Glucose deprivation contributes to the development of KRAS pathway mutations in tumor cells

Science

Volumn 325, Issue 5947, 2009, Pages 1555-1559

  Yun, Jihye ^a   Rago, Carlo ^a   Cheong, Ian ^a   Pagliarini, Ray ^a,d   Angenendt, Philipp ^a   Rajagopalan, Harith ^a,e   Schmidt, Kerstin ^a   Willson, James K V ^b   Markowitz, Sandy ^c   Zhou, Shibin ^a   Diaz Jr , Luis A ^a   Velculescu, Victor E ^a   Lengauer, Christoph ^a,f   Kinzler, Kenneth W ^a   Vogelstein, Bert ^a   Papadopoulos, Nickolas ^a  

^a JOHNS HOPKINS UNIVERSITY   (United States)

^b UNIVERSITY OF TEXAS SOUTHWESTERN MEDICAL CENTER   (United States)

^c CASE WESTERN RESERVE UNIVERSITY SCHOOL OF MEDICINE   (United States)

^d NOVARTIS INSTITUTES FOR BIOMEDICAL RESEARCH   (United States)

^e BRIGHAM AND WOMEN S HOSPITAL   (United States)

^f SANOFI   (France)

Author keywords

[No Author keywords available]

Indexed keywords

ADENOSINE DIPHOSPHATE; ADENOSINE TRIPHOSPHATE; B RAF KINASE; FLUORODEOXYGLUCOSE F 18; GLUCOSE; GLUCOSE TRANSPORTER 1; K RAS PROTEIN; LACTIC ACID; OXYGEN; SMALL INTERFERING RNA; TRANSCRIPTOME;

ALLELE; CYTOGENETICS; GENE EXPRESSION; GLUCOSE; GROWTH RATE; MUTATION; NUTRIENT UPTAKE; PHENOTYPE; TUMOR;

ALLELE; ARTICLE; CANCER CELL; CARCINOGENESIS; CELL GROWTH; CELL SURVIVAL; COLORECTAL CANCER; GENE EXPRESSION; GENE MUTATION; GENE OVEREXPRESSION; GENETIC ANALYSIS; GLUCOSE METABOLISM; GLUCOSE TRANSPORT; GLYCOLYSIS; GROWTH INHIBITION; HOMOLOGOUS RECOMBINATION; HUMAN; HUMAN CELL; HYPOGLYCEMIA; MISMATCH REPAIR; MITOCHONDRIAL RESPIRATION; MOLECULAR MIMICRY; NONHUMAN; ONCOGENE K RAS; OXYGEN CONSUMPTION; PHENOTYPE; POSITRON EMISSION TOMOGRAPHY; PRECANCER; PRIORITY JOURNAL; PROTEIN EXPRESSION; SERIAL ANALYSIS OF GENE EXPRESSION; UPREGULATION; WILD TYPE;

ANIMALS; CELL LINE, TUMOR; CELL PROLIFERATION; COLORECTAL NEOPLASMS; GENE EXPRESSION REGULATION, NEOPLASTIC; GENE TARGETING; GENES, RAS; GLUCOSE; GLUCOSE TRANSPORTER TYPE 1; GLYCOLYSIS; HUMANS; LACTIC ACID; MICE; MICE, NUDE; MUTATION; NEOPLASM TRANSPLANTATION; OLIGONUCLEOTIDE ARRAY SEQUENCE ANALYSIS; PROTO-ONCOGENE PROTEINS B-RAF; PYRUVATES; TRANSPLANTATION, HETEROLOGOUS;

EID: 70349331678     PISSN: 00368075     EISSN: 10959203     Source Type: Journal    
DOI: 10.1126/science.1174229     Document Type: Article

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42. We thank Y. He for helpful discussions, W. Yu for help with the microarray experiments, and E. Watson for expert technical assistance. This work was supported by the Virginia and D. K. Ludwig Fund for Cancer Research and NIH grants CA43460 and CA62924. Under agreements between the Johns Hopkins University, Genzyme Molecular Oncology, Novartis, Wyeth, Amgen, Glaxo-Smith-Kline, and Horizon, J.Y., V.E.V., H.R., R.P., C.L., K.W.K., B.V., and N.P. are entitled to a share of the royalties and licensing fees received by the university on cell lines described in this paper, some of which are the subject of patent applications. The Johns Hopkins University and V.E.V., K.W.K., and B.V. also own stock in Genzyme, which is subject to certain restrictions under university policy. The terms of these arrangements are being managed by the university in accordance with its conflict of interest policies.