Comment
obeticholic acid was pruritus, clearly more frequent and more intense in the obeticholic acid group, although just one patient was discontinued. Whether a lower dose might reduce the incidence of pruritus, while maintaining histological efficacy, needs to be tested. Patients with non-alcoholic steatohepatitis for whom diet and lifestyle measures fail to work need pharmacological therapy. FLINT provides a clear indication of the efficacy of obeticholic acid in alleviating liver injury and should be followed by more in-depth assessment of efficacy and safety. But there is a substantial proportion of non-responders, which, together with the multiplicity of pathways that result in steatohepatitis and fibrosis progression, mandates testing of other pharmacological agents with strong preclinical rationale: dual peroxisome proliferator-activated receptor α/Δ (GFT505), C-C motif chemokine receptor type 2 (CCR2) and CCR5 antagonists (cenicriviroc), antifibrotic agents (simtuzumab), Takeda G-protein coupled receptor 5 (TGR5) agonists or dual TGR5–farnesoid X receptor agonists, or fatty acid–bile acid conjugates (aramchol). Most of these agents are already in advanced, phase 2b and phase 3, clinical trials. The drug pipeline is slowly building to address the clinical need in this silent but damaging liver disease.
VR has received consulting fees from Abbott, AstraZeneca, Galmed, Genfit, Gilead, Intercept, Roche-Genentech, and Tobira. 1
2
3
4 5
6
7
8
9
10
11
12 13
Vlad Ratziu
Charlton MR, Burns JM, Pedersen RA, Watt KD, Heimbach JK, Dierkhising RA. Frequency and outcomes of liver transplantation for nonalcoholic steatohepatitis in the United States. Gastroenterology 2011; 141: 1249–53. Wong RJ, Cheung R, Ahmed A. Nonalcoholic steatohepatitis is the most rapidly growing indication for liver transplantation in patients with hepatocellular carcinoma in the US. Hepatology 2014; 59: 2188–95. Neuschwander-Tetri BA, Loomba R, Sanyal AJ, et al, for the NASH Clinical Research Network. Farnesoid X nuclear receptor ligand obeticholic acid for non-cirrhotic, non-alcoholic steatohepatitis (FLINT): a multicentre, randomised, placebo-controlled trial. Lancet 2014; published online Nov 7. http://dx.doi.org/10.1016/S0140-6736(14)61933-4. Sanyal AJ, Chalasani N, Kowdley KV, et al. Pioglitazone, vitamin E, or placebo for nonalcoholic steatohepatitis. N Engl J Med 2010; 362: 1675–85. Albanis E, Alvarez CE, Pruzansky M, Friedman SL, Fiorucci S. Anti-fibrotic activity of INT-747, a novel FXR activator, in vitro and in experimental liver fibrosis and cirrhosis. Hepatology 2005; 42: 1040A. Fickert P, Fuchsbichler A, Moustafa T, et al. Farnesoid X receptor critically determines the fibrotic response in mice but is expressed to a low extent in human hepatic stellate cells and periductal myofibroblasts. Am J Pathol 2009; 175: 2392–405. Younossi ZM, Stepanova M, Rafiq N, et al. Pathologic criteria for nonalcoholic steatohepatitis: interprotocol agreement and ability to predict liver-related mortality. Hepatology 2011; 53: 1874–82. Ekstedt M, Franzen LE, Mathiesen UL, Kechagias S. Low clinical relevance of the nonalcoholic fatty liver disease activity score (NAS) in predicting fibrosis progression. Scand J Gastroenterol 2012; 47: 108–15. Ekstedt M, Franzen LE, Mathiesen UL, et al. Long-term follow-up of patients with NAFLD and elevated liver enzymes. Hepatology 2006; 44: 865–73. Bassler D, Briel M, Montori VM, et al. Stopping randomized trials early for benefit and estimation of treatment effects: systematic review and metaregression analysis. JAMA 2010; 303: 1180–87. Hartman HB, Gardell SJ, Petucci CJ, Wang S, Krueger JA, Evans MJ. Activation of farnesoid X receptor prevents atherosclerotic lesion formation in LDLR–/– and apoE–/– mice. J Lipid Res 2009; 50: 1090–100. Mencarelli A, Renga B, Distrutti E, Fiorucci S. Antiatherosclerotic effect of farnesoid X receptor. Am J Physiol Heart Circ Physiol 2009; 296: H272–81. Li YT, Swales KE, Thomas GJ, Warner TD, Bishop-Bailey D. Farnesoid X receptor ligands inhibit vascular smooth muscle cell inflammation and migration. Arterioscler Thromb Vasc Biol 2007; 27: 2606–11.
Institute for Cardiometabolism and Nutrition, Université Pierre et Marie Curie, Assistance Publique Hôpitaux de Paris, Hôpital Pitié Salpêtrière, INSERM UMR_S 893, Paris 75013, France [email protected]
Progress with the global tobacco epidemic See Editorial page 915 See Comment page 918 See Articles page 966 See Series page 1029
924
During the 20th century, tobacco smoking killed some 100 million people, most of them in high-income countries.1 In the 21st century the corresponding figure is likely to be about 1 billion, most in lowincome and middle-income countries.1,2 Similar to the evolution of smoking within populations of highincome countries, the global smoking epidemic is now moving from the rich to the poor. Driven by the financial heft of transnational tobacco companies with a combined income higher than most individual countries,3 built on a business model of peddling an
addictive product to children and young people, and sustained by practices that prioritise corporate profit over health, the current global epidemic of smoking represents a triumph of corporate self-interest over human wellbeing.4 It is also a challenge that national and international health systems remain ill-equipped to face. The WHO Framework Convention on Tobacco Control (FCTC) is a global treaty, indeed the first ever global health treaty, designed to counter the smoking epidemic.5 The FCTC aims to equip countries, poor www.thelancet.com Vol 385 March 14, 2015
or rich and at any stage of evolution of the smoking epidemic,6 with effective tobacco control policies and practices. The core components—banning advertising, prohibition of smoking in public and work places, imposition of high taxes, media campaigns, and help for smokers to quit—are all effective,7 and most cost next to nothing. There are no good reasons not to use them. So, after 10 years of the FCTC, and now with 180 of the world’s countries declared as parties to the convention, how are things progressing? The answer, according to an analysis of global trends in tobacco use published by Ver Bilano and colleagues in The Lancet,8 is not very well. The study fits and extrapolates trends in national data for smoking prevalence to predict the likelihood that individual countries will achieve a WHO target, set in 2013, of reducing adult smoking prevalence by 30% from 2010 levels by 2025. Of the 178 countries for which projections could be made, the investigators conclude that despite generally decreasing prevalence, just under half of all countries (88 [49%]) are on track to meet the target for women, and only 37 countries (21%) are on target for men. African and eastern Mediterranean countries were among those with the worst outlook. The projections are inevitably speculative, being dependent on the validity of the prevalence data used to make them (the UK, for example, already has a reported cigarette smoking prevalence in women that is lower, at 18%, than the lower limit of the range predicted by the model for 2025),9 and susceptible to the effects of a range of political and commercial developments. Trends in prevalence are also only part of the story; demographic changes in developing countries mean that the number of smokers can increase substantially even as smoking prevalence falls.10 At face value, Bilano and colleagues’ findings add little that can’t be gleaned from a glance at tobacco companies’ regional sales figures, such as those in the 2013 British American Tobacco annual report,11 which spell out exactly where the tobacco industry is doing well and where it is doing less well. The outlook is not unremittingly bad, however; in the gloom, there are examples of success. Bilano and colleagues draw attention to Turkey,8 where a high degree of implementation of the FCTC is expected to deliver a substantial reduction in prevalence, and to www.thelancet.com Vol 385 March 14, 2015
Tim Wimborne/Reuters/Corbis
Comment
Norway and Sweden, which have achieved striking reductions in smoking prevalence attributable at least partly to substitution with smokeless tobacco. A previous report identified Uruguay as an early example of success for a middle-income country, with smoking prevalence among adults falling by 3·3% per year since the introduction of a comprehensive package of tobacco control policies in 2005.12 However, many more countries, rich and poor, have a smoking prevalence that is high or rising, with policies not yet in place to reverse these trends; in other countries where the smoking epidemic has yet to begin, governments are too preoccupied with other demands to act on tobacco. The issue is that, although the FCTC provides a framework and guidance for smoking prevention, without implementation it cannot succeed. Signing up to prevalence reductions or so-called endgame strategies with targets set comfortably far into the future is easy for politicians. Delivery is another matter, and the challenge for public health research and practice in the 21st century is to develop effective means to achieve it. Conventional health advocacy has proved successful in many countries, but more innovative political and economic incentives and drivers of change are desperately needed. Where the tobacco industry has gone, so the alcohol and fast food industries are following. Eradication of smoking will save millions of lives, but application of lessons from tobacco to other commercially driven epidemics will save many more. 925
Comment
John Britton UK Centre for Tobacco and Alcohol Studies, Division of Epidemiology and Public Health, University of Nottingham, City Hospital, Nottingham NG5 1PB, UK [email protected] I declare no competing interests. 1 2 3
4
Jha P. Avoidable global cancer deaths and total deaths from smoking. Nat Rev Cancer 2009; 9: 655–64. Mathers CD, Loncar D. Projections of global mortality and burden of disease from 2002 to 2030. PLoS Med 2006; 3: e442. Callard C. Follow the money: how the billions of dollars that flow from smokers in poor nations to companies in rich nations greatly exceed funding for global tobacco control and what might be done about it. Tob Control 2010; 19: 285–90. Gilmore AB, Fooks G, Drope J, Bialous SA, Jackson RR. Exposing and addressing tobacco industry conduct in low-income and middle-income countries. Lancet 2015; 385: 1029–43.
5 6 7 8
9
10 11 12
WHO. WHO Framework Convention on Tobacco Control. Geneva: World Health Organization, 2003. Lopez AD, Collishaw NE, Piha T. A descriptive model of the cigarette epidemic in developed countries. Tob Control 1994; 3: 242–47. Jha P, Chaloupka FJ. The economics of global tobacco control. BMJ 2000; 321: 358–61. Bilano V, Gilmour S, Moffiet T, et al. Global trends and projections for tobacco use, 1990–2025: an analysis of smoking indicators from the WHO Comprehensive Information Systems for Tobacco Control. Lancet 2015; 385: 966–76. Office for National Statistics. Adult smoking habits in Great Britain, 2013. http://www.ons.gov.uk/ons/dcp171778_386291.pdf (accessed March 6, 2015). Ng M, Freeman MK, Fleming TD. Smoking prevalence and cigarette consumption in 187 countries, 1980–2012. JAMA 2014; 311: 183–92. British American Tobacco. Annual review 2013. http://www.bat.com/ ar/2013/index.html#ar/2013/index (accessed Feb 27, 2015). Abascal W, Esteves E, Goja B, et al. Tobacco control campaign in Uruguay: a population-based trend analysis. Lancet 2012; 380: 1575–82.
Global survival patterns: potential for cancer control Published Online November 26, 2014 http://dx.doi.org/10.1016/ S0140-6736(14)62251-0
Ajay Verma/Reuters/Corbis
See Articles page 977
926
In 2011, member states of the UN General Assembly established an objective to reduce premature deaths from non-communicable diseases (including cancer) by 25% by 2025.1 A reduction in cancer mortality can only be achieved through disease control programmes that include prevention, early diagnosis, and treatment of malignant disease. Nearly a decade ago, the World Health Assembly called on its member states to create “national cancer plans and programs”.2 The need for such initiatives has escalated in the intervening years. The burden of cancer is growing worldwide, not only because the population is ageing in many countries (attributable in part to improved control of communicable diseases) but also because of changes
in risk factors (eg, increasing prevalence of tobacco smoking and obesity).3 To establish priorities for cancer control programmes, governments must have sufficient information to record the burden of cancer in their countries. Comprehensive, high-quality cancer registration is a key component needed to assess the effectiveness of disease control programmes, and cancer registries have been endorsed by WHO.4 In The Lancet, Claudia Allemani and colleagues in the CONCORD Working Group5 describe the efforts of the CONCORD-2 programme to initiate global surveillance of cancer survival, examining survival trends from 1995 to 2009. They assembled a global cancer dataset, with information for almost 26 million individual cancer patients provided by 279 population-based cancer registries in 67 countries.5 The group must be commended for the technical, scientific, and political efforts needed to obtain these data. Allemani and colleagues5 report an increase in 5-year survival from colon, rectal, and breast cancer in most developed countries. One striking finding was for childhood acute lymphoblastic leukaemia, for which very wide variations in survival were noted globally—eg, less than 60% in several countries but 90% or higher in Canada and four European countries (Austria, Belgium, Germany, and Norway)—which suggests an absence of adequate treatment for children in particular regions of the world. The potential for cancer prevention programmes was highlighted by poor survival in most countries from lung and liver cancer—generally 10–20% www.thelancet.com Vol 385 March 14, 2015
obeticholic acid was pruritus, clearly more frequent and more intense in the obeticholic acid group, although just one patient was discontinued. Whether a lower dose might reduce the incidence of pruritus, while maintaining histological efficacy, needs to be tested. Patients with non-alcoholic steatohepatitis for whom diet and lifestyle measures fail to work need pharmacological therapy. FLINT provides a clear indication of the efficacy of obeticholic acid in alleviating liver injury and should be followed by more in-depth assessment of efficacy and safety. But there is a substantial proportion of non-responders, which, together with the multiplicity of pathways that result in steatohepatitis and fibrosis progression, mandates testing of other pharmacological agents with strong preclinical rationale: dual peroxisome proliferator-activated receptor α/Δ (GFT505), C-C motif chemokine receptor type 2 (CCR2) and CCR5 antagonists (cenicriviroc), antifibrotic agents (simtuzumab), Takeda G-protein coupled receptor 5 (TGR5) agonists or dual TGR5–farnesoid X receptor agonists, or fatty acid–bile acid conjugates (aramchol). Most of these agents are already in advanced, phase 2b and phase 3, clinical trials. The drug pipeline is slowly building to address the clinical need in this silent but damaging liver disease.
VR has received consulting fees from Abbott, AstraZeneca, Galmed, Genfit, Gilead, Intercept, Roche-Genentech, and Tobira. 1
2
3
4 5
6
7
8
9
10
11
12 13
Vlad Ratziu
Charlton MR, Burns JM, Pedersen RA, Watt KD, Heimbach JK, Dierkhising RA. Frequency and outcomes of liver transplantation for nonalcoholic steatohepatitis in the United States. Gastroenterology 2011; 141: 1249–53. Wong RJ, Cheung R, Ahmed A. Nonalcoholic steatohepatitis is the most rapidly growing indication for liver transplantation in patients with hepatocellular carcinoma in the US. Hepatology 2014; 59: 2188–95. Neuschwander-Tetri BA, Loomba R, Sanyal AJ, et al, for the NASH Clinical Research Network. Farnesoid X nuclear receptor ligand obeticholic acid for non-cirrhotic, non-alcoholic steatohepatitis (FLINT): a multicentre, randomised, placebo-controlled trial. Lancet 2014; published online Nov 7. http://dx.doi.org/10.1016/S0140-6736(14)61933-4. Sanyal AJ, Chalasani N, Kowdley KV, et al. Pioglitazone, vitamin E, or placebo for nonalcoholic steatohepatitis. N Engl J Med 2010; 362: 1675–85. Albanis E, Alvarez CE, Pruzansky M, Friedman SL, Fiorucci S. Anti-fibrotic activity of INT-747, a novel FXR activator, in vitro and in experimental liver fibrosis and cirrhosis. Hepatology 2005; 42: 1040A. Fickert P, Fuchsbichler A, Moustafa T, et al. Farnesoid X receptor critically determines the fibrotic response in mice but is expressed to a low extent in human hepatic stellate cells and periductal myofibroblasts. Am J Pathol 2009; 175: 2392–405. Younossi ZM, Stepanova M, Rafiq N, et al. Pathologic criteria for nonalcoholic steatohepatitis: interprotocol agreement and ability to predict liver-related mortality. Hepatology 2011; 53: 1874–82. Ekstedt M, Franzen LE, Mathiesen UL, Kechagias S. Low clinical relevance of the nonalcoholic fatty liver disease activity score (NAS) in predicting fibrosis progression. Scand J Gastroenterol 2012; 47: 108–15. Ekstedt M, Franzen LE, Mathiesen UL, et al. Long-term follow-up of patients with NAFLD and elevated liver enzymes. Hepatology 2006; 44: 865–73. Bassler D, Briel M, Montori VM, et al. Stopping randomized trials early for benefit and estimation of treatment effects: systematic review and metaregression analysis. JAMA 2010; 303: 1180–87. Hartman HB, Gardell SJ, Petucci CJ, Wang S, Krueger JA, Evans MJ. Activation of farnesoid X receptor prevents atherosclerotic lesion formation in LDLR–/– and apoE–/– mice. J Lipid Res 2009; 50: 1090–100. Mencarelli A, Renga B, Distrutti E, Fiorucci S. Antiatherosclerotic effect of farnesoid X receptor. Am J Physiol Heart Circ Physiol 2009; 296: H272–81. Li YT, Swales KE, Thomas GJ, Warner TD, Bishop-Bailey D. Farnesoid X receptor ligands inhibit vascular smooth muscle cell inflammation and migration. Arterioscler Thromb Vasc Biol 2007; 27: 2606–11.
Institute for Cardiometabolism and Nutrition, Université Pierre et Marie Curie, Assistance Publique Hôpitaux de Paris, Hôpital Pitié Salpêtrière, INSERM UMR_S 893, Paris 75013, France [email protected]
Progress with the global tobacco epidemic See Editorial page 915 See Comment page 918 See Articles page 966 See Series page 1029
924
During the 20th century, tobacco smoking killed some 100 million people, most of them in high-income countries.1 In the 21st century the corresponding figure is likely to be about 1 billion, most in lowincome and middle-income countries.1,2 Similar to the evolution of smoking within populations of highincome countries, the global smoking epidemic is now moving from the rich to the poor. Driven by the financial heft of transnational tobacco companies with a combined income higher than most individual countries,3 built on a business model of peddling an
addictive product to children and young people, and sustained by practices that prioritise corporate profit over health, the current global epidemic of smoking represents a triumph of corporate self-interest over human wellbeing.4 It is also a challenge that national and international health systems remain ill-equipped to face. The WHO Framework Convention on Tobacco Control (FCTC) is a global treaty, indeed the first ever global health treaty, designed to counter the smoking epidemic.5 The FCTC aims to equip countries, poor www.thelancet.com Vol 385 March 14, 2015
or rich and at any stage of evolution of the smoking epidemic,6 with effective tobacco control policies and practices. The core components—banning advertising, prohibition of smoking in public and work places, imposition of high taxes, media campaigns, and help for smokers to quit—are all effective,7 and most cost next to nothing. There are no good reasons not to use them. So, after 10 years of the FCTC, and now with 180 of the world’s countries declared as parties to the convention, how are things progressing? The answer, according to an analysis of global trends in tobacco use published by Ver Bilano and colleagues in The Lancet,8 is not very well. The study fits and extrapolates trends in national data for smoking prevalence to predict the likelihood that individual countries will achieve a WHO target, set in 2013, of reducing adult smoking prevalence by 30% from 2010 levels by 2025. Of the 178 countries for which projections could be made, the investigators conclude that despite generally decreasing prevalence, just under half of all countries (88 [49%]) are on track to meet the target for women, and only 37 countries (21%) are on target for men. African and eastern Mediterranean countries were among those with the worst outlook. The projections are inevitably speculative, being dependent on the validity of the prevalence data used to make them (the UK, for example, already has a reported cigarette smoking prevalence in women that is lower, at 18%, than the lower limit of the range predicted by the model for 2025),9 and susceptible to the effects of a range of political and commercial developments. Trends in prevalence are also only part of the story; demographic changes in developing countries mean that the number of smokers can increase substantially even as smoking prevalence falls.10 At face value, Bilano and colleagues’ findings add little that can’t be gleaned from a glance at tobacco companies’ regional sales figures, such as those in the 2013 British American Tobacco annual report,11 which spell out exactly where the tobacco industry is doing well and where it is doing less well. The outlook is not unremittingly bad, however; in the gloom, there are examples of success. Bilano and colleagues draw attention to Turkey,8 where a high degree of implementation of the FCTC is expected to deliver a substantial reduction in prevalence, and to www.thelancet.com Vol 385 March 14, 2015
Tim Wimborne/Reuters/Corbis
Comment
Norway and Sweden, which have achieved striking reductions in smoking prevalence attributable at least partly to substitution with smokeless tobacco. A previous report identified Uruguay as an early example of success for a middle-income country, with smoking prevalence among adults falling by 3·3% per year since the introduction of a comprehensive package of tobacco control policies in 2005.12 However, many more countries, rich and poor, have a smoking prevalence that is high or rising, with policies not yet in place to reverse these trends; in other countries where the smoking epidemic has yet to begin, governments are too preoccupied with other demands to act on tobacco. The issue is that, although the FCTC provides a framework and guidance for smoking prevention, without implementation it cannot succeed. Signing up to prevalence reductions or so-called endgame strategies with targets set comfortably far into the future is easy for politicians. Delivery is another matter, and the challenge for public health research and practice in the 21st century is to develop effective means to achieve it. Conventional health advocacy has proved successful in many countries, but more innovative political and economic incentives and drivers of change are desperately needed. Where the tobacco industry has gone, so the alcohol and fast food industries are following. Eradication of smoking will save millions of lives, but application of lessons from tobacco to other commercially driven epidemics will save many more. 925
Comment
John Britton UK Centre for Tobacco and Alcohol Studies, Division of Epidemiology and Public Health, University of Nottingham, City Hospital, Nottingham NG5 1PB, UK [email protected] I declare no competing interests. 1 2 3
4
Jha P. Avoidable global cancer deaths and total deaths from smoking. Nat Rev Cancer 2009; 9: 655–64. Mathers CD, Loncar D. Projections of global mortality and burden of disease from 2002 to 2030. PLoS Med 2006; 3: e442. Callard C. Follow the money: how the billions of dollars that flow from smokers in poor nations to companies in rich nations greatly exceed funding for global tobacco control and what might be done about it. Tob Control 2010; 19: 285–90. Gilmore AB, Fooks G, Drope J, Bialous SA, Jackson RR. Exposing and addressing tobacco industry conduct in low-income and middle-income countries. Lancet 2015; 385: 1029–43.
5 6 7 8
9
10 11 12
WHO. WHO Framework Convention on Tobacco Control. Geneva: World Health Organization, 2003. Lopez AD, Collishaw NE, Piha T. A descriptive model of the cigarette epidemic in developed countries. Tob Control 1994; 3: 242–47. Jha P, Chaloupka FJ. The economics of global tobacco control. BMJ 2000; 321: 358–61. Bilano V, Gilmour S, Moffiet T, et al. Global trends and projections for tobacco use, 1990–2025: an analysis of smoking indicators from the WHO Comprehensive Information Systems for Tobacco Control. Lancet 2015; 385: 966–76. Office for National Statistics. Adult smoking habits in Great Britain, 2013. http://www.ons.gov.uk/ons/dcp171778_386291.pdf (accessed March 6, 2015). Ng M, Freeman MK, Fleming TD. Smoking prevalence and cigarette consumption in 187 countries, 1980–2012. JAMA 2014; 311: 183–92. British American Tobacco. Annual review 2013. http://www.bat.com/ ar/2013/index.html#ar/2013/index (accessed Feb 27, 2015). Abascal W, Esteves E, Goja B, et al. Tobacco control campaign in Uruguay: a population-based trend analysis. Lancet 2012; 380: 1575–82.
Global survival patterns: potential for cancer control Published Online November 26, 2014 http://dx.doi.org/10.1016/ S0140-6736(14)62251-0
Ajay Verma/Reuters/Corbis
See Articles page 977
926
In 2011, member states of the UN General Assembly established an objective to reduce premature deaths from non-communicable diseases (including cancer) by 25% by 2025.1 A reduction in cancer mortality can only be achieved through disease control programmes that include prevention, early diagnosis, and treatment of malignant disease. Nearly a decade ago, the World Health Assembly called on its member states to create “national cancer plans and programs”.2 The need for such initiatives has escalated in the intervening years. The burden of cancer is growing worldwide, not only because the population is ageing in many countries (attributable in part to improved control of communicable diseases) but also because of changes
in risk factors (eg, increasing prevalence of tobacco smoking and obesity).3 To establish priorities for cancer control programmes, governments must have sufficient information to record the burden of cancer in their countries. Comprehensive, high-quality cancer registration is a key component needed to assess the effectiveness of disease control programmes, and cancer registries have been endorsed by WHO.4 In The Lancet, Claudia Allemani and colleagues in the CONCORD Working Group5 describe the efforts of the CONCORD-2 programme to initiate global surveillance of cancer survival, examining survival trends from 1995 to 2009. They assembled a global cancer dataset, with information for almost 26 million individual cancer patients provided by 279 population-based cancer registries in 67 countries.5 The group must be commended for the technical, scientific, and political efforts needed to obtain these data. Allemani and colleagues5 report an increase in 5-year survival from colon, rectal, and breast cancer in most developed countries. One striking finding was for childhood acute lymphoblastic leukaemia, for which very wide variations in survival were noted globally—eg, less than 60% in several countries but 90% or higher in Canada and four European countries (Austria, Belgium, Germany, and Norway)—which suggests an absence of adequate treatment for children in particular regions of the world. The potential for cancer prevention programmes was highlighted by poor survival in most countries from lung and liver cancer—generally 10–20% www.thelancet.com Vol 385 March 14, 2015
