Global burden of cancer.
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Biomedical subjects
Publications and source records attributed to P Boyle.
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Cigarette smoking has been clearly and unambiguously identified as a direct cause of cancers of the oral cavity, oesophagus, stomach, pancreas, larynx, lung, bladder, kidney and leukaemia, especially acute myeloid leukaemia. Additionally, cigarette smoking is a direct cause of ischaemic heart disease (the commonest cause of death in western countries), respiratory heart disease, aortic aneurysm, chronic obstructive lung disease, stroke, pneumonia and cirrhosis and cancer of the liver. Cigarette smoking can kill in 24 different ways and, although smoking protects against several fatal and non-fatal conditions, the adverse effect of smoking on health is largely negative. In developed countries as a whole, tobacco is responsible for 24% of all male deaths and 7% of all female deaths: these figures rise to over 40% in men in some countries of central and eastern Europe and to 17% in women in the United States. The average loss of life of smokers is 8 years. Among United Kingdom doctors followed for 40 years, overall death rates in middle age were about three times higher among doctors who smoked cigarettes as among doctors who had never smoked regularly. About half of all regular cigarette smokers will eventually be killed by their habit. The important information is that it is never too late to stop smoking: among United Kingdom doctors who stopped smoking, even in middle age, there was a substantial improvement in life expectancy. World-wide, smoking is killing three million people each year and this figure is increasing. In most countries the worst is yet to come, since by the time the young smokers of today reach middle or old age there will be about 10 million deaths/year from tobacco. Approximately 500 million individuals alive today can expect to be killed by tobacco, 250 million of these deaths will occur in middle age. Tobacco is already the biggest cause of adult death in developed countries. Over the next few decades tobacco could well become the biggest cause of adult death in the world. For men in developed countries, the full effects of smoking can already be seen. Tobacco now causes one-third of all male deaths in middle age (plus one fifth in old age). Tobacco is a cause of about half of all male cancer deaths in middle age (plus one-third in old age). Of those who start smoking in their teenage years and keep on smoking, about half will be killed by tobacco. Half of these deaths will be in middle age (35-69) and each will lose an average of 20-25 years of non-smoker life expectancy. In non-smokers in many countries, cancer mortality is decreasing slowly and total mortality rapidly. The war against cancer is being won slowly: the effects of cigarette smoking are holding back this victory. Lung cancer now kills more women in the United States each year than breast cancer. For women in developed countries, the peak of the tobacco epidemic has not yet arrived. Tobacco now causes almost one-third of all deaths in women in middle age in the United States. Although it has only 5% of the world's female population, the United States has 50% of the world's deaths from smoking in women. Tobacco smoking is a major cause of premature death. Throughout Europe, in 1990 tobacco smoking caused three quarters of a million deaths in middle age (between 35 and 69). In the Member States of the European Union in 1990 there were over one quarter of a million deaths in middle age directly caused by tobacco smoking: there were 219700 in men and 31900 in women. There were many more deaths caused by tobacco at older ages. In countries of central and eastern Europe, including the former USSR, there were 441200 deaths in middle age in men and 42100 deaths in women. There is a need for urgent action to help contain this important and unnecessary loss of life. In formulating Recommendations, the European Cancer Experts Consensus Committee recognised that Tobacco Control depends on various parts of society and not only on the individual.
A rapid increase of female breast cancer has been reported in many areas of the world and the reasons are not fully understood. While some have attributed the increase to the increasing detection of early stage breast cancer through mammography screening, few studies have directly examined the time trend of in situ breast cancer specifically. This study included all incident cases of female breast carcinoma in situ reported to the Connecticut Tumor Registry between 1973 and 1992. The age-adjusted incidence rates and age-specific incidence rates were calculated by histology and by race. The age-adjusted incidence rates were standardised to the 1970 United States standard million population. The study found that the overall age-adjusted incidence rate of in situ breast cancer has increased dramatically, from 3.53/100000 in 1973-1975 to 17.51/100000 in 1991-1992. The increase was not uniform during the past two decades of cancer registration. In fact, most of the observed rise has occurred since the early 1980s. This increase was found in both Caucasians and Blacks. The results by histology indicate that the dramatic increase in carcinoma in situ is mostly attributable to an increase in ductal carcinoma in situ. The increase was also observed in all age groups 40 years and over. These results are consistent with the use pattern and the reported effect of mammography screening. Therefore, these results are qualitatively consistent with the idea that mammography screening is largely responsible for the recent upsurge in female breast cancer incidence in this population. The study also found that the age group 40-49 years in whites experienced a rapid increase in incidence that began in the same time period as the older age groups, but it has since levelled off. The potential impact of the highly publicized debate regarding the efficacy of mammography in this age group in recent years is discussed.
Recent studies indicate that cancer of the tongue is increasing rapidly among the younger population in many parts of the world. Few studies, however, have directly examined the risk factors for the disease. A case-control study was conducted in Beijing, China to investigate risk factors for tongue cancer. A total of 111 cases and 111 controls aged 20-80 years were included in this study. The results show that risk of tongue cancer is significantly elevated among ex-smokers (OR = 2.24, 95% CI = 1.09-4.62) and among current smokers (OR = 2.73, 95% CI = 1.26-5.91). The risk increases with increasing tobacco consumption, as reflected by both cigarette equivalents smoked per day and lifetime pack-years of tobacco smoking. Quitting smoking was associated with a reduction of the risk of tongue cancer. The numbers of cases in the study, however, is small, preventing further analyses during the years after quitting smoking. Overall, alcohol drinking was not found to be significantly associated with the risk of tongue cancer in this study (OR = 1.20, 95% CI = 0.58-2.50 for current drinkers). However, a marginally significant association was found for those who drank spirits at least 5 days a week (OR = 2.34, 95% CI = 0.90-6.06). A suggestion of effect modification for smoking and alcohol drinking was observed in this study.
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BACKGROUND: Psoralens are potent tanning activators that have been introduced in France and in Belgium in some tanning lotions and sunscreens. It was shown that poor tanners who ever used psoralen tanning activators display a four-fold increase in melanoma risk when compared to poor tanners using regular sunscreens. Although psoralens have now banned from suntan lotions, it is likely that the increase in melanoma risk linked to their previous use will persist for several years. METHODS: The melanoma risk attributable to psoralens use was calculated to evaluate the population at risk in France and Belgium. RESULTS: Melanoma incidence for the year 1995 was estimated to be of 10.2 per 100,000 in France and of 10.0 per 100,000 in Belgium, representing 5,900 and 1,000 melanoma cases. From the melanoma incidence among poor tanner who ever used psoralens (52 per 100,000) and estimation of the percentage of psoralen users among poor tanners, it can be derived that, for the year 1995, 267 melanoma cases could be attributed to psoralen tanning activators. CONCLUSIONS: Subjects who used psoralen suntan activators should be informed of their increased melanoma risk and be encouraged to participate in clinical programmes for early detection of melanoma, more especially when they are poor tanners and display a high naevi count. Such an action could save a significant number of lives.
The interpretation of time trends in disease rates can be facilitated using estimable contrasts from age-period-cohort models. Cohort and period trends in breast cancer incidence and mortality rates in Scotland were investigated using contrasts that measure the changes in the linear trends. These contrasts were compared with estimates obtained from mortality rates in the USA and Japan. A significant moderation of both breast cancer incidence and mortality rates was observed in Scotland, associated with cohorts of women born after the Second World War compared with women born between the two world wars. The moderation of breast cancer mortality among cohorts born after 1925 compared with cohorts born before 1925 that was observed in the USA and Japan was also observed in this study. This moderation is not present in the incidence rates. The relative decline in the risk of breast cancer seen in younger cohorts seems to be contradictory to the temporal pattern present among breast cancer risk factors. It may well be that the alteration of eating patterns as a result of rationing in the wartime and immediate post-war period, and the subsequent influence on certain breast cancer risk factors probably produced by such changes, may have had some influence on the development of healthier girls and women. Such speculation could be addressed in a well-designed epidemiological study. There have been no changes in the mortality rate trends with period in Scotland, although the changes in the incidence rate trends with period are consistent with an increase in registration coverage.
BACKGROUND: Recent studies indicate that cancers of the salivary gland are increasing, and the factors responsible for the increase are unknown. Artefactual changes, such as shift in classifying cancers of the floor of the mouth to cancers of the salivary gland, could affect the time trend for salivary gland cancer. METHODS: The current study examined the time trends for cancers of the salivary gland and for cancers of the floor of the mouth and lower gum by using Connecticut Tumor Registry data for the time period 1935-1992. A regression model was used to identify the components of birth cohort, period and age as determinants of the observed time trend. RESULTS: Cancers of the salivary gland have recently increased in Connecticut, with a relative risk of 1.48 (95% CI: 1.06-2.08) for females in 1990-1992 compared to 1980-1984, and a comparable relative risk of 1.60 (95% CI: 1.16-2.22) for males. The increase was found in all age groups 40 and over, particularly among those aged 70 and over. The results from age-period-cohort modelling show a recent upturn in the trend for period slopes, with no clear increase from recent birth cohorts, which is consistent with the results from univariate analyses suggesting no clear increase among those under 40 years of age. CONCLUSION: Our results suggest that artifactual changes, such as a shift in designation of cancer sites, increasing use of the needle aspirate biopsies, and greater access to medical care for the elderly, may have largely contributed to the rising trend. The known risk factors, radiation exposure and a history of a prior cancer, can hardly explain the observed increase. The Epstein-Barr virus infection has only been associated with certain types of rare squamous cell carcinomas of the salivary gland in the Eskimo population. The AIDS epidemic also cannot explain why older age groups have accounted for most of the increase in incidence of the disease. An examination of the incidence rates for cancers of the salivary gland from other populations may help to clarify the issue.
BACKGROUND: Epidemiological studies of rare events, which are common in the medical literature, often involve modeling sparse data sets. Assessing the fit of these models may be complicated by the large numbers of observed zeros in the data set. METHODS: Poisson models, fitted as generalized linear models, were used to investigate the referral patterns of patients suffering from end-stage renal failure in south west Wales. The usual method for assessing the goodness of fit is to compare the deviance with a chi 2 distribution with appropriate degrees of freedom. However, this test may be invalid when the data set is sparse, as the deviance values may be unusually low compared to the degrees of freedom. This would suggest that there is a problem with underdispersion when, in fact, the large numbers of zeros in the data set make the comparison with the chi 2 distribution unreliable. A simulation approach is advocated as an alternative method of assessing model fit in these situations. RESULTS: Three models are considered in detail here. The first modelled the total referrals in each of the 245 wards in the study area and included two explanatory variables. These observations were not unusually sparse and both the chi 2 goodness of fit test and the simulation methodology outlined here suggested that the model did not fit. The second model included the population 'at risk' as an offset and the model improved considerably. Both the chi 2 test and the simulation approach suggested that this model did fit. Finally, the data were disaggregated into five age groups providing 1225 observations and a very sparse data set. According to the chi 2 goodness of fit test, the deviance was very low suggesting that the model was underdispersed. Using simulated data, it was shown that the deviance was not unusually low and that the model fitted the data reasonably well. CONCLUSION: In cases where the data set being modelled is sparse, it is useful to test the goodness of fit of a Poisson model using a simulation approach, rather than relying on the chi 2 test.
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Questionnaires to evaluate symptoms and quality of life are being increasingly used in urology. It is, however, important that these questionnaires show equivalence when they are used in international, collaborative studies. Precise linguistic and cultural validation should greatly increase their compatibility in different population and cultural groups. Indeed, recent progress in the validation of symptom scores, such as the International Prostate Symptom Score (I-PSS), has helped international comparability in epidemiology and clinical trials. The management of benign prostatic hyperplasia (BPH) increasingly focuses on quality of life and the development of a successful BPH-specific quality-of-life questionnaire is an important advance in the study of BPH. The nine-item BPH-specific quality-of-life scale is currently undergoing linguistic and cultural validation and appears to be satisfactory for extensive use in different cultures.
For human B lymphocytes, Epstein-Barr virus (EBV) is a polyclonal activator, inducing both proliferation and Ig secretion. It is also a transforming virus capable of generating immortalized B cell lines. These early and late functions of EBV are not apparently connected. The receptor for EBV, CD21, also serves as a receptor for some complement components and is called CR2. This molecule associates with CD19 and TAPA-1 on the surface of B cells. This complex is involved in signaling B cells and participates in many responses. We have observed that simultaneous ligation of CD40 and the CD21 complex, by exposure to anti-CD40 MAbs and EBV, enhances both the short-term proliferation as well as the long-term transformation rate of human B lymphocytes. B cell proliferation shows synergy between anti-CD40 MAb and EBV. CD19 also appears to be involved in the synergistic activation of B cells through CD40 and CD21, since ligation of CD19 with anti-CD19 MAbs, either prior to or concomitant with exposure to anti-CD40 and EBV, markedly inhibits both proliferation and subsequent B cell transformation. These observations do not elucidate the mechanisms of B cell transformation employed by EBV but the do suggest a relationship between early proliferation and later transformation induced by the virus. Anti-CD40 enhances both these effects and anti-CD19 is capable of inhibiting both.
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Tumour cells in malignant melanomas express molecules associated with tumour progression; however, up until now, no marker has been able to identify the tumour cells from which metastases are derived. It has recently been shown that in human melanoma cell lines, populations expressing peanut agglutinin (PNA)-binding glycoproteins are able to generate metastases, and that such cells do exist in primary human melanomas, their presence being associated with the degree of local invasion that governs the metastasis risk. To further investigate the correlation between the expression of PNA-binding glycoconjugates by cells from primary melanomas and the patient's individual risk of recurrence or metastasis, a molecular epidemiological approach employing histochemical techniques within a case-control design was developed. The main objective of this study is to determine whether an histochemical staining with the lectin PNA of cells in the primary lesion is associated with an increased risk of local recurrence of metastasis, and with survival, independently of Breslow's tumour thickness. The study comprises the comparison of the PNA labelling index and of the type and intratumour location of the staining as a function of clinical outcome in two matched series of patients with known clinical outcome: patients who had died at 5 years and patients alive at 5 years (to assess association with survival), and patients who experienced a recurrence within the first 5 years and patients alive without recurrence at 5 years (to assess association with risk of recurrence). A matched case-control design was used with a variable number of controls matched to each case. Apart from age (+/-5 years), sex and centre where diagnosis was made, matching was made on histogenetic type and primary tumour thickness (four categories being considered: <0.75, 0.76-1.5, 1.51-3 and >3 mm).
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The European Code Against Cancer is a set of ten recommendations which, if followed, can be the best measure that an individual can take to avoid developing and dying from cancer. Primary and secondary prevention are considered as an important part of cancer control if their use is rational, based on scientific evidence. Six recommendations have to do with primary prevention (smoking, alcohol, diet, overweight, sun exposure, industrial carcinogens), two with secondary prevention, preferably consisting in organized screening programmes (uterine cervix, breast), and two with early diagnosis based on initial symptoms. Considering that smoking is the most important single cause of cancer in Europe tobacco control should be a priority. It is never too late to stop smoking: stopping even in middle age, prior to the onset of tobacco related illness, has a beneficial effect on life expectancy. If the entire population of Europe were to follow these guidelines a minimum of 40% reduction in cancer incidence and an even greater decrease in mortality could be achieved. The revised recommendations are the result of an agreement following 6-year experience of initially practising the original rules, comments and views of cancer experts throughout Europe; they were approved by the European Community Cancer Experts at their meeting in Bonn on 28-29 November 1994. Comprehension and implementation of these principles is of importance both for medical professionals and the general population of all European countries, in particular for members and candidates of the European Union, including the Czech Republic.