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Peer Reviewed Papers, Books, Chapters

Year Title Citation Authors Review type Summary Keywords File filename File mime type
1. 2010 Hypoxia-induced autophagy: cell death or cell survival? Curr. Op. Cell Biol.,
2. 2009 Hypoxia-inducible carbonic anhydrase IX and XII promote tumor cell growth by counteracting acidosis through the regulation of the intracellular pH. J. Cancer Res. (2009) 69, 358-368
3. 2008 Tumor cell metabolism; cancer’s Achilles heel. Cancer Cell 13, 472-82
4. 2008 PHDs overactivation during chronic hypoxia "desensitizes" HIFalpha and protects cells from necrosis. Proc Natl Acad Sci USA. (2008) 105, 4745-50.
5. 2007 Hypoxia Signalling Controls Metabolic Demand. J. Curr. Op. Cell Biol. (2007) 19, 223-9.
6. 2006 Hypoxia signaling in Cancer and approaches to enforce Tumour Regression. Nature 441, 437-443
7. 2006 The Hypoxia-Inducible-Factor hydroxylases bring fresh air into Hypoxia Signaling. EMBO Rep 7: 41-5
8. 2004 A short synthetic peptide inhibits signal transduction migration and angiogenesus mediated by Tie2 receptor EMBO Rep. 5: 26. 2-7
9. 2003 HIF prolyl-hydroxylase 2 is the key oxygen sensor setting low steady-state levels of HIF-1a in normoxia EMBO J. 22, 4082-4090
10. 2001 Hypoxia-inducible factor-1a (HIF-1a) escapes O2-driven proteasomal degradation irrespective of its subcellular localization: nucleus or cytoplasm EMBO Rep. 2, 615-20
11. 2000 An Arresting Start for MAPK. Science 290, 1515-1518
12. 1999 Defective thymocyte maturation in p44 MAP kinase (Erk1) knock out mice. Science 286, 1374-1377
13. 1999 Regulation of MKP-1 degradation by p42/p44MAPK-dependent phosphorylation Science 286, 2514-2517
14. 1999 Nuclear translocation of p42/p44 mitogen-activated protein kinase is required for growth factor-induced gene expression and cell cycle entry EMBO J. 18, 664-674.
15. 1996 Identification of MAP kinase domains by re-directing stress signals into growth factor responses Science 272, 1652-1655
16. 1994 Constitutive mutant and putative regulatory serine phosphorylation site of mammalian MAP kinase kinase (MEK1) EMBO J. 13, 3003-3010.
17. 1993 A Point Mutation of the Na+/H+ Exchanger Gene (NHE1) and Amplification of the Mutated Allele Confer Amiloride-Resistance upon Chronic Acidosis. Proc. Natl. Acad. Sci. USA 90, 4508-4512.
18. 1993 The Mitogen-Activated Protein kinases p42 and p44 MAPK are required for fibroblast Cell Proliferation. Proc. Natl. Acad. Sci. USA 90, 8319-8323
19. 1992 The Na+/H+ antiporter cytoplasmic domain mediates growth factor signals and controls 'H+ -sensing'. Proc. Natl. Acad. Sci. USA 89, 2424-2428
20. 1990 Growth factors induce phosphorylation of the Na+/H+ antiporter, a glycoprotein of 110 kDa Science 247, 723-726.
21. 1989 Molecular cloning, primary structure and expression of the human growth factor-activatable Na+/H+ antiporter Cell 56, 271-280
22. 1988 Serotonin stimulates DNA synthesis in fibroblasts via 5-HT-1B receptors coupled to Gi-protein Nature 335, 254-257.
23. 1988 Deregulation of hamster fibroblast proliferation by mutated ras oncogenes is not mediated by constitutive activation of Phospholipase C EMBO J. 7, 161-168.
24. 1987 Two growth factor signalling pathways in fibroblasts distinguished by pertussis toxin Nature, 326, 800-803.
25. 1986 Pertussis toxin inhibits thrombin-induced activation of phosphoinositide hydrolysis and Na+/H+ exchange in hamster fibroblasts. EMBO J. 5, 55-60
26. 1986 Functional expression of a transfected Na+/H+ antiporter human gene into antiporter-deficient mouse L cells. Proc.Natl.Acad.Sci USA. 83, 9388-9392
27. 1985 a-thrombin-induced early mitogenic signalling events and G0 to S-phase transition of fibroblasts require continual external stimulation EMBO J. 4, 2927-2932
28. 1985 The growth factor activatable Na+/H+ exchange system. A genetic approach Trends in Biochem.Sci. 10, 453-455
29. 1984 A specific mutation abolishing Na+/H+ antiport activity in hamster fibroblasts precludes growth at neutral and acidic pH. Proc.Natl.Acad.Sci. USA 81, 4833-37
30. 1982 Growth factor activation of an amiloride sensitive Na+/H+ exchange system in quiescent fibroblasts: coupling to ribosomal protein S6 phosphorylation Proc.Natl.Acad.Sci. USA 79, 3935-3939
31. 1980 Isolation of a Chinese hamster fibroblasts mutant defective in hexose transport and aerobic glycolysis: its use to dissect the malignant phenotype Proc.Natl.Acad.Sci. USA 77, 2698-2701
32. 1980 Relationship between increased aerobic glycolysis and DNA synthesis initiation studied using glycolytic mutant fibroblasts Nature 287, 445-447
33. 1980 Identification of tetrodotoxin-sensitive Na+ channel in a variety of fibroblasts lines Nature 28, 162-164
34. 1978 Adenylate cyclase in fibroblast mutant defective in glycolipid and glycoprotein synthesis Nature 275, 223-224
35. 1978 Isolation and immunological characterization of a glucose-regulated fibroblasts cell surface glycosylation precursor Cell 13, 139-150
36. 1977 Induction of two transformation-sensitive membrane polypeptides in normal fibroblasts by a block in glycoprotein systhesis or glucose deprivation. Cell 11, 941-947
37. 1977 Role of cell surface carbohydrate and proteins in cell behavior: studies on the biochemical reversion of an N-acetyl-glucosamine deficient fibroblasts mutant Proc.Natl.Acad.Sci. USA 74, 243-247
38. 1976 Mutants of Balb/c 3T3 fibroblasts defective in adhesiveness to substratum: evidence for alteration in cell surface proteins Proc.Natl.Acad.Sci. USA 73, 544-548
39. As Otto Warburg first observed, cancer cells largely favor fermentative glycolysis for growth even under aerobic conditions. Pubmed As Otto Warburg first observed, cancer cells largely favor fermentative glycolysis for growth even under aerobic conditions. This energy paradox also extends to rapidly growing normal cells indicating that glycolysis is optimal for fast growth and biomass production. Here we further explored this concept by genetic ablation of fermentative glycolysis in two fast growing cancer cell lines: human colon adenocarcinoma LS174T and B16 mouse melanoma. We disrupted the upstream glycolytic enzyme, glucose-6-phosphate isomerase (GPI), to allow cells to re-route glucose-6-phosphate flux into the pentose-phosphate branch. Indeed, GPI-KO severely reduced glucose consumption and suppressed lactic acid secretion, which reprogrammed these cells to rely on oxidative phosphorylation and mitochondrial ATP production to maintain viability. In contrast to previous pharmacological inhibition of glycolysis that suppressed tumor growth, GPI-KO surprisingly demonstrated only a moderate impact on normoxic cell growth. However, hypoxic (1% O2) cell growth was severely restricted. Despite in vitro growth restriction under hypoxia, tumor growth rates in vivo were reduced less than 2-fold for both GPI-KO cancer cell lines. Combined our results indicate that exclusive use of oxidative metabolism has the capacity to provide metabolic precursors for biomass synthesis and fast growth. This work and others clearly indicate that metabolic cancer cell plasticity poses a strong limitation to anticancer strategies. OXPHOS; glucose-6-phosphate isomerase; glycolysis; pentose phosphate pathway; tumor growth


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