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'THE ‘UNIQUENESS’ OF CANCER' by Professor Graham Mann - Sick or Treat Sessions
- 1. Official Opening 9 October 2014 Graham Mann Centre for Cancer Research Westmead Institute for Medical Research Melanoma Institute Australia Cancer: what we know … and what we don’t
- 2. 2 Cancer – the big picture (Australia 2011) • 119,000 people newly diagnosed each year • 43,000 deaths • burden >$100b Commonest: • Women: breast, bowel, melanoma, lung • Men: prostate, bowel, melanoma, lung
- 3. Australian Melanoma Statistics and Trends 0 10 20 30 40 50 60 70 1965 1970 1975 1980 1985 1990 1995 2000 2005 2010 2015 Age-standardisedrate Year Age-standardised incidence (to 2011) and mortality (to 2012) rates by year M. inc. F. inc. M. mort. F. mort. Australian Institute of Health and Welfare (AIHW) 2015. Australian Cancer Incidence and Mortality (ACIM) books: Melanoma. Canberra. • 3rd most common cancer in men and women, 4th overall • commonest cancer in younger adults
- 4. 4 What is cancer? • A group of related cells that is growing and multiplying, if … • some of them never stop • and some can move elsewhere in the body They are our own cells, malfunctioning • growing when they should have stopped • living longer than they are supposed to • moving out of the places where they belong
- 5. 5 How? All these normal functions are controlled in cells by genes, e.g. • cell multiplication genes • lifespan and cell death genes • genes that keep a cell where it should be • we have about 20,000 genes They are our own cells, malfunctioning • growing when they should have stopped • living longer than they are allowed to • moving from the places where they belong
- 6. 6 What causes cancer? All these normal functions are controlled in cells by genes e.g. • cell multiplication genes • lifespan and cell death genes • genes that keep a cell where it should be Cancer is caused by things that damage (mutate) genes (DNA) • some chemicals • some kinds of radiation • some infections • wear and tear (oxygen)
- 7. M. Lawrence 1st Annual TCGA Scientific Symposium, 2011
- 8. Australian Melanoma Statistics and Trends 0 10 20 30 40 50 60 70 1965 1970 1975 1980 1985 1990 1995 2000 2005 2010 2015 Age-standardisedrate Year Age-standardised incidence (to 2011) and mortality (to 2012) rates by year M. inc. F. inc. M. mort. F. mort. Australian Institute of Health and Welfare (AIHW) 2015. Australian Cancer Incidence and Mortality (ACIM) books: Melanoma. Canberra. • 3rd most common cancer in men and women, 4th overall • commonest cancer in younger adults
- 9. 9 Why me? • Unlucky • Ageing • Exposed to more DNA damage, or DNA damage to a particular site • (Rarely) a strong inherited predisposition to cancer • (Commonly) a genetic background that raises the odds
- 10. Bishop et al. Nature Genetics 2011 Common genetic risk DNA markers found more often in people with melanoma MC1R ATMCASP8 TYR
- 11. 11 … different tumours of the same type
- 12. M. Lawrence 1st Annual TCGA Scientific Symposium, 2011
- 13. International Cancer Genome Consortium (ICGC) Nature. 2010 Apr 15;464(7291):993-8 Original goal: sequence 500 tumours from 50 different cancer types International Cancer Genome Consortium
- 14. The Cancer Genome Atlas Network. Cell 2015 Diversity and commonality in 311 melanomas
- 15. The Cancer Genome Atlas Network. Cell 2015 Genes, pathways, targets
- 16. The Cancer Genome Atlas Network. Cell (in press) Immune response
- 17. 17 What works? PREVENTION – but there are limits • new hope: individualised EARLY DETECTION • new hope: target screening by risk DESTRUCTION, if you can get it all • Surgery – newer, better • Radiotherapy – newer, better
- 18. 18 What works? NEW FRONTIERS • Drugs that target the specific mutations driving the tumour: ”personalised therapy” • Overcoming the way tumours hide from the immune system • They work!
- 19. PLX4720 co-Structure with kinase domain of BRAFV600E (Tsai J et al. 2008 PNAS) New generation of kinase inhibitors w specificity for oncogenic BRAF (V600E) from cancer genomics “1.0” 2002
- 20. 20 Why isn’t it fixed yet? Getting there … • it is fixed for some • we understand what works and (mostly) why things fail • the end is in sight But … • our system can fall short • more targets = more drugs • early days for immune therapy
- 21. 21 Thanks and questions Casey Dunlop CRUK scienceblog.cancerresearchuk.org Bernie Stewart IARC The Conversation