Oncogenic Kras Maintains Pancreatic Tumors through Regulation of Anabolic Glucose Metabolism

[1]  J. Asara,et al.  A positive/negative ion–switching, targeted mass spectrometry–based metabolomics platform for bodily fluids, cells, and fresh and fixed tissue , 2012, Nature Protocols.

[2]  Gregory Stephanopoulos,et al.  Amplification of phosphoglycerate dehydrogenase diverts glycolytic flux and contributes to oncogenesis , 2012, BMC Proceedings.

[3]  Scott E. Kern,et al.  Oncogene-induced Nrf2 transcription promotes ROS detoxification and tumorigenesis , 2011, Nature.

[4]  A. Caudy,et al.  Riboneogenesis in Yeast , 2011, Cell.

[5]  D. Hanahan,et al.  Hallmarks of Cancer: The Next Generation , 2011, Cell.

[6]  F. McCormick,et al.  Therapeutic strategies for targeting ras proteins. , 2011, Genes & cancer.

[7]  A. Mancuso,et al.  p53 regulates biosynthesis through direct inactivation of glucose-6-phosphate dehydrogenase , 2011, Nature Cell Biology.

[8]  E. Petricoin,et al.  Proteomic analysis of pancreatic ductal adenocarcinoma cells reveals metabolic alterations. , 2011, Journal of proteome research.

[9]  이연수.  Functional genomics reveal that the serine synthesis pathway is essential in breast cancer , 2011 .

[10]  H. Coller,et al.  The hexosamine biosynthetic pathway couples growth factor-induced glutamine uptake to glucose metabolism. , 2010, Genes & development.

[11]  A. Levine,et al.  The Control of the Metabolic Switch in Cancers by Oncogenes and Tumor Suppressor Genes , 2010, Science.

[12]  Gerald W. Hart,et al.  Glycomics Hits the Big Time , 2010, Cell.

[13]  Lin Cui,et al.  &agr;-Smooth Muscle Actin Expressing Stroma Promotes an Aggressive Tumor Biology in Pancreatic Ductal Adenocarcinoma , 2010, Pancreas.

[14]  Malte Buchholz,et al.  Stromal biology and therapy in pancreatic cancer , 2010, Gut.

[15]  W. Wheaton,et al.  Mitochondrial metabolism and ROS generation are essential for Kras-mediated tumorigenicity , 2010, Proceedings of the National Academy of Sciences.

[16]  K. Kinzler,et al.  Glucose Deprivation Contributes to the Development of KRAS Pathway Mutations in Tumor Cells , 2009, Science.

[17]  J. Settleman,et al.  Oncogenic K-ras “addiction” and synthetic lethality , 2009, Cell cycle.

[18]  Patricia Greninger,et al.  A gene expression signature associated with "K-Ras addiction" reveals regulators of EMT and tumor cell survival. , 2009, Cancer cell.

[19]  L. Cantley,et al.  Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation , 2009, Science.

[20]  C. Thompson,et al.  The molecular determinants of de novo nucleotide biosynthesis in cancer cells. , 2009, Current opinion in genetics & development.

[21]  Tsung-Cheng Chang,et al.  c-Myc suppression of miR-23 enhances mitochondrial glutaminase and glutamine metabolism , 2009, Nature.

[22]  B. Seliger,et al.  Altered detoxification status and increased resistance to oxidative stress by K-ras transformation. , 2008, Cancer research.

[23]  Anthony Mancuso,et al.  Myc regulates a transcriptional program that stimulates mitochondrial glutaminolysis and leads to glutamine addiction , 2008, Proceedings of the National Academy of Sciences.

[24]  Gerald C. Chu,et al.  P53 and Pten control neural and glioma stem/progenitor cell renewal and differentiation , 2008, Nature.

[25]  G. Evan,et al.  Modelling Myc inhibition as a cancer therapy , 2008, Nature.

[26]  Ralph J Deberardinis,et al.  Brick by brick: metabolism and tumor cell growth. , 2008, Current opinion in genetics & development.

[27]  R. Deberardinis,et al.  The biology of cancer: metabolic reprogramming fuels cell growth and proliferation. , 2008, Cell metabolism.

[28]  S. Henderson,et al.  Transformation of human mesenchymal stem cells increases their dependency on oxidative phosphorylation for energy production , 2007, Proceedings of the National Academy of Sciences.

[29]  R. DePinho,et al.  Genetics and biology of pancreatic ductal adenocarcinoma. , 2006, Genes & development.

[30]  M. Lerner,et al.  [1,2-13C2]-D-Glucose Profiles of the Serum, Liver, Pancreas, and DMBA-Induced Pancreatic Tumors of Rats , 2005, Pancreas.

[31]  Pablo Tamayo,et al.  Gene set enrichment analysis: A knowledge-based approach for interpreting genome-wide expression profiles , 2005, Proceedings of the National Academy of Sciences of the United States of America.

[32]  Marta Cascante,et al.  K-ras Codon-Specific Mutations Produce Distinctive Metabolic Phenotypes in Human Fibroblasts , 2005 .

[33]  J. Esko,et al.  The sweet and sour of cancer: glycans as novel therapeutic targets , 2005, Nature Reviews Cancer.

[34]  J. Whitsett,et al.  Conditional and inducible transgene expression in mice through the combinatorial use of Cre-mediated recombination and tetracycline induction , 2005, Nucleic acids research.

[35]  Marta Cascante,et al.  K-ras codon-specific mutations produce distinctive metabolic phenotypes in NIH3T3 mice [corrected] fibroblasts. , 2005, Cancer research.

[36]  J. Hecht,et al.  Multicenter phase II study of the oral MEK inhibitor, CI-1040, in patients with advanced non-small-cell lung, breast, colon, and pancreatic cancer. , 2004, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[37]  Gordon K Smyth,et al.  Statistical Applications in Genetics and Molecular Biology Linear Models and Empirical Bayes Methods for Assessing Differential Expression in Microarray Experiments , 2011 .

[38]  R. DePinho,et al.  Activated Kras and Ink4a/Arf deficiency cooperate to produce metastatic pancreatic ductal adenocarcinoma. , 2003, Genes & development.

[39]  E. Petricoin,et al.  Preinvasive and invasive ductal pancreatic cancer and its early detection in the mouse. , 2003, Cancer cell.

[40]  Manuel Serrano,et al.  Tumor induction by an endogenous K-ras oncogene is highly dependent on cellular context. , 2003, Cancer cell.

[41]  Mitchell D Schnall,et al.  Conditional activation of Neu in the mammary epithelium of transgenic mice results in reversible pulmonary metastasis. , 2002, Cancer cell.

[42]  C. Wright,et al.  The role of the transcriptional regulator Ptf1a in converting intestinal to pancreatic progenitors , 2002, Nature Genetics.

[43]  H. Varmus,et al.  Induction and apoptotic regression of lung adenocarcinomas by regulation of a K-Ras transgene in the presence and absence of tumor suppressor genes. , 2001, Genes & development.

[44]  T. Jacks,et al.  Somatic activation of the K-ras oncogene causes early onset lung cancer in mice , 2001, Nature.

[45]  A. Berns,et al.  Induction of medulloblastomas in p53-null mutant mice by somatic inactivation of Rb in the external granular layer cells of the cerebellum. , 2000, Genes & development.

[46]  D. Felsher,et al.  Reversible tumorigenesis by MYC in hematopoietic lineages. , 1999, Molecular cell.

[47]  L. Chin,et al.  Essential role for oncogenic Ras in tumour maintenance , 1999, Nature.

[48]  M. Cascante,et al.  Nonoxidative pentose phosphate pathways and their direct role in ribose synthesis in tumors: is cancer a disease of cellular glucose metabolism? , 1998, Medical hypotheses.

[49]  P. Paty,et al.  Beta 1-6 branching of N-linked carbohydrate is associated with K-ras mutation in human colon carcinoma cell lines. , 1995, Biochemical and biophysical research communications.

[50]  J. Russo,et al.  Cell surface glycosylation changes accompanying immortalization and transformation of normal human mammary epithelial cells. , 1991, Cancer letters.

[51]  J. Dennis,et al.  Oncogenes conferring metastatic potential induce increased branching of Asn-linked oligosaccharides in rat2 fibroblasts. , 1989, Oncogene.

[52]  J. Neefjes,et al.  Ras (proto)oncogene induces N‐linked carbohydrate modification: temporal relationship with induction of invasive potential. , 1988, The EMBO journal.

[53]  J. Williams,et al.  The pentose pathway: a random harvest. Impediments which oppose acceptance of the classical (F-type) pentose cycle for liver, some neoplasms and photosynthetic tissue. The case for the L-type pentose pathway. , 1987, The International journal of biochemistry.

[54]  E. Racker,et al.  Glycolysis and methylaminoisobutyrate uptake in rat-1 cells transfected with ras or myc oncogenes. , 1985, Proceedings of the National Academy of Sciences of the United States of America.