The relationship between body mass index (BMI) at different ages and subsequent endometrial-cancer risk was investigated in a multicentre case-control study conducted between 1988 and 1991 in Vaud, Switzerland, and Northern Italy on 272 histologically confirmed incident cases of endometrial cancer and 571 controls admitted to hospital for acute, non-neoplastic conditions, unrelated to known or potential risk factors for endometrial cancer. The risk of endometrial cancer increased with increasing BMI in the 3rd decade of age (20 to 29 years), in the 5th decade (40 to 49 years) and in the 7th decade (60 to 69 years), although the risk estimates tended to be substantially higher at older ages: compared with women whose BMI (kg m-2) was less than 20, the relative risks (RR) were 1.8 for BMI greater than or equal to 25 at age 20 to 29, 2.7 for BMI greater than or equal to 30 at age 40 to 49 and 3.8 at age 60 to 69. All the trends in risk were significant, except that for BMI at age 25 after allowance for current BMI. When data were examined in separate strata of current BMI, among women of normal body mass at diagnosis no significant effect of past overweight was observed. In contrast, among subjects over-weight at diagnosis, there were significant direct relationships with BMI at ages 20 to 29 and 40 to 49. To reduce endometrial cancer risk, it is therefore important to avoid obesity in later middle and older age, and the benefit can be even greater for women who were overweight at younger age.

The relationships between age at first birth, parity, and the risk of ovarian cancer were evaluated in a case-control study of 272 women with histologically confirmed epithelial ovarian cancer and 544 age-matched controls with a spectrum of acute conditions unrelated to any of the established or potential risk factors for ovarian cancer. Late age at first birth was associated with increased risk: Compared to women who first had a child before the age of 22 years, the relative risks (RR) for those who first gave birth at ages 22-24, 25-27, and 28 or more were 2.7, 3.2, and 4.0, respectively. Nulliparous women showed increased RR (3.9) comparable to the RR among women who first bore a child at age 25 or more, regardless of the number of births. The elevated risk associated with later age at first birth was not accounted for by low parity. The risk of ovarian cancer, as expected, increased with decreasing parity: RR estimates for women having 5 or more, 3 or 4, and 1 or 2 children and for nulliparae were 1.0, 1.7, 1.9, and 2.6, respectively. However, the inverse association between parity and ovarian cancer could be accounted for largely by the importance of age at first birth, because when adjustment was made for that variable, the RR for 3 or 4 and 1 or 2 children decreased to 1.3 and 1.2, respectively. Thus the results of the present study show a strong independent effect of age at first birth on the risk of epithelial ovarian cancer, whereas the association with parity can be explained largely or totally in terms of a high correlation between total parity and age at first birth. The pattern of ovarian cancer risk that emerges from this study, therefore, is similar to the epidemiology of breast cancer. General evidence on this issue from various other studies, however, is rather controversial, and similar analysis of other data-sets would be useful.

Between November 1981 and March 1983, data were collected to evaluate risk factors for benign breast lesions in a case-control study based on 288 women with histologically proven benign breast disease, admitted for biopsy to the Tumor Institute of Milan, and 285 age-matched controls. Questions were asked about menstrual and reproductive characteristics, marital status, education, history of various diseases, and lifetime use of oral contraceptives and other hormonal treatments. Nulliparity or low parity, late age at first birth, and late menopause were associated with an increased risk of benign breast disease. The elevated risk associated with late age at first birth was not accounted for by parity. Early age at menarche was associated with an increased risk, but the estimate was not statistically significant. The data do not suggest that the use of oral contraceptives or other female hormones (such as estrogen replacement therapy) is related to the risk of benign breast disease. Risk was apparently lower, however, among current and long-term oral contraceptive users. There was no evidence of a trend with reference to body mass index. The present data indicate a substantial agreement between the risk factors for (pathologically confirmed) benign and malignant breast disease, not only directly, by showing a relationship with parity, age at first birth, and age at menopause, but also indirectly, by failing to produce evidence that greater weight or the use of oral contraceptives has a protective effect.

Progestins have become normal medical practice in the treatment of endometrial carcinoma. An accurate review of the literature on the subject, involving about 1500 treated cases since 1951, reveals that a positive response is obtained in about 30% of cases. However, authors differ greatly as to the kind of progestin to be administered, and especially as to the dosage, which can go from 0.2 to 5.6 gr. According to the authors of this article great importance must be given to plasmatic levels and to the analysis of hormonal receptors before deciding on the type of therapy. Results from their personal observations of 45 cases show that some patients would benefit more from progestin thersapy, and others from traditional chemothersapy.

Research Articles| September 29 2008 Bakterien aus der Klebsiella- (Friedländer-) Gruppe als Erreger einer Pseudodysenterie in Gemeinschaft mit einer croupösen Pneumonie Subject Area: Further Areas , Oncology , Pathology and Cell Biology J. Kahler J. Kahler (Aus dem Pathologischen Institut der Universität München) Search for other works by this author on: This Site PubMed Google Scholar Schweizerische Zeitschrift für allgemeine Pathologie und Bakteriologie (1951) 14 (6): 684–691. https://doi.org/10.1159/000160038 Article history Published Online: September 29 2008 Content Tools Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn Email Tools Icon Tools Get Permissions Cite Icon Cite Search Site Citation J. Kahler; Bakterien aus der Klebsiella- (Friedländer-) Gruppe als Erreger einer Pseudodysenterie in Gemeinschaft mit einer croupösen Pneumonie. Schweizerische Zeitschrift für allgemeine Pathologie und Bakteriologie 1 June 1951; 14 (6): 684–691. https://doi.org/10.1159/000160038 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsSchweizerische Zeitschrift für allgemeine Pathologie und Bakteriologie Search Advanced Search Article PDF first page preview Close Modal This content is only available via PDF. 1951Copyright / Drug Dosage / DisclaimerCopyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements. You do not currently have access to this content.

Despite a small elevation in RR for lung cancer among MMVF production workers, the lack of excess risk among end users, the absence of any dose-risk relation, the likelihood of detection bias, and the potential for residual confounding by smoking and asbestos exposure argue against a carcinogenic effect of MMVF, RW, or GW at this time. Similar conclusions apply to HN cancer risk among workers exposed to MMVF.

In order to provide a more precise quantification of the association between alcohol consumption and pancreatic cancer risk, we performed a meta-analysis of relevant dose-risk results. We conducted a PubMed search of all case-control (N=21) and cohort (N=11) studies published up to March 2009. We computed summary relative risk (RR) estimates using either fixed- or, in the presence of heterogeneity, random-effects models. The pooled RR was 0.92 (95% confidence interval, 95% CI, 0.86-0.97) for <3 drinks/day and 1.22 (95% CI, 1.12-1.34) for > or = 3 drinks/day. The increased risk for heavy drinking was similar in women and men, but apparently stronger in cohort studies (RR=1.29), in studies with high quality index (RR=1.30), and did not appear to be explained by residual confounding by either history of pancreatitis or tobacco smoking. This meta-analysis provides strong evidence for the absence of a role of moderate drinking in pancreatic carcinogenesis, coupled to an increased risk for heavy alcohol drinking. Given the moderate increase in risk and the low prevalence of heavy drinkers in most populations, alcohol appears to be responsible only for a small fraction of all pancreatic cancers.

In an Italian case-control study of oral cancer, number of missing teeth and other aspects of dental care were similar, but the general condition of the mouth, as indicated by gum bleeding, tartar deposits and mucosal irritation, was worse among oral cancer cases than controls. No differences were detected in sexual practices (including oral sex) and (previous) sexually transmitted infections.

aDepartments of Epidemiology, Istituto di Ricerche Farmacologiche Mario Negri bOccupational Health, Università di Milano, Italy Correspondence to Professor Carlo La Vecchia, MD, Istituto Mario Negri, Via G. La Masa, 19, Milano 20156, Italy Tel: +39 02 3901 4527; fax: +39 02 3320 02321; e-mail: [email protected] Received February 21, 2011 Accepted February 21, 2011

Abstract Neoplasms are a group of diverse diseases with complex distributions in human populations and with different aetiological factors. Current knowledge of the causes of human neoplasms and the development of control strategies have led to the elaboration of lists of recommendations for their prevention. A comprehensive strategy for cancer control might lead to the avoidance of a sizeable proportion of human cancers, and the greatest benefit can be achieved via tobacco control. Nevertheless, neoplasms will continue to be a major source of human disease and death. Considerable efforts are made in the public and private domains to develop effective therapeutic approaches. Even if major discoveries in the clinical management of cancer patients will be accomplished in the near future, the changes will mainly affect the affluent part of the world population. Prevention of the known causes of cancer remains the most promising approach in reducing the consequences of cancer, in particular in countries with limited resources. Control of tobacco smoking and of smokeless tobacco products, reduced overweight and obesity, moderation in alcohol intake, increased physical activity, avoidance of exposure to solar radiation and control of known occupational carcinogens are the main approaches we currently have to reduce the burden of human neoplasms.

Laryngeal cancer is the neoplasm with the largest male to female sex ratio in most populations. Thus, inadequate data are available on women. We analyzed several risk factors in the combined dataset from two case-control studies conducted between 1986 and 2000 in northern Italy and Switzerland. Cases were 68 women under age 79 years, with incident, histologically confirmed cancer of the larynx. Controls were 340 women, admitted to the same network of hospitals as cases, for acute, nonmalignant conditions, unrelated to tobacco and alcohol consumption. Odds ratios (ORs) and corresponding 95% confidence intervals (CIs) were estimated by logistic regression models, conditioned by age, study center and year of interview, and including terms for education, body mass index, tobacco, alcohol drinking, and nonalcohol energy intake. Laryngeal cancer was strongly associated with cigarette smoking (OR = 435.7, 95% CI: 38.2–4964.4 for smokers of ≥25 cigarettes/day) and alcohol drinking (OR = 4.3, 95% CI: 0.8–24.1 for ≥5 drinks/day). An inverse relation was found for vegetables (OR = 0.3, 95% CI: 0.1–0.9 for the highest level of consumption), fruit (OR = 0.5, 95% CI: 0.2–1.3), and olive oil (OR = 0.3, 95% CI: 0.1–0.9). Reproductive and hormonal factors were not consistently associated to laryngeal cancer risk. This investigation, based on a uniquely large number of laryngeal cancers in women, provides definite evidence that cigarette smoking is the prominent risk factor for laryngeal cancer in women, accounting for 78% of cases in this population. Alcohol and selected dietary aspects account for ∼30% of cases, whereas menstrual and hormonal factors do not appear to have a consistent role in laryngeal carcinogenesis.