Pub Date : 2000-12-01DOI: 10.1097/00008469-200012000-00002
F. Levi, C. la Vecchia, P. Boyle
{"title":"The rise and fall of prostate cancer.","authors":"F. Levi, C. la Vecchia, P. Boyle","doi":"10.1097/00008469-200012000-00002","DOIUrl":"https://doi.org/10.1097/00008469-200012000-00002","url":null,"abstract":"","PeriodicalId":11950,"journal":{"name":"European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2000-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75101807","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2000-12-01DOI: 10.1097/00008469-200012000-00001
M J Hill
{"title":"Tobacco and cancer.","authors":"M J Hill","doi":"10.1097/00008469-200012000-00001","DOIUrl":"10.1097/00008469-200012000-00001","url":null,"abstract":"","PeriodicalId":11950,"journal":{"name":"European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2000-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1097/00008469-200012000-00001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87294719","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2000-06-01DOI: 10.1097/00008469-200006000-00004
L. Signorello, H. Kuper, P. Lagiou, J. Wuu, L. Mucci, D. Trichopoulos, H. Adami
Insulin-like growth factor 1 (IGF-1) is a potentially important determinant of disease; hence epidemiological identification of factors that influence circulating IGF-1 is merited. We therefore analysed data collected in Greece to determine the relationship between anthropometric, lifestyle and dietary variables and serum levels of IGF-1 among elderly men. We identified 51 men with prostate cancer, 50 men with benign prostatic hyperplasia, and 52 apparently healthy elderly men (controls), all matched for age (+/- 1 year). These 153 men provided blood specimens and were interviewed using a validated lifestyle and food frequency questionnaire. We performed multivariate linear regression to identify potential predictors of circulating IGF-1. After controlling for age, body mass index, smoking habits, alcohol drinking and coffee consumption, each 5 cm increase in height predicted a 13.0% increase in IGF-1 (95% CI 0.4-27.2%) among the controls and a 11.3% increase in IGF-1 (95% CI 4.5-18.6%) among the entire study group. None of the investigated dietary factors (total fat, carbohydrate, protein, dairy products, tomatoes, calcium) were strongly related to IGF-1 levels. The positive association between IGF-1 and height integrates the empirical evidence linking IGF-1 and height with prostate cancer risk.
胰岛素样生长因子1 (IGF-1)是疾病的潜在重要决定因素;因此，有必要对影响循环IGF-1的因素进行流行病学鉴定。因此，我们分析了在希腊收集的数据，以确定老年男性中人体测量、生活方式和饮食变量与血清IGF-1水平之间的关系。我们确定了51名前列腺癌男性，50名良性前列腺增生男性和52名明显健康的老年男性(对照组)，所有年龄匹配(±1岁)。这153名男性提供了血液样本，并使用有效的生活方式和食物频率问卷进行了访谈。我们采用多元线性回归来确定循环IGF-1的潜在预测因子。在控制了年龄、体重指数、吸烟习惯、饮酒和喝咖啡等因素后，身高每增加5厘米，对照组中IGF-1水平增加13.0% (95% CI 0.4-27.2%)，整个研究组中IGF-1水平增加11.3% (95% CI 4.5-18.6%)。所有被调查的饮食因素(总脂肪、碳水化合物、蛋白质、乳制品、西红柿、钙)都与IGF-1水平没有密切关系。IGF-1和身高之间的正相关整合了将IGF-1和身高与前列腺癌风险联系起来的经验证据。
{"title":"Lifestyle factors and insulin-like growth factor 1 levels among elderly men.","authors":"L. Signorello, H. Kuper, P. Lagiou, J. Wuu, L. Mucci, D. Trichopoulos, H. Adami","doi":"10.1097/00008469-200006000-00004","DOIUrl":"https://doi.org/10.1097/00008469-200006000-00004","url":null,"abstract":"Insulin-like growth factor 1 (IGF-1) is a potentially important determinant of disease; hence epidemiological identification of factors that influence circulating IGF-1 is merited. We therefore analysed data collected in Greece to determine the relationship between anthropometric, lifestyle and dietary variables and serum levels of IGF-1 among elderly men. We identified 51 men with prostate cancer, 50 men with benign prostatic hyperplasia, and 52 apparently healthy elderly men (controls), all matched for age (+/- 1 year). These 153 men provided blood specimens and were interviewed using a validated lifestyle and food frequency questionnaire. We performed multivariate linear regression to identify potential predictors of circulating IGF-1. After controlling for age, body mass index, smoking habits, alcohol drinking and coffee consumption, each 5 cm increase in height predicted a 13.0% increase in IGF-1 (95% CI 0.4-27.2%) among the controls and a 11.3% increase in IGF-1 (95% CI 4.5-18.6%) among the entire study group. None of the investigated dietary factors (total fat, carbohydrate, protein, dairy products, tomatoes, calcium) were strongly related to IGF-1 levels. The positive association between IGF-1 and height integrates the empirical evidence linking IGF-1 and height with prostate cancer risk.","PeriodicalId":11950,"journal":{"name":"European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2000-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75043640","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2000-06-01DOI: 10.1097/00008469-200006000-00008
K. Almendingen, B. Hofstad, K. Trygg, G. Hoff, A. Hussain, M. Vatn
A positive association between tobacco and colorectal adenomas has been suggested. Smoking is, however, also associated with 'poor' dietary habits, which in turn may be related to risk of adenomas. It is therefore of interest to study the relationship between smoking, diet and risk of colorectal adenomas in follow-up studies. We compared 87 adenoma cases to 35 'hospital' and 35 healthy controls (all controls were age- and sex-matched and proven to be free of adenomas). Smoking data were collected by an interview and a self-administrated questionnaire with a time interval of at least one month. After 3 years of follow-up, all polyps were removed. Our data indicate that smoking is associated with adenoma prevalence, but not necessarily with size, multiplicity, growth or recurrence of adenomas. Compared to both sets of controls, cases reported to have smoked more than 15 pack-years, or who are current smokers, had a fourfold increased frequency of adenomas (odds ratios 3.6-5.9). Smokers with adenomas had dietary habits that may also be associated with adenomas. The smoking estimates remained largely unchanged even after adjustments for dietary variables in multivariate analysis. This study lends support to the theory of an initiating role of tobacco smoke in neoplasia formation.
{"title":"Smoking and colorectal adenomas: a case-control study.","authors":"K. Almendingen, B. Hofstad, K. Trygg, G. Hoff, A. Hussain, M. Vatn","doi":"10.1097/00008469-200006000-00008","DOIUrl":"https://doi.org/10.1097/00008469-200006000-00008","url":null,"abstract":"A positive association between tobacco and colorectal adenomas has been suggested. Smoking is, however, also associated with 'poor' dietary habits, which in turn may be related to risk of adenomas. It is therefore of interest to study the relationship between smoking, diet and risk of colorectal adenomas in follow-up studies. We compared 87 adenoma cases to 35 'hospital' and 35 healthy controls (all controls were age- and sex-matched and proven to be free of adenomas). Smoking data were collected by an interview and a self-administrated questionnaire with a time interval of at least one month. After 3 years of follow-up, all polyps were removed. Our data indicate that smoking is associated with adenoma prevalence, but not necessarily with size, multiplicity, growth or recurrence of adenomas. Compared to both sets of controls, cases reported to have smoked more than 15 pack-years, or who are current smokers, had a fourfold increased frequency of adenomas (odds ratios 3.6-5.9). Smokers with adenomas had dietary habits that may also be associated with adenomas. The smoking estimates remained largely unchanged even after adjustments for dietary variables in multivariate analysis. This study lends support to the theory of an initiating role of tobacco smoke in neoplasia formation.","PeriodicalId":11950,"journal":{"name":"European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2000-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86991390","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2000-01-01DOI: 10.1097/00008469-200006000-00005
C. la Vecchia, A. Decarli, J. Peto, F. Levi, F. Tomei, E. Negri
Death certification data from pleural cancer in eight European countries providing data to the World Health Organization database over the period 1970-1994 were analysed using a log-linear Poisson model to disentangle the effects of age, birth cohort and period of death. The age effect reached values between 10 and 15/100,000 males at age 80-84 in most countries, except Hungary (6.7), Switzerland (18.0), France (20.6) and the Netherlands (36.5). Cohort effects were steadily and appreciably upwards in all countries up to the generations born in 1940 or 1945, and levelled off for the 1950 cohort, except in Hungary, where persistent rises were observed. Thus, most rises in pleural cancer mortality in Europe were on a cohort of birth basis. Since most pleural cases were asbestos-related mesotheliomas, and since asbestos has an early-stage effect on subsequent mesothelioma risk, exposure early in life is important for determining the subsequent mesothelioma risk of each generation. Consequently, the data indicate that the peak mortality from pleural cancer in most western European countries will be reached in the first decades of the 21st century, i.e. around 2010-2020, when the generations born between 1940 and 1950 will reach the peak age for mesothelioma incidence and mortality. This contrasts with US data, where the peak of pleural cancer incidence has been reached at the end of the 20th century, and reflects a delay in adopting adequate prevention measures since the 1940-1945 generations entered the workforce in the 1960s, when cancer risk from asbestos exposure was already recognized.
{"title":"An age, period and cohort analysis of pleural cancer mortality in Europe.","authors":"C. la Vecchia, A. Decarli, J. Peto, F. Levi, F. Tomei, E. Negri","doi":"10.1097/00008469-200006000-00005","DOIUrl":"https://doi.org/10.1097/00008469-200006000-00005","url":null,"abstract":"Death certification data from pleural cancer in eight European countries providing data to the World Health Organization database over the period 1970-1994 were analysed using a log-linear Poisson model to disentangle the effects of age, birth cohort and period of death. The age effect reached values between 10 and 15/100,000 males at age 80-84 in most countries, except Hungary (6.7), Switzerland (18.0), France (20.6) and the Netherlands (36.5). Cohort effects were steadily and appreciably upwards in all countries up to the generations born in 1940 or 1945, and levelled off for the 1950 cohort, except in Hungary, where persistent rises were observed. Thus, most rises in pleural cancer mortality in Europe were on a cohort of birth basis. Since most pleural cases were asbestos-related mesotheliomas, and since asbestos has an early-stage effect on subsequent mesothelioma risk, exposure early in life is important for determining the subsequent mesothelioma risk of each generation. Consequently, the data indicate that the peak mortality from pleural cancer in most western European countries will be reached in the first decades of the 21st century, i.e. around 2010-2020, when the generations born between 1940 and 1950 will reach the peak age for mesothelioma incidence and mortality. This contrasts with US data, where the peak of pleural cancer incidence has been reached at the end of the 20th century, and reflects a delay in adopting adequate prevention measures since the 1940-1945 generations entered the workforce in the 1960s, when cancer risk from asbestos exposure was already recognized.","PeriodicalId":11950,"journal":{"name":"European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2000-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77748777","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1999-12-01DOI: 10.1097/00008469-199912001-00002
C. Bonithon‐Kopp, A M Benhamiche
The knowledge of descriptive epidemiology of colorectal cancer is a prerequisite essential to a better understanding of the aetiology of the disease and the development of prevention strategies. This work provides an update of descriptive epidemiological data on colorectal cancer incidence in the world. In 1988-1992, incidence rates of colorectal cancer varied from 15- to 25-fold according to the geographical area. The highest rates were observed in Western countries, especially in North America, Australasia and, to a lesser extent, in northern and western Europe. The geographical distribution of colorectal cancer was similar in men and women. An examination of incidence data by subsites showed that the magnitude of geographical variations was more important for colon cancer than for rectal cancer. Contrasting with the male predominance for rectal cancer and, to a lesser degree, for left colon cancer, cancers of the right colon were found to be as frequent in women as in men. Examination of time trends during the last decades reveals a sharp increase in incidence of colorectal cancer in Japan and in eastern and southern Europe. On the other hand, incidence rates show some stagnation in North America and western Europe in recent years. In fact, there are some suggestions for differential time trends according to the anatomical subsite, with a recent proximal shift in the distribution of cancers of the large bowel in Western countries. In conclusion, descriptive epidemiological data support the notion that distinct pathogenic mechanisms may be involved in the carcinogenesis of the proximal and distal bowel.
{"title":"Are there several colorectal cancers? Epidemiological data.","authors":"C. Bonithon‐Kopp, A M Benhamiche","doi":"10.1097/00008469-199912001-00002","DOIUrl":"https://doi.org/10.1097/00008469-199912001-00002","url":null,"abstract":"The knowledge of descriptive epidemiology of colorectal cancer is a prerequisite essential to a better understanding of the aetiology of the disease and the development of prevention strategies. This work provides an update of descriptive epidemiological data on colorectal cancer incidence in the world. In 1988-1992, incidence rates of colorectal cancer varied from 15- to 25-fold according to the geographical area. The highest rates were observed in Western countries, especially in North America, Australasia and, to a lesser extent, in northern and western Europe. The geographical distribution of colorectal cancer was similar in men and women. An examination of incidence data by subsites showed that the magnitude of geographical variations was more important for colon cancer than for rectal cancer. Contrasting with the male predominance for rectal cancer and, to a lesser degree, for left colon cancer, cancers of the right colon were found to be as frequent in women as in men. Examination of time trends during the last decades reveals a sharp increase in incidence of colorectal cancer in Japan and in eastern and southern Europe. On the other hand, incidence rates show some stagnation in North America and western Europe in recent years. In fact, there are some suggestions for differential time trends according to the anatomical subsite, with a recent proximal shift in the distribution of cancers of the large bowel in Western countries. In conclusion, descriptive epidemiological data support the notion that distinct pathogenic mechanisms may be involved in the carcinogenesis of the proximal and distal bowel.","PeriodicalId":11950,"journal":{"name":"European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1999-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79491477","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1999-12-01DOI: 10.1097/00008469-199912001-00012
B. Glinghammar, J. Rafter
At last, inroads are beginning to be made into the hitherto unknown and complex area of gene-environment interactions in the colon. Interestingly, many of the studies to date would suggest: that the Apc gene is a target for such interactions; that luminal factors can regulate the level of cellular proteins of central importance in the control of cell growth/arrest; and that some of the newly discovered members of the nuclear hormone receptor superfamily may be mediating gene-environment interactions in the colon. This is a very exciting area and will presumably be the subject of intense research in the near future. By characterizing the dietary/luminal factors that interact with the genes implicated in tumour development in the colon, we will reach another level of certainty regarding the dietary components responsible for tumour formation and their underlying mechanisms. It is gratifying to see at last the fields of epidemiology and molecular biology begin to overlap, and without doubt results from this new area of research will give a new and better status to the field of making dietary recommendations to decrease the risk of developing colorectal cancer.
{"title":"Carcinogenesis in the colon: interaction between luminal factors and genetic factors.","authors":"B. Glinghammar, J. Rafter","doi":"10.1097/00008469-199912001-00012","DOIUrl":"https://doi.org/10.1097/00008469-199912001-00012","url":null,"abstract":"At last, inroads are beginning to be made into the hitherto unknown and complex area of gene-environment interactions in the colon. Interestingly, many of the studies to date would suggest: that the Apc gene is a target for such interactions; that luminal factors can regulate the level of cellular proteins of central importance in the control of cell growth/arrest; and that some of the newly discovered members of the nuclear hormone receptor superfamily may be mediating gene-environment interactions in the colon. This is a very exciting area and will presumably be the subject of intense research in the near future. By characterizing the dietary/luminal factors that interact with the genes implicated in tumour development in the colon, we will reach another level of certainty regarding the dietary components responsible for tumour formation and their underlying mechanisms. It is gratifying to see at last the fields of epidemiology and molecular biology begin to overlap, and without doubt results from this new area of research will give a new and better status to the field of making dietary recommendations to decrease the risk of developing colorectal cancer.","PeriodicalId":11950,"journal":{"name":"European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1999-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82329764","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1999-12-01DOI: 10.1097/00008469-199912001-00008
Silvia Franceschi
Several uncertainties remain with respect to the role of intake of fat and/or total energy in the aetiology of cancer of the colon-rectum. Between 1992 and 1996, 1953 subjects with cancer of the colon-rectum (median age = 62 years) and 4154 hospital controls were interviewed in six Italian areas. The validated food-frequency questionnaire included questions on 78 foods and recipes, and specific questions on individual fat intake pattern. Significant trends of increasing colorectal cancer risk with increasing intake emerged for bread and pasta, cakes and desserts, and refined sugar. Most vegetables, including pulses, were inversely associated with cancer of the colon and rectum. High fruit intake was associated only with a reduction of rectal cancer. Total energy intake was directly associated with colorectal cancer risk. Among macronutrients, a high intake of starch and saturated fat seemed to lead to an increased risk of cancer. High intakes of polyunsaturated fatty acids (chiefly derived from olive oil and seed oils) showed a marginal inverse association with colorectal cancer risk. Among micronutrients, beta-carotene, vitamin E and calcium showed the most consistent inverse associations. An excess of energy intake, particularly from refined bread and pasta, can be an unfavourable feature of the Mediterranean diet with respect to colorectal cancer risk, especially in the presence of sedentary life.
{"title":"Nutrients and food groups and large bowel cancer in Europe.","authors":"Silvia Franceschi","doi":"10.1097/00008469-199912001-00008","DOIUrl":"https://doi.org/10.1097/00008469-199912001-00008","url":null,"abstract":"Several uncertainties remain with respect to the role of intake of fat and/or total energy in the aetiology of cancer of the colon-rectum. Between 1992 and 1996, 1953 subjects with cancer of the colon-rectum (median age = 62 years) and 4154 hospital controls were interviewed in six Italian areas. The validated food-frequency questionnaire included questions on 78 foods and recipes, and specific questions on individual fat intake pattern. Significant trends of increasing colorectal cancer risk with increasing intake emerged for bread and pasta, cakes and desserts, and refined sugar. Most vegetables, including pulses, were inversely associated with cancer of the colon and rectum. High fruit intake was associated only with a reduction of rectal cancer. Total energy intake was directly associated with colorectal cancer risk. Among macronutrients, a high intake of starch and saturated fat seemed to lead to an increased risk of cancer. High intakes of polyunsaturated fatty acids (chiefly derived from olive oil and seed oils) showed a marginal inverse association with colorectal cancer risk. Among micronutrients, beta-carotene, vitamin E and calcium showed the most consistent inverse associations. An excess of energy intake, particularly from refined bread and pasta, can be an unfavourable feature of the Mediterranean diet with respect to colorectal cancer risk, especially in the presence of sedentary life.","PeriodicalId":11950,"journal":{"name":"European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1999-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76512984","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1999-12-01DOI: 10.1097/00008469-199912001-00013
M. Hill
There is consistent and strong evidence that a high risk of colorectal cancer is associated with obesity and with a low intake of vegetables, of whole grain cereals and of fish. Many other food groups or nutrients have been associated with this cancer, but the evidence for them is inconsistent and therefore untenable. Vegetables contain a wide range of protective agents that protect against cancer at many other sites as well as the large bowel. The same is true of whole grain cereals; these can also protect against colorectal cancer by mechanisms specific to the large bowel. Fish are rich in n-3 polyunsaturated fatty acids that are thought to protect the colon against malignancy via the prostaglandin pathway. Overweight is the result of an excess of energy intake over energy output, and there is good evidence to suggest that overweight might be a surrogate measure of lack of exercise.
{"title":"Mechanisms of diet and colon carcinogenesis.","authors":"M. Hill","doi":"10.1097/00008469-199912001-00013","DOIUrl":"https://doi.org/10.1097/00008469-199912001-00013","url":null,"abstract":"There is consistent and strong evidence that a high risk of colorectal cancer is associated with obesity and with a low intake of vegetables, of whole grain cereals and of fish. Many other food groups or nutrients have been associated with this cancer, but the evidence for them is inconsistent and therefore untenable. Vegetables contain a wide range of protective agents that protect against cancer at many other sites as well as the large bowel. The same is true of whole grain cereals; these can also protect against colorectal cancer by mechanisms specific to the large bowel. Fish are rich in n-3 polyunsaturated fatty acids that are thought to protect the colon against malignancy via the prostaglandin pathway. Overweight is the result of an excess of energy intake over energy output, and there is good evidence to suggest that overweight might be a surrogate measure of lack of exercise.","PeriodicalId":11950,"journal":{"name":"European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1999-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81113289","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1999-12-01DOI: 10.1097/00008469-199912001-00007
Pierre Laurent-Puig, H. Bons, P. Cugnenc
Intensive screening for genetic alteration in colorectal cancer led to the identification of two types of colorectal tumours that are distinct by their carcinogenesis processes. The first group, named LOH (for loss of heterozygosity)-positive, is characterized by hyperploidy and allelic losses involving preferentially chromosome 18q and chromosome 17p. More than two-thirds of colorectal cancers belong to this group. The second group, called multiple microsatellite loci (MSI)-positive cancers, is characterized by genetic instability at microsatellite loci. Although colorectal cancer cells are characterized by specific microsatellite alterations, the same four different signalling pathways, WNT/Wingless pathway, K-ras pathway, transforming growth factor (TGF)beta pathway and p53 pathway, could be implicated in tumour progression. The WNT/Wingless pathway could be altered in two different ways according to whether the cancer cells belong to the group of LOH-positive or MSI-positive tumours. LOH-positive tumours activate the WNT/Wingless signalling pathway through an adenomatous polyposis coli (APC) mutation, whereas the MSI-positive tumours activate this pathway through a beta-catenin stabilizing mutation. Beta-catenin and APC mutations were observed as early as the adenomatous stage of colorectal neoplasia. In TGFbeta pathways LOH-positive tumours inactivated SMAD2 (similar to mother against decapentaplegic drosophilia) or SMAD4, whereas in MSI-positive tumours the TGFbeta type II receptor is frequently deleted. Alteration of these genes correlated closely with the progression of the adenoma to cancer. In the p53 pathway LOH-positive tumours showed frequent p53 mutation, whereas MSI-positive tumours demonstrated BAX (BCL-2-associated X protein)-inactivating mutation. These alterations contribute to the adenoma-carcinoma transition.
{"title":"Sequence of molecular genetic events in colorectal tumorigenesis.","authors":"Pierre Laurent-Puig, H. Bons, P. Cugnenc","doi":"10.1097/00008469-199912001-00007","DOIUrl":"https://doi.org/10.1097/00008469-199912001-00007","url":null,"abstract":"Intensive screening for genetic alteration in colorectal cancer led to the identification of two types of colorectal tumours that are distinct by their carcinogenesis processes. The first group, named LOH (for loss of heterozygosity)-positive, is characterized by hyperploidy and allelic losses involving preferentially chromosome 18q and chromosome 17p. More than two-thirds of colorectal cancers belong to this group. The second group, called multiple microsatellite loci (MSI)-positive cancers, is characterized by genetic instability at microsatellite loci. Although colorectal cancer cells are characterized by specific microsatellite alterations, the same four different signalling pathways, WNT/Wingless pathway, K-ras pathway, transforming growth factor (TGF)beta pathway and p53 pathway, could be implicated in tumour progression. The WNT/Wingless pathway could be altered in two different ways according to whether the cancer cells belong to the group of LOH-positive or MSI-positive tumours. LOH-positive tumours activate the WNT/Wingless signalling pathway through an adenomatous polyposis coli (APC) mutation, whereas the MSI-positive tumours activate this pathway through a beta-catenin stabilizing mutation. Beta-catenin and APC mutations were observed as early as the adenomatous stage of colorectal neoplasia. In TGFbeta pathways LOH-positive tumours inactivated SMAD2 (similar to mother against decapentaplegic drosophilia) or SMAD4, whereas in MSI-positive tumours the TGFbeta type II receptor is frequently deleted. Alteration of these genes correlated closely with the progression of the adenoma to cancer. In the p53 pathway LOH-positive tumours showed frequent p53 mutation, whereas MSI-positive tumours demonstrated BAX (BCL-2-associated X protein)-inactivating mutation. These alterations contribute to the adenoma-carcinoma transition.","PeriodicalId":11950,"journal":{"name":"European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1999-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86976199","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
京公网安备 11010802042870号
京ICP备2023020795号-1
扫码关注我们
求助内容：
应助结果提醒方式：