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54. Periconceptional environment and the developmental origins of disease

Author

Velazquez, Miguel A., Fleming, Tom P., and Watkins, Adam J.

Abstract

The concept emerging from Professor David Barker’s seminal research on the developmental origins of later-life disease has progressed in many directions since it was first published. One critical question being when during gestation might environment alter the developmental programme with such enduring consequences. Here, we review the growing consensus from clinical and animal research that the period around conception, embracing gamete maturation and early embryogenesis might be the most vulnerable period. We focus on four types of environmental exposure shown to modify periconceptional reproduction and offspring development and health: maternal overnutrition and obesity; maternal undernutrition; paternal diet and health; and assisted reproductive technology. These conditions may act through diverse epigenetic, cellular and physiological mechanisms to alter gene expression and cellular signalling and function in the conceptus affecting offspring growth and metabolism leading to increased risk for cardiometabolic and neurological disease in later life.

Published
2019

58. Epithelial differentiation in the mouse preimplantation embryo: making adhesive cell contacts for the first time

Author

Collins, Jane E. and Fleming, Tom P.

Subjects
Mice -- Physiological aspects, Embryology -- Research, Epithelial cells -- Analysis, Biological sciences, Chemistry
Abstract

The preimplantation embryo generates two distinct tissues, the trophectoderm, which is a transporting polarized epithelium, and the inner cell mass. Epithelial differentiation and tissue segregation, here examined in relation to the maturation of membrane adhesion and cell junction systems, are coordinated events regulated by a combination of the zygotic gene expression programme, kinase-mediated protein activation and cell-cell interactions.

Published
1995

59. Advanced maternal age perturbs mouse embryo development and alters the phenotype of derived embryonic stem cells

Author

Khurana, Pooja, Smyth, Neil R., Sheth, Bhavwanti, Velazquez, Miguel A., Eckert, Judith J., and Fleming, Tom P.

Abstract

AbstractAdvanced maternal age (AMA) is known to reduce fertility, increases aneuploidy in oocytes and early embryos and leads to adverse developmental consequences which may associate with offspring lifetime health risks. However, investigating underlying effects of AMA on embryo developmental potential is confounded by the inherent senescence present in maternal body systems further affecting reproductive success. Here, we describe a new model for the analysis of early developmental mechanisms underlying AMA by the derivation and characterisation of mouse embryonic stem cell (mESC-like) lines from naturally conceived embryos. Young (7–8 weeks) and Old (7–8 months) C57BL/6 female mice were mated with young males. Preimplantation embryos from Old dams displayed developmental retardation in blastocyst morphogenesis. mESC lines established from these blastocysts using conventional techniques revealed differences in genetic, cellular and molecular criteria conserved over several passages in the standardised medium. mESCs from embryos from AMA dams displayed increased incidence of aneuploidy following Giemsa karyotyping compared with those from Young dams. Moreover, AMA caused an altered pattern of expression of pluripotency markers (Sox2, OCT4) in mESCs. AMA further diminished mESC survival and proliferation and reduced the expression of cell proliferation marker, Ki-67. These changes coincided with altered expression of the epigenetic marker, Dnmt3a and other developmental regulators in a sex-dependent manner. Collectively, our data demonstrate the feasibility to utilise mESCs to reveal developmental mechanisms underlying AMA in the absence of maternal senescence and with reduced animal use.

Published
2022
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63. Mouse maternal systemic inflammation at the zygote stage causes blunted cytokine responsiveness in lipopolysaccharide-challenged adult offspring

Author

Fleming Tom P, Perry V Hugh, Teeling Jessica L, and Williams Charlotte L

Subjects
Biology (General), QH301-705.5
Abstract

Abstract Background The preimplantation embryo is sensitive to culture conditions in vitro and poor maternal diet in vivo. Such environmental perturbations can have long-lasting detrimental consequences for offspring health and physiology. However, early embryo susceptibility to other aspects of maternal health and their potential long-term influence into adulthood is relatively unexplored. In this study, we established an in vivo mouse model of maternal periconceptional systemic inflammation by intraperitoneal lipopolysaccharide (LPS) administration on the day of zygote formation and investigated the consequences into adulthood. Results In the short term, maternal LPS challenge induced a transient and typical maternal sickness response (elevated serum proinflammatory cytokines and hypoactive behaviour). Maternal LPS challenge altered preimplantation embryo morphogenesis and cell lineage allocation, resulting in reduced blastocyst inner cell mass (ICM) cell number and a reduced ICM:trophectoderm cell ratio. In the long term, diverse aspects of offspring physiology were affected by maternal LPS treatment. Whilst birthweight, growth and adult blood pressure were unaltered, reduced activity in an open-field behaviour test, increased fat pad:body weight ratio and increased body mass index were observed in male, but not female, offspring. Most importantly, the maternal LPS challenge caused corticosterone-independent blunting of the serum proinflammatory cytokine response to innate immune challenge in both male and female offspring. The suppressed state of innate immunity in challenged offspring was dose-dependent with respect to the maternal LPS concentration administered. Conclusions These results demonstrate for the first time that the preimplantation embryo in vivo is sensitive to maternal systemic inflammation, with effects on blastocyst cell lineage allocation and consequences for behaviour, adiposity and innate immune response in adult offspring. Critically, we identify a novel mechanism mediated through maternal-embryonic interactions that confers plasticity in the development of the innate immune system, which is potentially important in setting postnatal tolerance to environmental pathogens. Our study extends the concept of developmental programming of health and disease to include maternal health at the time of conception.

Published
2011
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64. Periconception maternal low-protein diet adversely affects male mouse fetal bone growth and mineral density quality in late gestation.

Author

Lanham, Stuart A., Smith, Stephanie J., Watkins, Adam J., Lucas, Emma S., MacCaoilte, Niamh, Oreffo, Richard O.C., Fleming, Tom P., and Eckert, Judith J.

Abstract

Adverse programming of adult non-communicable disease can be induced by poor maternal nutrition during pregnancy and the periconception period has been identified as a vulnerable period. In the current study, we used a mouse maternal low-protein diet fed either for the duration of pregnancy (LPD) or exclusively during the preimplantation period (Emb-LPD) with control nutrition provided thereafter and postnatally to investigate effects on fetal bone development and quality. This model has been shown previously to induce cardiometabolic and neurological disease phenotypes in offspring. Micro 3D computed tomography examination at fetal stages Embryonic day E14.5 and E17.4, reflecting early and late stages of bone formation, demonstrated LPD treatment caused increased bone formation of relative high mineral density quality in males, but not females, at E14.5, disproportionate to fetal growth, with bone quality maintained at E17.5. In contrast, Emb-LPD caused a late increase in male fetal bone growth, proportionate to fetal growth, at E17.5, affecting central and peripheral skeleton and of reduced mineral density quality relative to controls. These altered dynamics in bone growth coincide with increased placental efficiency indicating compensatory responses to dietary treatments. Overall, our data show fetal bone formation and mineral quality is dependent upon maternal nutritional protein content and is sex-specific. In particular, we find the duration and timing of poor maternal diet to be critical in the outcomes with periconceptional protein restriction leading to male offspring with increased bone growth but of poor mineral density, thereby susceptible to later disease risk. [ABSTRACT FROM AUTHOR]

Published
2021
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73. Do little embryos make big decisions? How maternal dietary protein restriction can permanently change an embryo's potential, affecting adult health

Author

Fleming, Tom P., Watkins, Adam J., Sun, Congshan, Velazquez, Miguel A., Smyth, Neil R., and Eckert, Judith J.

Abstract

Periconceptional environment may influence embryo development, ultimately affecting adult health. Here, we review the rodent model of maternal low-protein diet specifically during the preimplantation period (Emb-LPD) with normal nutrition during subsequent gestation and postnatally. This model, studied mainly in the mouse, leads to cardiovascular, metabolic and behavioural disease in adult offspring, with females more susceptible. We evaluate the sequence of events from diet administration that may lead to adult disease. Emb-LPD changes maternal serum and/or uterine fluid metabolite composition, notably with reduced insulin and branched-chain amino acids. This is sensed by blastocysts through reduced mammalian target of rapamycin complex 1 signalling. Embryos respond by permanently changing the pattern of development of their extra-embryonic lineages, trophectoderm and primitive endoderm, to enhance maternal nutrient retrieval during subsequent gestation. These compensatory changes include stimulation in proliferation, endocytosis and cellular motility, and epigenetic mechanisms underlying them are being identified. Collectively, these responses act to protect fetal growth and likely contribute to offspring competitive fitness. However, the resulting growth adversely affects long-term health because perinatal weight positively correlates with adult disease risk. We argue that periconception environmental responses reflect developmental plasticity and 'decisions' made by embryos to optimise their own development, but with lasting consequences.

Published
2015

76. Maternal nutrition modifies trophoblast giant cell phenotype and fetal growth in mice

Author

Watkins, Adam J., Lucas, Emma S., Marfy-Smith, Stephanie, Bates, Nicola, Kimber, Susan J., Fleming, Tom P., Watkins, Adam J., Lucas, Emma S., Marfy-Smith, Stephanie, Bates, Nicola, Kimber, Susan J., and Fleming, Tom P.

Abstract

Mammalian placentation is dependent upon the action of trophoblast cells at the time of implantation. Appropriate fetal growth, regulated by maternal nutrition and nutrient transport across the placenta, is a critical factor for adult offspring long-term health. We have demonstrated that a mouse maternal low-protein diet (LPD) fed exclusively during preimplantation development (Emb-LPD) increases offspring growth but programmes adult cardiovascular and metabolic disease. In this study, we investigate the impact of maternal nutrition on post-implantation trophoblast phenotype and fetal growth. Ectoplacental cone explants were isolated at day 8 of gestation from female mice fed either normal protein diet (NPD: 18% casein), LPD (9% casein) or Emb-LPD and cultured in vitro. We observed enhanced spreading and cell division within proliferative and secondary trophoblast giant cells (TGCs) emerging from explants isolated from LPD-fed females when compared with NPD and Emb-LPD explants after 24 and 48 h. Moreover, both LPD and Emb-LPD explants showed substantial expansion of TGC area during 24-48 h, not observed in NPD. No difference in invasive capacity was observed between treatments using Matrigel transwell migration assays. At day 17 of gestation, LPD- and Emb-LPD-fed conceptuses displayed smaller placentas and larger fetuses respectively, resulting in increased fetal:placental ratios in both groups compared with NPD conceptuses. Analysis of placental and yolk sac nutrient signalling within the mammalian target of rapamycin complex 1 pathway revealed similar levels of total and phosphorylated downstream targets across groups. These data demonstrate that early post-implantation embryos modify trophoblast phenotype to regulate fetal growth under conditions of poor maternal nutrition.

Published
2015

83. The preimplantation embryo:handle with care

Author

Watkins, Adam J., Papenbrock, Tom, and Fleming, Tom P.

Abstract

The past decade has seen considerable advances in our understanding of intrinsic developmental mechanisms associated with gametogenesis and embryogenesis and accompanying applications in the fields of reproductive medicine, embryonic stem cell biology, and nuclear reprogramming. However, a new focus has recently emerged concerning the homeostatic regulation of embryonic cells, how this is set, and how it may influence the longitudinal progression and optimization of the developmental program and indeed the phenotype of the offspring. Attention has been drawn to the preimplantation stage of development as a sensitive "window" when in vitro and in vivo manipulations, such as culture conditions or maternal diet, may have critical consequences. In this article, we review how changes in environmental conditions, mediated via a range of epigenetic, cellular, and metabolic mechanisms in the preimplantation embryo, may alter the pattern of cell division, gene expression, morphology, and potential. We consider how fetal and postnatal phenotype may become susceptible to the plasticity of the preimplantation embryo and the risks for adult health and physiology.

Published
2008

84. People person.

Author

Fleming, Tom

Abstract

The article reviews the exhibition "Lucian Freud: New Perspectives" at the National Gallery in London, Great Britain from October 1, 2022 to January 22, 2023.

Published
2023

85. The influence of mouse Ped gene expression on postnatal development

Author

Watkins, Adam, Wilkins, Adrian, Osmond, Clive, Warner, Carol M, Comiskey, Martina, Hanson, Mark, and Fleming, Tom P

Subjects
Male, Sex Characteristics, Histocompatibility Antigens Class I, Embryonic Development, Gene Expression Regulation, Developmental, Blood Pressure, Mice, Inbred Strains, Growth, Organ Size, Peptidyl-Dipeptidase A, Cardiovascular Physiological Phenomena, Mice, Integrative, Animals, Birth Weight, Female, Lung
Abstract

The Ped (preimplantation embryo development) gene, whose product is Qa-2 protein, is correlated with a faster rate of preimplantation development (Ped fast phenotype) in mice that express Qa-2 protein compared with mice with an absence of Qa-2 protein (Ped slow phenotype). In the current study, we have used two congenic mouse strains differentially expressing the Ped gene, strain B6.K1 (Ped slow; Qa-2 negative) and strain B6.K2 (Ped fast; Qa-2 positive), to investigate the effects of Ped gene expression on postnatal growth profiles, systolic blood pressure and adult organ allometry. At birth, B6.K1 mice were moderately lighter than B6.K2 mice. B6.K1 mice became heavier during postnatal life (P < 0.05) and had elevated systolic blood pressure at 21 weeks of age when compared with B6.K2 mice (P = 0.006). B6.K1 mice also demonstrated elevated serum angiotensin-converting enzyme (ACE) activity, a known regulator of blood pressure (P = 0.037). Altered organ:body weight ratios were also observed, with the B6.K1 females having a higher ratio for lungs than B6. K2 females (P = 0.014). These data provide evidence of an association between the rate of preimplantation embryo development, postnatal growth and later cardiovascular function.

Published
2005

92. Metabolic induction and early responses of mouse blastocyst developmental programming following maternal low protein diet affecting life-long health

Author

Eckert, Judith J., Porter, Richard, Watkins, Adam J., Burt, Elizabeth, Brooks, Suzanne, Leese, Henry J., Humpherson, Peter G., Cameron, Iain T., Fleming, Tom P., Eckert, Judith J., Porter, Richard, Watkins, Adam J., Burt, Elizabeth, Brooks, Suzanne, Leese, Henry J., Humpherson, Peter G., Cameron, Iain T., and Fleming, Tom P.

Abstract

Previously, we have shown that a maternal low protein diet, fed exclusively during the preimplantation period of mouse development (Emb-LPD), is sufficient to induce by the blastocyst stage a compensatory growth phenotype in late gestation and postnatally, correlating with increased risk of adult onset cardiovascular disease and behavioural dysfunction. Here, we examine mechanisms of induction of maternal Emb-LPD programming and early compensatory responses by the embryo. Emb-LPD induced changes in maternal serum metabolites at the time of blastocyst formation (E3.5), notably reduced insulin and increased glucose, together with reduced levels of free amino acids (AAs) including branched chain AAs leucine, isoleucine and valine. Emb-LPD also caused reduction in the branched chain AAs within uterine fluid at the blastocyst stage. These maternal changes coincided with an altered content of blastocyst AAs and reduced mTORC1 signalling within blastocysts evident in reduced phosphorylation of effector S6 ribosomal protein and its ratio to total S6 protein but no change in effector 4E-BP1 phosphorylated and total pools. These changes were accompanied by increased proliferation of blastocyst trophectoderm and total cells and subsequent increased spreading of trophoblast cells in blastocyst outgrowths. We propose that induction of metabolic programming following Emb-LPD is achieved through mTORC1signalling which acts as a sensor for preimplantation embryos to detect maternal nutrient levels via branched chain AAs and/or insulin availability. Moreover, this induction step associates with changes in extra-embryonic trophectoderm behaviour occurring as early compensatory responses leading to later nutrient recovery.

Published
2012

93. Maternal periconceptional and gestational low protein diet affects mouse offspring growth, cardiovascular and adipose phenotype at 1 year of age

Author

Watkins, Adam J., Lucas, Emma S., Wilkins, Adrian, Cagampang, Felino R.A., Fleming, Tom P., Watkins, Adam J., Lucas, Emma S., Wilkins, Adrian, Cagampang, Felino R.A., and Fleming, Tom P.

Abstract

Human and animal studies have revealed a strong association between periconceptional environmental factors, such as poor maternal diet, and an increased propensity for cardiovascular and metabolic disease in adult offspring. Previously, we reported cardiovascular and physiological effects of maternal low protein diet (LPD) fed during discrete periods of periconceptional development on 6-month-old mouse offspring. Here, we extend the analysis in 1 year aging offspring, evaluating mechanisms regulating growth and adiposity. Isocaloric LPD (9% casein) or normal protein diet (18% casein; NPD) was fed to female MF-1 mice either exclusively during oocyte maturation (for 3.5 days prior to mating; Egg-LPD, Egg-NPD, respectively), throughout gestation (LPD, NPD) or exclusively during preimplantation development (for 3.5 days post mating; Emb-LPD). LPD and Emb-LPD female offspring were significantly lighter and heavier than NPD females respectively for up to 52 weeks. Egg-LPD, LPD and Emb-LPD offspring displayed significantly elevated systolic blood pressure at 52 weeks compared to respective controls (Egg-NPD, NPD). LPD females had significantly reduced inguinal and retroperitoneal fat pad: body weight ratios compared to NPD females. Expression of the insulin receptor (Insr) and insulin-like growth factor I receptor (Igf1r) in retroperitoneal fat was significantly elevated in Emb-LPD females (P&0.05), whilst Emb-LPD males displayed significantly decreased expression of the mitochondrial uncoupling protein 1 (Ucp1) gene compared to NPD offspring. LPD females displayed significantly increased expression of Ucp1 in interscapular brown adipose tissue when compared to NPD offspring. Our results demonstrate that aging offspring body weight, cardiovascular and adiposity homeostasis can be programmed by maternal periconceptional nutrition. These adverse outcomes further exemplify the criticality of dietary behaviour around the time of conception on long-term offspring health.

Published
2011

96. Global, Regional, and National Cancer Incidence, Mortality, Years of Life Lost, Years Lived With Disability, and Disability-Adjusted Life-years for 32 Cancer Groups, 1990 to 2015: A Systematic Analysis for the Global Burden of Disease Study

Author

Fitzmaurice, Christina, Allen, Christine, Barber, Ryan M., Barregard, Lars, Bhutta, Zulfiqar A., Brenner, Hermann, Dicker, Daniel J., Chimed-Orchir, Odgerel, Dandona, Rakhi, Dandona, Lalit, Fleming, Tom, Forouzanfar, Mohammad H., Hancock, Jamie, Hay, Roderick J., Hunter-Merrill, Rachel, Huynh, Chantal, Hosgood, H. Dean, Johnson, Catherine O., Jonas, Jost B., Khubchandani, Jagdish, Kumar, G. Anil, Kutz, Michael, Lan, Qing, Larson, Heidi J., Liang, Xiaofeng, Lim, Stephen S., Lopez, Alan D., MacIntyre, Michael F., Marczak, Laurie, Marquez, Neal, Mokdad, Ali H., Pinho, Christine, Pourmalek, Farshad, Salomon, Joshua A., Sanabria, Juan Ramon, Sandar, Logan, Sartorius, Benn, Schwartz, Stephen M., Shackelford, Katya A., Shibuya, Kenji, Stanaway, Jeff, Steiner, Caitlyn, Sun, Jiandong, Takahashi, Ken, Vollset, Stein Emil, Vos, Theo, Wagner, Joseph A., Wang, Haidong, Westerman, Ronny, Zeeb, Hajo, Zoeckler, Leo, Abd-Allah, Foad, Ahmed, Muktar Beshir, Alabed, Samer, Alam, Noore K., Aldhahri, Saleh Fahed, Alem, Girma, Alemayohu, Mulubirhan Assefa, Ali, Raghib, Al-Raddadi, Rajaa, Amare, Azmeraw, Amoako, Yaw, Artaman, Al, Asayesh, Hamid, Atnafu, Niguse, Awasthi, Ashish, Saleem, Huda Ba, Barac, Aleksandra, Bedi, Neeraj, Bensenor, Isabela, Berhane, Adugnaw, Bernabé, Eduardo, Betsu, Balem, Binagwaho, Agnes, Boneya, Dube, Campos-Nonato, Ismael, Castañeda-Orjuela, Carlos, Catalá-López, Ferrán, Chiang, Peggy, Chibueze, Chioma, Chitheer, Abdulaal, Choi, Jee-Young, Cowie, Benjamin, Damtew, Solomon, das Neves, José, Dey, Suhojit, Dharmaratne, Samath, Dhillon, Preet, Ding, Eric, Driscoll, Tim, Ekwueme, Donatus, Endries, Aman Yesuf, Farvid, Maryam, Farzadfar, Farshad, Fernandes, Joao, Fischer, Florian, G/hiwot, Tsegaye Tewelde, Gebru, Alemseged, Gopalani, Sameer, Hailu, Alemayehu, Horino, Masako, Horita, Nobuyuki, Husseini, Abdullatif, Huybrechts, Inge, Inoue, Manami, Islami, Farhad, Jakovljevic, Mihajlo, James, Spencer, Javanbakht, Mehdi, Jee, Sun Ha, Kasaeian, Amir, Kedir, Muktar Sano, Khader, Yousef S., Khang, Young-Ho, Kim, Daniel, Leigh, James, Linn, Shai, Lunevicius, Raimundas, El Razek, Hassan Magdy Abd, Malekzadeh, Reza, Malta, Deborah Carvalho, Marcenes, Wagner, Markos, Desalegn, Melaku, Yohannes A., Meles, Kidanu G, Mendoza, Walter, Mengiste, Desalegn Tadese, Meretoja, Tuomo J., Miller, Ted R., Mohammad, Karzan Abdulmuhsin, Mohammadi, Alireza, Mohammed, Shafiu, Moradi-Lakeh, Maziar, Nagel, Gabriele, Nand, Devina, Le Nguyen, Quyen, Nolte, Sandra, Ogbo, Felix A., Oladimeji, Kelechi E., Oren, Eyal, Pa, Mahesh, Park, Eun-Kee, Pereira, David M, Plass, Dietrich, Qorbani, Mostafa, Radfar, Amir, Rafay, Anwar, Rahman, Mahfuzar, Rana, Saleem M., Søreide, Kjetil, Satpathy, Maheswar, Sawhney, Monika, Sepanlou, Sadaf G., Shaikh, Masood Ali, She, Jun, Shiue, Ivy, Shore, Hirbo Roba, Shrime, Mark G., So, Samuel, Soneji, Samir, Stathopoulou, Vasiliki, Stroumpoulis, Konstantinos, Sufiyan, Muawiyyah Babale, Sykes, Bryan L., Tabarés-Seisdedos, Rafael, Tadese, Fentaw, Tedla, Bemnet Amare, Tessema, Gizachew Assefa, Thakur, J. S., Tran, Bach Xuan, Ukwaja, Kingsley Nnanna, Uzochukwu, Benjamin S. Chudi, Vlassov, Vasiliy Victorovich, Weiderpass, Elisabete, Wubshet Terefe, Mamo, Yebyo, Henock Gebremedhin, Yimam, Hassen Hamid, Yonemoto, Naohiro, Younis, Mustafa Z., Yu, Chuanhua, Zaidi, Zoubida, Zaki, Maysaa El Sayed, Zenebe, Zerihun Menlkalew, Murray, Christopher J. L., and Naghavi, Mohsen

Abstract

IMPORTANCE: Cancer is the second leading cause of death worldwide. Current estimates on the burden of cancer are needed for cancer control planning. OBJECTIVE: To estimate mortality, incidence, years lived with disability (YLDs), years of life lost (YLLs), and disability-adjusted life-years (DALYs) for 32 cancers in 195 countries and territories from 1990 to 2015. EVIDENCE REVIEW: Cancer mortality was estimated using vital registration system data, cancer registry incidence data (transformed to mortality estimates using separately estimated mortality to incidence [MI] ratios), and verbal autopsy data. Cancer incidence was calculated by dividing mortality estimates through the modeled MI ratios. To calculate cancer prevalence, MI ratios were used to model survival. To calculate YLDs, prevalence estimates were multiplied by disability weights. The YLLs were estimated by multiplying age-specific cancer deaths by the reference life expectancy. DALYs were estimated as the sum of YLDs and YLLs. A sociodemographic index (SDI) was created for each location based on income per capita, educational attainment, and fertility. Countries were categorized by SDI quintiles to summarize results. FINDINGS: In 2015, there were 17.5 million cancer cases worldwide and 8.7 million deaths. Between 2005 and 2015, cancer cases increased by 33%, with population aging contributing 16%, population growth 13%, and changes in age-specific rates contributing 4%. For men, the most common cancer globally was prostate cancer (1.6 million cases). Tracheal, bronchus, and lung cancer was the leading cause of cancer deaths and DALYs in men (1.2 million deaths and 25.9 million DALYs). For women, the most common cancer was breast cancer (2.4 million cases). Breast cancer was also the leading cause of cancer deaths and DALYs for women (523 000 deaths and 15.1 million DALYs). Overall, cancer caused 208.3 million DALYs worldwide in 2015 for both sexes combined.Between 2005 and 2015, age-standardized incidence rates for all cancers combined increased in 174 of 195 countries or territories. Age-standardized death rates (ASDRs) for all cancers combined decreased within that timeframe in 140 of 195 countries or territories. Countries with an increase in the ASDR due to all cancers were largely located on the African continent.Of all cancers, deaths between 2005 and 2015 decreased significantly for Hodgkin lymphoma (−6.1% [95% uncertainty interval (UI), −10.6% to −1.3%]). The number of deaths also decreased for esophageal cancer, stomach cancer, and chronic myeloid leukemia, although these results were not statistically significant. CONCLUSION AND RELEVANCE: As part of the epidemiological transition, cancer incidence is expected to increase in the future, further straining limited health care resources. Appropriate allocation of resources for cancer prevention, early diagnosis, and curative and palliative care requires detailed knowledge of the local burden of cancer. The GBD 2015 study results demonstrate that progress is possible in the war against cancer. However, the major findings also highlight an unmet need for cancer prevention efforts, including tobacco control, vaccination, and the promotion of physical activity and a healthy diet.

Published
2017
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