Christian Frezza MRC Cancer Unit
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1 Christian Frezza MRC Cancer Unit
2 What is cancer?
3 What is cancer? Douglas Hanahan, Robert A. Weinberg; The Hallmarks of Cancer Cell, Volume 100, Issue 1, 7 January 2000, Pages 57 70
4 Cancer cells need energy to proliferate EAT, SURVIVE, REPRODU CE cell
5 Metabolism is an emerging hallmark of cancer Douglas Hanahan, Robert A. Weinberg; Hallmarks of Cancer: next generation Cell, Volume 144, Issue 5, p , 4 March 2011
6 The timeline of cancer research Muller observed aberrant metabolism in urine of cancer patients Warburg observed the increased glycolysis in cancer cell Wassermann hypothesised a role of deregulated respiration in cancer cell Otto Warburg
7 The timeline of cancer research Warburg observed the increased glycolysis in cancer cell Kovacevic observed increased glutaminolysis in cancer cell Warburg published On the origin of cancer cell p53 was identified cmyc was discovered Biochemistry era Genomic era I was born debate between Weinhouse and Warburg on mitochondria and cancer
8 Cancer: a genetic disease activated oncogene/ tumour suppressor Cell transformation
9 The timeline of cancer research Warburg observed the increased glycolysis in cancer cell Kovacevic observed increased glutaminolysis in cancer cell Warburg published On the origin of cancer cell p53 was identified Src/Ras regulate glycolysis c-myc regulates glycolysis c-myc was discovered Biochemistry era Genomic era I was born debate between Weinhouse and Warburg on mitochondria and cancer
10 Cancer and Metabolism activated oncogene/ tumour suppressor metabolic transformation Cell transformation
11 The timeline of cancer research Warburg observed the increased glycolysis in cancer cell Kovacevic observed increased glutaminolysis in cancer cell Warburg published On the origin of cancer cell p53 was identified cmyc was discovered cmyc regulates glycolysis Biochemistry era Genomic era Debate between Weinhouse and Warburg on mitochondria and cancer I was born mutations in mitochondrial proteins SDH and FH are cause of cancer
12 The timeline of cancer research Warburg observed the increased glycolysis in cancer cell Kovacevic observed increased glutaminolysis in cancer cell Warburg published On the origin of cancer cell p53 was identified cmyc was discovered cmyc regulates glycolysis p53 regulates cell metabolism via TIGAR, PGHDH is amplified in PGM, Sco2 breast cancer Biochemistry era Genomic era Metabolomic era Debate between Weinhouse and Warburg on mitochondria and cancer I was born mutations in mitochondrial proteins SDH and FH are cause of cancer mutations in IDH are found in glioblastoma accumulation of succinate in SDH mutants stabilizes HIF 2HG is sufficient to induce leukemogenesis 2HG is produced by mutant IDHs and inhibits DNA and histone demethylation Fumarate induces EMT
13 Cancer: a metabolic disease?
14 A system view of cancer
15 An historical perspective on CANCER METABOLISM
16 Metabolism in the 19 th century Pasteur effect glucose fermentation lactate pyruvate respiration CO 2 21% O 2 0 % O 2 Oxygen concentration
17 Warburg experiments
18 Aerobic glycolysis in cancer cells normal cells cancer cells
19 The Warburg hypothesis The prime cause of cancer is the replacement of the respiration of oxygen by a fermentation of sugar Injury of respiration Aerobic glycolysis De-differentiation Phase I Phase II Phase III
20 The Warburg hypothesis Injury of respiration Aerobic glycolysis De-differentiation Phase I Phase II Phase III
21 Is respiration injured in cancer cells? there is no evidence that the respiration in cancer cell is either quantitatively lowered or fails to lower glycolysis Sidney Weinhouse Weinhouse, Z. Krebsforsh, 1976
22 Is hypoxia the cause of mitochondrial dysfunction? all Warburg s experiment were performed using well oxygenated tissues
23 Metabolic changes in cancer vs normal tissues Gaude and Frezza, Nat Comms 2016
24 Mitochondrial genes are suppressed in cancer Gaude and Frezza, Nat Comms 2016
25 Mitochondrial genes as oncogenes and TSGs Gaude and Frezza, Cancer & Metab, 2014
26 Oncogenic roles of dysfunctional mitochondria
27 Mitochondrial dysfunction can be oncogenic
28 Mitochondrial tumour suppressors and oncometabolites
29 Succinate and fumarate activate HIF pathway akg prolyl hydroxylases fumarate succinate HIF HIF-OH O 2 CO 2 HIF degradation
30 Succinate, fumarate, and 2HG as epigenetic modifiers 2HG IDH* akg DNA-CH 3 TETs fumarate succinate DNA O 2 CO 2
31 Fumarate and succination protein-sh
32 Succination of Keap1 activates Nrf2 pathway Keap1 fumarate Nrf2 Nrf2-Keap1 Nrf2 degradation
33 The emerging concept of oncometabolites the somatic mutation theory acts like a tranquilizer on those who believe in it (Rous, 1959).
34 Mitochondria dysfunction in cancer? Mitochondrial function is rewired in cancer cells, but mitochondria are required for cancer cell growth and proliferation
35 The Warburg hypothesis Injury of respiration Aerobic glycolysis De-differentiation Phase I Phase II Phase III
36 Aerobic glycolysis in cancer: increase in glucose uptake [ 18 F]flouro-2-deoxyglucose (FDG) Positron Emission Tomography (PET)
37 Aerobic glycolysis in cancer: increase in glucose uptake
38 Aerobic glycolysis in cancer: hyperpolarised glucose
39 Aerobic glycolysis in cancer: increased lactate secretion subcutaneously implanted EL4 tumour ph map
40 Is glycolysis up-regulated in cancer? YES! aerobic glycolysis is a hallmark of cancer Disclaimer: Aerobic glycolysis is a characteristic of most proliferating cells
41 Is it all about ATP?
42 Aerobic glycolysis supports proliferation
43 Aerobic glycolysis and migration
44 The Warburg hypothesis Injury of respiration Aerobic glycolysis De-differentiation Phase I Phase II Phase III
45 Aerobic glycolysis and stemness
46 Cancer stem cells and plasticity
47 Can we exploit altered cancer metabolism as therapeutic strategy? metabolism
48 The first example of targeting cancer metabolism?
49 Targeting cancer metabolism 2HG IDH*
50 IDH and GLS inhibitors are in clinic
51
52 Resistance through metabolic reprogramming
53 Conclusions Metabolism of cancer cells is different from that of normal cells Dysregulated metabolism can drive oncogenic processes Altered metabolism offers a therapeutic window to target cancer cells
54 Key references & links O. Warburg, On the origin of cancer cells, Science, 1956 JS. Flier et al. Elevated levels of glucose transport and transporter messenger RNA are induced by ras or src oncogenes. Science, 1987 H. Shim et al. c-myc transactivation of LDH-A: Implications for tumor metabolism and growth, PNAS, 1998 D. Hanahan and RA. Weinberg, Hallmarks of Cancer: next generation, Cell, 2011 Gaude and Frezza, Tissue-specific and convergent metabolic transformation of cancer correlates with metastatic potential and patient survival, Nat Comms, 2016 Pavlova and Thompson, The emerging hallmarks of cancer metabolism, Cell Metabolism,
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