Pub Date : 2002-08-01DOI: 10.1097/00008469-200208000-00012
A. McKinlay, E. Breitbart, U. Ringborg, R. Greinert
{"title":"'Children under the Sun'-- UV radiation and children's skin. WHO Workshop -- Children's sun protection education.","authors":"A. McKinlay, E. Breitbart, U. Ringborg, R. Greinert","doi":"10.1097/00008469-200208000-00012","DOIUrl":"https://doi.org/10.1097/00008469-200208000-00012","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":"2002-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81651191","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 : 2002-06-01DOI: 10.1097/00008469-200206000-00001
M. Hill
{"title":"The changing spectrum of gastroesophageal cancer.","authors":"M. Hill","doi":"10.1097/00008469-200206000-00001","DOIUrl":"https://doi.org/10.1097/00008469-200206000-00001","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":"2002-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80708620","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 : 2002-06-01DOI: 10.1097/00008469-200206000-00002
M. Mignogna, S. Fedele, L. Lo Russo, E. Ruoppo, L. Lo Muzio
Oropharyngeal cancer is estimated to be the ninth most common cancer worldwide. Its prognosis is largely dependent upon tumour-stage at the time of diagnosis. Stage I and II oropharyngeal cancers are characterized by a 5-year survival rate ranging from 70% to 90%, and the management of these early carcinomas is usually of short duration, easy and very cost-effective. On the other hand, the diagnostic evaluation, treatment and management of complications and recurrences of advanced stage oral tumours (stage III and IV) are often very long, complex and costly. They also have very poor prognosis with survival figures dropping to about 20%. Nowadays, most oropharyngeal cancers are detected at a late stage with an overall 5-year survival rate of around 45-50%, and with a conspicuous increase in treatment costs and a worsening of prognosis. Even if formal and comprehensive cost-effectiveness and cost-benefit analyses are not currently available in the oropharyngeal cancer literature, it seems clear that, in the care of these patients, the enormous consumption of resources is not associated with acceptable outcomes. New initiatives should be evaluated, planned and developed for the care of patients with oral and pharyngeal cancer. These strategies should be directed at prevention and early diagnosis in order to increase patient survival and quality of life and decrease the consumption of health care resources.
{"title":"Costs and effectiveness in the care of patients with oral and pharyngeal cancer: analysis of a paradox.","authors":"M. Mignogna, S. Fedele, L. Lo Russo, E. Ruoppo, L. Lo Muzio","doi":"10.1097/00008469-200206000-00002","DOIUrl":"https://doi.org/10.1097/00008469-200206000-00002","url":null,"abstract":"Oropharyngeal cancer is estimated to be the ninth most common cancer worldwide. Its prognosis is largely dependent upon tumour-stage at the time of diagnosis. Stage I and II oropharyngeal cancers are characterized by a 5-year survival rate ranging from 70% to 90%, and the management of these early carcinomas is usually of short duration, easy and very cost-effective. On the other hand, the diagnostic evaluation, treatment and management of complications and recurrences of advanced stage oral tumours (stage III and IV) are often very long, complex and costly. They also have very poor prognosis with survival figures dropping to about 20%. Nowadays, most oropharyngeal cancers are detected at a late stage with an overall 5-year survival rate of around 45-50%, and with a conspicuous increase in treatment costs and a worsening of prognosis. Even if formal and comprehensive cost-effectiveness and cost-benefit analyses are not currently available in the oropharyngeal cancer literature, it seems clear that, in the care of these patients, the enormous consumption of resources is not associated with acceptable outcomes. New initiatives should be evaluated, planned and developed for the care of patients with oral and pharyngeal cancer. These strategies should be directed at prevention and early diagnosis in order to increase patient survival and quality of life and decrease the consumption of health care resources.","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":"2002-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88738356","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 : 2002-04-01DOI: 10.1097/00008469-200204000-00013
B. Berra, I. Colombo, E. Sottocornola, A. Giacosa
Sphingolipids are widespread membrane components that are found in all eukaryotic cells. They consist of a long chain sphingoid-base, usually sphingosine, which is acylated at the 2-amino position, forming a ceramide. All together, sphingolipids may represent the most structurally diverse category of lipids in nature. There is no known nutritional requirement for sphingolipids. Nonetheless, studies with experimental animals have shown that consumption of sphingolipids inhibits colon carcinogenesis, reduces serum low-density lipoprotein cholesterol and elevates high-density lipoproteins, which suggest that they are 'functional' components of food. In animal models (CF1 mice) sphingomyelin supplementation reduces the number of aberrant colonic crypt foci by approximately 70% and, with longer feeding, reduces the number of colonic adenocarcinomas. A possible mechanism of action of sphingolipids in suppressing colon carcinogenesis is that exogenously supplied sphingolipids bypass a sphingolipid signalling defect that is important in cancer (for example, a loss of cellular sphingomyelin turnover to produce ceramide and sphingosine). Indirect evidence suggests that sphingolipids can inhibit colon cancer in humans: sphingosine and ceramide induce apoptosis in a human adenocarcinoma cell line and feeding sphingolipids to Min mice reduces the number of colon tumours.
{"title":"Dietary sphingolipids in colorectal cancer prevention.","authors":"B. Berra, I. Colombo, E. Sottocornola, A. Giacosa","doi":"10.1097/00008469-200204000-00013","DOIUrl":"https://doi.org/10.1097/00008469-200204000-00013","url":null,"abstract":"Sphingolipids are widespread membrane components that are found in all eukaryotic cells. They consist of a long chain sphingoid-base, usually sphingosine, which is acylated at the 2-amino position, forming a ceramide. All together, sphingolipids may represent the most structurally diverse category of lipids in nature. There is no known nutritional requirement for sphingolipids. Nonetheless, studies with experimental animals have shown that consumption of sphingolipids inhibits colon carcinogenesis, reduces serum low-density lipoprotein cholesterol and elevates high-density lipoproteins, which suggest that they are 'functional' components of food. In animal models (CF1 mice) sphingomyelin supplementation reduces the number of aberrant colonic crypt foci by approximately 70% and, with longer feeding, reduces the number of colonic adenocarcinomas. A possible mechanism of action of sphingolipids in suppressing colon carcinogenesis is that exogenously supplied sphingolipids bypass a sphingolipid signalling defect that is important in cancer (for example, a loss of cellular sphingomyelin turnover to produce ceramide and sphingosine). Indirect evidence suggests that sphingolipids can inhibit colon cancer in humans: sphingosine and ceramide induce apoptosis in a human adenocarcinoma cell line and feeding sphingolipids to Min mice reduces the number of colon tumours.","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":"2002-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81441856","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 : 2002-04-01DOI: 10.1097/00008469-200204000-00015
L. Ovesen
{"title":"But baby, it's cold outside.","authors":"L. Ovesen","doi":"10.1097/00008469-200204000-00015","DOIUrl":"https://doi.org/10.1097/00008469-200204000-00015","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":"2002-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86710578","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 : 2002-04-01DOI: 10.1097/00008469-200204000-00002
C. L. Vecchia, A. Tavani
H2-receptor antagonists have been widely used since the late 1970s for the treatment of gastrointestinal ulcers and other benign conditions of the stomach, oesophagus and duodenum. Several case reports suggested that long-term therapy with H2-receptor antagonists, mainly cimetidine and ranitidine, might increase the risk of gastric cancer. After early case reports, at least six analytical epidemiological studies (two cohort and four case-control) were published, including a total of about 1000 cases of gastric cancer. The relative risks (RR) were systematically and substantially elevated in the first year since starting H2-receptor antagonist use, and levelled off in the following years. Some excess risk was still apparent during the first 5 years of drug use, probably due to incorrect diagnosis and treatment of pre-existing neoplastic gastric lesions, but the estimated RR was not above unity for > or = 10 years since starting drug treatment in the two studies including information on long-term use. The findings of analytical epidemiological studies are thus consistent with the absence of a causal association between H2-receptor antagonist use and gastric cancer risk. Data on oesophageal and colorectal cancer do not support a relevant relation between cimetidine use and the risk of these neoplasms. With reference to total cancer mortality, in a Danish cohort study, for males the RR was 1.9 in the first year, and 1.4 in the first 5 years; corresponding values for females were 1.7 and 1.5. In a British cohort study, the RR was 3.4 in the first year, and 1.3 in the years 2-10. The excess risk in the first year was essentially due to gastric cancer. Post-marketing surveillance data for omeprazole and other proton pump inhibitors are much scantier than for H2-receptor antagonists, particularly on long-term use.
{"title":"A review of epidemiological studies on cancer in relation to the use of anti-ulcer drugs.","authors":"C. L. Vecchia, A. Tavani","doi":"10.1097/00008469-200204000-00002","DOIUrl":"https://doi.org/10.1097/00008469-200204000-00002","url":null,"abstract":"H2-receptor antagonists have been widely used since the late 1970s for the treatment of gastrointestinal ulcers and other benign conditions of the stomach, oesophagus and duodenum. Several case reports suggested that long-term therapy with H2-receptor antagonists, mainly cimetidine and ranitidine, might increase the risk of gastric cancer. After early case reports, at least six analytical epidemiological studies (two cohort and four case-control) were published, including a total of about 1000 cases of gastric cancer. The relative risks (RR) were systematically and substantially elevated in the first year since starting H2-receptor antagonist use, and levelled off in the following years. Some excess risk was still apparent during the first 5 years of drug use, probably due to incorrect diagnosis and treatment of pre-existing neoplastic gastric lesions, but the estimated RR was not above unity for > or = 10 years since starting drug treatment in the two studies including information on long-term use. The findings of analytical epidemiological studies are thus consistent with the absence of a causal association between H2-receptor antagonist use and gastric cancer risk. Data on oesophageal and colorectal cancer do not support a relevant relation between cimetidine use and the risk of these neoplasms. With reference to total cancer mortality, in a Danish cohort study, for males the RR was 1.9 in the first year, and 1.4 in the first 5 years; corresponding values for females were 1.7 and 1.5. In a British cohort study, the RR was 3.4 in the first year, and 1.3 in the years 2-10. The excess risk in the first year was essentially due to gastric cancer. Post-marketing surveillance data for omeprazole and other proton pump inhibitors are much scantier than for H2-receptor antagonists, particularly on long-term use.","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":"2002-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74226525","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 : 2002-04-01DOI: 10.1097/00008469-200204000-00001
C. la Vecchia, S. Franceschi
{"title":"Progestogen-only contraceptives and cancer risk.","authors":"C. la Vecchia, S. Franceschi","doi":"10.1097/00008469-200204000-00001","DOIUrl":"https://doi.org/10.1097/00008469-200204000-00001","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":"2002-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86468577","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 : 2002-02-01DOI: 10.1097/00008469-200202000-00011
C. Bonaïti‐pellié
Most diseases arise through the joint action of genetic susceptibilities and environmental factors. This is particularly true for cancers in which both types of factors have already been identified or strongly suspected. There may, however, be other as yet unidentified factors. Recent advances in molecular genetics will make it easier to study the gene– environment interactions in these diseases. Synergism (i.e. assessment of whether the effect of the genotype on risk is modified by the exposure level or whether the effect of exposure on risk is modified by the genotype) has important scientific and public health implications. Indeed, it could help to elucidate the mechanisms underlying these interactions and to evaluate the risks for individuals. The definition of interaction is dependent on a model and on how the effects are measured. When the effects are measured in terms of relative risks of disease, which is usually the case, interaction means that the joint effects of genetic and environmental factors cannot simply be multiplied. There are a number of potential situations: (1) a genetic factor and an environmental factor have already been evidenced and the aim is to specify their joint effect; (2) some genetic and environmental factors are only suspected of playing a role in the aetiology of the disease and some kind of interaction is thought to be hiding the main effects, which could be overcome by taking it into account; and (3) oblivious to potential causes, a search is made for a large number of factors in the hope of being lucky enough to find something. In the case of gene–nutrient interactions, all these situations are applicable. Although some genetic factors (Bonaı̈ti-Pellié, 1999; Olschwang, 1999) and the role of some nutritional factors (Franceschi, 1999; Giacosa et al., 1999) have already been identified, several uncertainties remain and there are numerous inconsistencies across studies on possible interactions between these factors (Little and Faivre, 1999). The objective of this paper is to review some available methods for evidencing genetic factors and assessing gene–environment interactions, to compare their respective advantages and limitations, and to consider the possible applications to the study of gene–nutrient interactions in colorectal cancer.
大多数疾病是遗传易感性和环境因素共同作用的结果。对于已经确定或强烈怀疑这两种因素的癌症来说尤其如此。然而，可能还有其他尚未查明的因素。分子遗传学的最新进展将使研究这些疾病的基因-环境相互作用变得更加容易。协同作用(即评估基因型对风险的影响是否因暴露水平而改变，或暴露对风险的影响是否因基因型而改变)具有重要的科学和公共卫生意义。事实上，它可以帮助阐明这些相互作用的机制，并评估个人的风险。相互作用的定义取决于模型和如何测量影响。当以疾病的相对风险来衡量这些影响时(通常是这种情况)，相互作用意味着遗传和环境因素的共同影响不能简单地成倍增加。有几种可能的情况:(1)遗传因素和环境因素已经得到证实，目的是确定它们的共同作用;(2)一些遗传因素和环境因素在疾病的病因学中只被怀疑起作用，而某种相互作用被认为隐藏了主要影响，通过考虑这些因素可以克服这些影响;(3)忽略潜在的原因，对大量的因素进行搜索，希望幸运地找到一些东西。在基因-营养相互作用的情况下，所有这些情况都适用。虽然一些遗传因素(bonavia ti- pelli， 1999;Olschwang, 1999)和一些营养因素的作用(Franceschi, 1999;Giacosa et al.， 1999)已经确定，仍然存在一些不确定性，并且在这些因素之间可能的相互作用的研究中存在许多不一致的地方(Little和Faivre, 1999)。本文的目的是综述一些现有的证据遗传因素和评估基因-环境相互作用的方法，比较它们各自的优点和局限性，并考虑可能的应用研究基因-营养相互作用在结直肠癌。
{"title":"Methodological aspects of investigating gene-nutrient interactions.","authors":"C. Bonaïti‐pellié","doi":"10.1097/00008469-200202000-00011","DOIUrl":"https://doi.org/10.1097/00008469-200202000-00011","url":null,"abstract":"Most diseases arise through the joint action of genetic susceptibilities and environmental factors. This is particularly true for cancers in which both types of factors have already been identified or strongly suspected. There may, however, be other as yet unidentified factors. Recent advances in molecular genetics will make it easier to study the gene– environment interactions in these diseases. Synergism (i.e. assessment of whether the effect of the genotype on risk is modified by the exposure level or whether the effect of exposure on risk is modified by the genotype) has important scientific and public health implications. Indeed, it could help to elucidate the mechanisms underlying these interactions and to evaluate the risks for individuals. The definition of interaction is dependent on a model and on how the effects are measured. When the effects are measured in terms of relative risks of disease, which is usually the case, interaction means that the joint effects of genetic and environmental factors cannot simply be multiplied. There are a number of potential situations: (1) a genetic factor and an environmental factor have already been evidenced and the aim is to specify their joint effect; (2) some genetic and environmental factors are only suspected of playing a role in the aetiology of the disease and some kind of interaction is thought to be hiding the main effects, which could be overcome by taking it into account; and (3) oblivious to potential causes, a search is made for a large number of factors in the hope of being lucky enough to find something. In the case of gene–nutrient interactions, all these situations are applicable. Although some genetic factors (Bonaı̈ti-Pellié, 1999; Olschwang, 1999) and the role of some nutritional factors (Franceschi, 1999; Giacosa et al., 1999) have already been identified, several uncertainties remain and there are numerous inconsistencies across studies on possible interactions between these factors (Little and Faivre, 1999). The objective of this paper is to review some available methods for evidencing genetic factors and assessing gene–environment interactions, to compare their respective advantages and limitations, and to consider the possible applications to the study of gene–nutrient interactions in 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":"2002-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81117436","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 : 2002-02-01DOI: 10.1097/00008469-200202000-00001
M. Hill
{"title":"Vegetables, fruits, fibre and colorectal cancer.","authors":"M. Hill","doi":"10.1097/00008469-200202000-00001","DOIUrl":"https://doi.org/10.1097/00008469-200202000-00001","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":"2002-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87650418","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 : 2002-02-01DOI: 10.1097/00008469-200202000-00015
N. Haites
IntroductionDNA for studying gene–nutrient or other interactions and for testing hypotheses relating to the causes of human diseases can be obtained from a wide range of tissue types. The main limitation to obtaining DNA is, in fact, the availability of tissue, which can affect the number of cases a
{"title":"Sources of DNA for studying gene-nutrition interactions.","authors":"N. Haites","doi":"10.1097/00008469-200202000-00015","DOIUrl":"https://doi.org/10.1097/00008469-200202000-00015","url":null,"abstract":"IntroductionDNA for studying gene–nutrient or other interactions and for testing hypotheses relating to the causes of human diseases can be obtained from a wide range of tissue types. The main limitation to obtaining DNA is, in fact, the availability of tissue, which can affect the number of cases a","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":"2002-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80990189","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}
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