The global burden of cancer continues to increase largely because of the aging and growth of the world population alongside an increasing adoption of cancer-causing behaviors, particularly smoking, in economically developing countries. Based on the GLOBOCAN 2008 estimates, about 12.7 million cancer cases and 7.6 million cancer deaths are estimated to have occurred in 2008; of these, 56% of the cases and 64% of the deaths occurred in the economically developing world. Breast cancer is the most frequently diagnosed cancer and the leading cause of cancer death among females, accounting for 23% of the total cancer cases and 14% of the cancer deaths. Lung cancer is the leading cancer site in males, comprising 17% of the total new cancer cases and 23% of the total cancer deaths. Breast cancer is now also the leading cause of cancer death among females in economically developing countries, a shift from the previous decade during which the most common cause of cancer death was cervical cancer. Further, the mortality burden for lung cancer among females in developing countries is as high as the burden for cervical cancer, with each accounting for 11% of the total female cancer deaths. Although overall cancer incidence rates in the developing world are half those seen in the developed world in both sexes, the overall cancer mortality rates are generally similar. Cancer survival tends to be poorer in developing countries, most likely because of a combination of a late stage at diagnosis and limited access to timely and standard treatment. A substantial proportion of the worldwide burden of cancer could be prevented through the application of existing cancer control knowledge and by implementing programs for tobacco control, vaccination (for liver and cervical cancers), and early detection and treatment, as well as public health campaigns promoting physical activity and a healthier dietary intake. Clinicians, public health professionals, and policy makers can play an active role in accelerating the application of such interventions globally.

/pdf/global-cancer-statistics-49zjx478re.pdf

Global cancer statistics

Cancer constitutes an enormous burden on society in more and less economically developed countries alike. The occurrence of cancer is increasing because of the growth and aging of the population, as well as an increasing prevalence of established risk factors such as smoking, overweight, physical inactivity, and changing reproductive patterns associated with urbanization and economic development. Based on GLOBOCAN estimates, about 14.1 million new cancer cases and 8.2 million deaths occurred in 2012 worldwide. Over the years, the burden has shifted to less developed countries, which currently account for about 57% of cases and 65% of cancer deaths worldwide. Lung cancer is the leading cause of cancer death among males in both more and less developed countries, and has surpassed breast cancer as the leading cause of cancer death among females in more developed countries; breast cancer remains the leading cause of cancer death among females in less developed countries. Other leading causes of cancer death in more developed countries include colorectal cancer among males and females and prostate cancer among males. In less developed countries, liver and stomach cancer among males and cervical cancer among females are also leading causes of cancer death. Although incidence rates for all cancers combined are nearly twice as high in more developed than in less developed countries in both males and females, mortality rates are only 8% to 15% higher in more developed countries. This disparity reflects regional differences in the mix of cancers, which is affected by risk factors and detection practices, and/or the availability of treatment. Risk factors associated with the leading causes of cancer death include tobacco use (lung, colorectal, stomach, and liver cancer), overweight/obesity and physical inactivity (breast and colorectal cancer), and infection (liver, stomach, and cervical cancer). A substantial portion of cancer cases and deaths could be prevented by broadly applying effective prevention measures, such as tobacco control, vaccination, and the use of early detection tests.

/pdf/global-cancer-statistics-2012-18pecqxl5v.pdf

Global cancer statistics, 2012

Most medical researchers, whether clinical or non-clinical, receive some background in statistics as undergraduates. However, it is most often brief, a long time ago, and largely forgotten by the time it is needed. Furthermore, many introductory texts fall short of adequately explaining the underlying concepts of statistics, and often are divorced from the reality of conducting and assessing medical research.

Practical Statistics for Medical Research is a problem-based text for medical researchers, medical students, and others in the medical arena who need to use statistics but have no specialized mathematics background. 

The author draws on twenty years of experience as a consulting medical statistician to provide clear explanations to key statistical concepts, with a firm emphasis on practical aspects of designing and analyzing medical research. The text gives special attention to the presentation and interpretation of results and the many real problems that arise in medical research

/pdf/practical-statistics-for-medical-research-1ijulrzqv3.pdf

Practical statistics for medical research

Viral hepatitis in all its forms is a major public health problem throughout the world, affecting several hundreds of millions of people. Viral hepatitis is a cause of considerable morbidity and mortality both from acute infection and chronic sequelae which include, in the case of hepatitis B, C and D, chronic active hepatitis and cirrhosis. Hepatocellular carcinoma, which is one of the 10 commonest cancers worldwide, is closely associated with hepatitis B and, at least in some regions of the world, with hepatitis C virus. This timely monograph is a distillation of knowledge of hepatitis B, C and D, based on a review of 1000 studies by a small group of scientists. (It is interesting to note in passing that some 5000 papers on viral hepatitis are published annually in the world literature.) The epidemiological, clinical and experimental data on the association between infection with hepatitis B virus and primary liver cancer in humans are reviewed in a readable and succinct format. The available information on hepatitis C and progression to chronic infection is also evaluated and it is concluded (perhaps a little prematurely) that hepatitis C virus is carcinogenic. However, it is concluded that hepatitis D virus, an unusual virus with a number of similarities to certain plant viral satellites and viroids, cannot be classified as a human carcinogen. There are some minor criticisms: there are few illustrations and some complex tabulations (for example, Table 6) and no subject index. A cumulative cross index to IARC Monographs is of little value and occupies nearly 30 pages. This small volume is a useful addition to the overwhelming literature on viral hepatitis, and the presentation is similar to the excellent World Health Organisation Technical Reports series on the subject published in the past. It is strongly recommended as a readable up-to-date summary of a complex subject; and at a cost of 65 Sw.fr (approximately £34) is excellent value. A J ZUCKERMAN

https://jcp.bmj.com/content/jclinpath/48/7/691.1.full.pdf

IARC Monographs on the Evaluation of Carcinogenic Risks to Humans

Mutations in the evolutionarily conserved codons of the p53 tumor suppressor gene are common in diverse types of human cancer. The p53 mutational spectrum differs among cancers of the colon, lung, esophagus, breast, liver, brain, reticuloendothelial tissues, and hemopoietic tissues. Analysis of these mutations can provide clues to the etiology of these diverse tumors and to the function of specific regions of p53. Transitions predominate in colon, brain, and lymphoid malignancies, whereas G:C to T:A transversions are the most frequent substitutions observed in cancers of the lung and liver. Mutations at A:T base pairs are seen more frequently in esophageal carcinomas than in other solid tumors. Most transitions in colorectal carcinomas, brain tumors, leukemias, and lymphomas are at CpG dinucleotide mutational hot spots. G to T transversions in lung, breast, and esophageal carcinomas are dispersed among numerous codons. In liver tumors in persons from geographic areas in which both aflatoxin B1 and hepatitis B virus are cancer risk factors, most mutations are at one nucleotide pair of codon 249. These differences may reflect the etiological contributions of both exogenous and endogenous factors to human carcinogenesis.

https://zenodo.org/record/1230948/files/article.pdf

p53 mutations in human cancers

In a large matched population-based case-control study of acute myelogenous leukemia (AML), we did not find incident AML in Los Angeles County (1987-1994) to be associated with previous exposure to electric blankets, electrically heated waterbeds, or occupations with presumed high exposure to electromagnetic fields.

Adult onset acute myelogenous leukemia and electromagnetic fields in Los Angeles County: bed-heating and occupational exposures.

Members of prepaid health plans are often considered a group for which complete histories of exposure to medically-related risk factors are known. In a population-based case-control study of radiography as a risk factor for acute myelogenous leukemia, extensive retrospective exposure data from an average of 71% of subjects' health care providers were collected. It was determined that at least 21% of prepaid health plan members received diagnostic imaging procedures outside of their plans over the 10-y period of interest and that these "outside" procedures constituted 43% of their total red bone marrow dose from all radiographic imaging. Procedures significantly more likely to have been received outside of prepaid health plans were conventional spine x rays (p = 0.004) and coronary angiograms (p < 0.0001). All "outside" coronary angiograms and 50% of "outside" spine x rays were received at hospitals. Epidemiologic studies that restrict exposure to that received within prepaid health plans may miss a substantial portion of exposure, resulting in underestimated risk estimates and a loss of statistical power.

The potential impact of incomplete radiography histories in epidemiologic studies that rely on prepaid health plan records.

Processed meats and risk of

In recently published results from a Canadian case–control study on lifestyle factors and risk of adult leukemia, Kasim et al. reported a significantly increased risk of acute myeloid leukemia (AML) associated with cigarette smoking, based on 307 AML cases [1]. Specifically, they observed an odds ratio (OR) of 1.4 [95% confidence interval (CI) = 1.1, 1.8] for current smokers compared to neversmokers and positive trends relating smoking status (never, ex, current) and total pack-years of smoking with AML risk. Smoking was not associated with other forms of adult leukemia (acute lymphoid, chronic myeloid, chronic lymphoid, hairy cell). In a case–control study of AML conducted in Los Angeles, California, we observed increased risks associated with smoking that were particularly strong for French–American–British (FAB) subtype M2; OR for ‘ever smoked’ was 1.2 (CI = 0.9, 1.6) among all cases and 2.3 (CI = 1.1, 4.4) among M2 cases [2]. Among all cases, we observed weak evidence of dose-response. However, among M2 cases we observed significant doseresponse for total number of years smoked, average cigarettes/day, and type of product smoked (filtered versus non-filtered). In general, results were stronger for older cases (‡60 years). We hypothesized that the age effect may be due to decreased ability to repair DNA damage in older subjects, higher exposure levels among older subjects due to smoking habits that differed from those of younger subjects, and long latency for the smoking effect

Smoking and risk of acute myeloid leukemia in adults.

Using BEIR V risk estimates and age-specific population dose estimates, we estimate that approximately 12% of leukemias may be attributable to diagnostic x-rays. Earlier estimates were markedly lower (< or = 1%) because of their use of earlier risk coefficients, different dose rate effectiveness factors, and, in one case, a methodological error.

Risk of leukemia caused by diagnostic x-rays.

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