cell carcinomas. 
  • ras oncogene mutations in diethylnitrosamine-induced hepatic tumors in medaka (Oryzias latipes), a teleost fish. 
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  Keywords of People

  • Berchuck, Andrew, James M. Ingram Professor of Gynecologic Oncology, Obstetrics and Gynecology, Gynecologic Oncology