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<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns="http://purl.org/rss/1.0/"><channel rdf:about="http://www.cancerepidemiology.net/?rss=yes"><title>Cancer Epidemiology</title><description>Cancer Epidemiology RSS feed: Current Issue. 
 Cancer Epidemiology: the international journal for cancer epidemiology, detection and prevention  is dedicated to advancing cancer 
prevention and control.  The scope of the journal includes:

 
 •  Descriptive cancer epidemiology and cancer statistics • 
 Epidemiological studies on risk factors for the development of cancer •  Genetic and molecular cancer epidemiology • 
 Methodological papers in the field of cancer epidemiology, detection and prevention •  New concepts and approaches for early 
detection of cancer •  New concepts and approaches for population-based cancer prevention •  Chemoprevention, screening 
and other interventions to prevent cancer •  Epidemiological studies on late effects after cancer

 
 The journal publishes 
original research articles (full length and short communications), review articles including meta-analysis, methodological papers, editorials, 
commentaries, letters to the Editor commenting on previously published work in the journal, and special issues.  Methodological papers 
include validation studies, study designs, statistical methods and practical experiences. 

 
 
 Cancer Epidemiology (Cancer Epidemiol.)  
is indexed and abstracted in: MEDLINE/PubMed, Current Contents/Clinical Medicine, the Science Citation Index Expanded, and Thomson Reuters 
Journal Citation Reports (Science Edition).


</description><link>http://www.cancerepidemiology.net/?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2010 Published by Elsevier Inc. All rights reserved. </dc:rights><prism:publicationName>Cancer Epidemiology</prism:publicationName><prism:issn>1877-7821</prism:issn><prism:volume>34</prism:volume><prism:number>1</prism:number><prism:publicationDate>February 2010</prism:publicationDate><prism:copyright> © 2010 Published by Elsevier Inc. All rights reserved. </prism:copyright><prism:rightsAgent>healthpermissions@elsevier.com</prism:rightsAgent><items><rdf:Seq><rdf:li rdf:resource="http://www.cancerepidemiology.net/article/PIIS1877782110000135/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cancerepidemiology.net/article/PIIS1877782110000159/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cancerepidemiology.net/article/PIIS187778211000010X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cancerepidemiology.net/article/PIIS1877782109001726/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cancerepidemiology.net/article/PIIS1877782109001908/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cancerepidemiology.net/article/PIIS1877782109001751/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cancerepidemiology.net/article/PIIS1877782109001477/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cancerepidemiology.net/article/PIIS1877782109001830/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cancerepidemiology.net/article/PIIS1877782109001921/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cancerepidemiology.net/article/PIIS1877782109001842/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cancerepidemiology.net/article/PIIS187778210900191X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cancerepidemiology.net/article/PIIS1877782109001933/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cancerepidemiology.net/article/PIIS1877782109001829/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cancerepidemiology.net/article/PIIS1877782109001866/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cancerepidemiology.net/article/PIIS1877782109001854/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cancerepidemiology.net/article/PIIS1877782109001805/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cancerepidemiology.net/article/PIIS1877782109001817/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cancerepidemiology.net/article/PIIS1877782109001465/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cancerepidemiology.net/article/PIIS187778210900188X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cancerepidemiology.net/article/PIIS1877782109001763/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cancerepidemiology.net/article/PIIS1877782109001945/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cancerepidemiology.net/article/PIIS1877782109001489/abstract?rss=yes"/><rdf:li rdf:resource="http://www.cancerepidemiology.net/article/PIIS1877782109001738/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.cancerepidemiology.net/article/PIIS1877782110000135/abstract?rss=yes"><title>Editorial Board</title><link>http://www.cancerepidemiology.net/article/PIIS1877782110000135/abstract?rss=yes</link><description></description><dc:title>Editorial Board</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1877-7821(10)00013-5</dc:identifier><dc:source>Cancer Epidemiology 34, 1 (2010)</dc:source><dc:date>2010-02-01</dc:date><prism:publicationName>Cancer Epidemiology</prism:publicationName><prism:publicationDate>2010-02-01</prism:publicationDate><prism:volume>34</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1877-7821(10)X0002-9</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>i</prism:startingPage><prism:endingPage>i</prism:endingPage></item><item rdf:about="http://www.cancerepidemiology.net/article/PIIS1877782110000159/abstract?rss=yes"><title>Table of contents</title><link>http://www.cancerepidemiology.net/article/PIIS1877782110000159/abstract?rss=yes</link><description></description><dc:title>Table of contents</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1877-7821(10)00015-9</dc:identifier><dc:source>Cancer Epidemiology 34, 1 (2010)</dc:source><dc:date>2010-02-01</dc:date><prism:publicationName>Cancer Epidemiology</prism:publicationName><prism:publicationDate>2010-02-01</prism:publicationDate><prism:volume>34</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1877-7821(10)X0002-9</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>iii</prism:startingPage><prism:endingPage>iii</prism:endingPage></item><item rdf:about="http://www.cancerepidemiology.net/article/PIIS187778211000010X/abstract?rss=yes"><title>A tribute to Herbert E. Nieburgs MD</title><link>http://www.cancerepidemiology.net/article/PIIS187778211000010X/abstract?rss=yes</link><description>As this journal changes to a new editor and from Cancer Detection and Prevention to the new title of Cancer Epidemiology, it is appropriate to recognize the contributions to this journal of Herbert E. Nieburgs MD who served as Editor in Chief of Cancer Detection and Prevention for 32 years. Dr. Nieburgs brought Cancer Detection and Prevention from a minor publication depending on the membership of the International Society of Preventive Oncology (ISPO) to a major voice in mechanisms of cancer induction as well as its many causes and many aspects of detection and prevention.</description><dc:title>A tribute to Herbert E. Nieburgs MD</dc:title><dc:creator>V.E. (Ted) Valli</dc:creator><dc:identifier>10.1016/j.canep.2010.01.007</dc:identifier><dc:source>Cancer Epidemiology 34, 1 (2010)</dc:source><dc:date>2010-02-01</dc:date><prism:publicationName>Cancer Epidemiology</prism:publicationName><prism:publicationDate>2010-02-01</prism:publicationDate><prism:volume>34</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1877-7821(10)X0002-9</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>1</prism:startingPage><prism:endingPage>2</prism:endingPage></item><item rdf:about="http://www.cancerepidemiology.net/article/PIIS1877782109001726/abstract?rss=yes"><title>Contributions of leukocytes to tumor invasion and metastasis: The “piggy-back” hypothesis</title><link>http://www.cancerepidemiology.net/article/PIIS1877782109001726/abstract?rss=yes</link><description>The epithelium, which is the origin of over 85% of human malignant tumors, is physically separated from the stroma by the basement membrane. In breast, prostate, and major salivary glands, the epithelium is further segregated form the stroma by a layer of myoepithelial or basal cells. The epithelium is normally devoid of lymphatic ducts and blood vessels, and thus, totally relies on the stroma for its essential needs. Due to these structural relationships, the disruption of these structures is a prerequisite for tumor invasion or metastasis, which is believed to be a multistage process, progressing sequentially from normal to hyperplasia, to in situ, and to invasive or metastatic stages . Progression from an in situ to invasive stage is believed to be triggered by overproduction of proteolytic enzymes primarily by cancer cells, which cause degradation of the basement membrane .</description><dc:title>Contributions of leukocytes to tumor invasion and metastasis: The “piggy-back” hypothesis</dc:title><dc:creator>Yan-gao Man, Russell Harley, Jeffrey Mason, William A. Gardner</dc:creator><dc:identifier>10.1016/j.canep.2009.11.005</dc:identifier><dc:source>Cancer Epidemiology 34, 1 (2010)</dc:source><dc:date>2009-12-08</dc:date><prism:publicationName>Cancer Epidemiology</prism:publicationName><prism:publicationDate>2009-12-08</prism:publicationDate><prism:volume>34</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1877-7821(10)X0002-9</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>3</prism:startingPage><prism:endingPage>6</prism:endingPage></item><item rdf:about="http://www.cancerepidemiology.net/article/PIIS1877782109001908/abstract?rss=yes"><title>Benzene and the risk of non-Hodgkin lymphoma: A review and meta-analysis of the literature</title><link>http://www.cancerepidemiology.net/article/PIIS1877782109001908/abstract?rss=yes</link><description>Abstract: Benzene, an accepted leukemogen, has been suggested to cause other hemato- and lymphopoietic cancers. Here we review the published literature for non-Hodgkin lymphoma (NHL) and occupational exposure to benzene. Six cohorts, sixteen case–control studies and two studies of other designs were identified through keyword searches of bibliographic databases. Twenty-two of twenty-four studies found no association between NHL and ever exposed to benzene compared to never; a random-effects meta-analysis gave a pooled risk estimate of 1.11 (95% confidence interval 0.94–1.30). Our finding of no effect agrees with one of two previous meta-analyses. The other meta-analysis examined if high benzene exposure increased NHL risk but a lack of consistent exposure categories within the same metric should have precluded pooling risks by exposure level. Instead, we reviewed whether dose–response relationships existed. The best available data came from six studies where exposure was estimated from historical measurements and on the whole, no trends in risks of NHL with rising cumulative, average, peak, or duration of benzene exposure were found. NHL is a heterogeneous group of malignancies and although less well-studied, benzene was not associated with any NHL subtype. In conclusion, benzene at either low or high doses does not increase the risk of NHL.</description><dc:title>Benzene and the risk of non-Hodgkin lymphoma: A review and meta-analysis of the literature</dc:title><dc:creator>Eleanor V. Kane, Rob Newton</dc:creator><dc:identifier>10.1016/j.canep.2009.12.011</dc:identifier><dc:source>Cancer Epidemiology 34, 1 (2010)</dc:source><dc:date>2009-12-25</dc:date><prism:publicationName>Cancer Epidemiology</prism:publicationName><prism:publicationDate>2009-12-25</prism:publicationDate><prism:volume>34</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1877-7821(10)X0002-9</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>7</prism:startingPage><prism:endingPage>12</prism:endingPage></item><item rdf:about="http://www.cancerepidemiology.net/article/PIIS1877782109001751/abstract?rss=yes"><title>A novel approach to estimate the German-wide incidence of testicular cancer</title><link>http://www.cancerepidemiology.net/article/PIIS1877782109001751/abstract?rss=yes</link><description>Abstract: Background: Currently, only 7 out of 16 Federal States of Germany provide testicular cancer incidence rates with an estimated completeness of at least 90% which complicates the regional comparison of incidence rates. The aim of this study was to provide a novel approach to estimate the testicular cancer incidence in Germany by using nationwide hospitalization data. Methods: We used the nationwide hospitalization data (DRG statistics) of the years 2005–2006 including 16,6 million hospitalizations among men. We identified incident testicular cancer cases by the combination of a diagnosis of testicular cancer and an orchiectomy during the same hospitalization and estimated the age-specific and age-standardized (World Standard Population) incidence of testicular cancer across Federal States. We also analyzed available cancer registry data from 2005 to 2006. Results: A total of 8544 hospitalizations indicated incident testicular cancer cases in 2005–2006. The nationwide crude incidence rate of testicular cancer was 10,6 per 100.000 person-years. The ratio of the number of registered cases (cancer registry) to the estimated number of cases based on the hospitalization statistics ranged between 79% and 100%. There was only little variation of the age-standardized DRG-based incidence estimates across Federal States (range: 8,2–10,6 per 100.000 person-years). Discussion: We provided testicular cancer incidence estimates for each of the 16 Federal States of Germany based on hospitalization data for the first time. The low within-population incidence variability in Germany and high between-population incidence variability in Europe may indicate that ecologic factors play a causal role in the European variation of testicular cancer.</description><dc:title>A novel approach to estimate the German-wide incidence of testicular cancer</dc:title><dc:creator>Andreas Stang, Alexander Katalinic, Klaus-Peter Dieckmann, Ron Pritzkuleit, Roland Stabenow, on behalf of the Network of German Cancer Registries (GEKID)</dc:creator><dc:identifier>10.1016/j.canep.2009.11.007</dc:identifier><dc:source>Cancer Epidemiology 34, 1 (2010)</dc:source><dc:date>2009-12-11</dc:date><prism:publicationName>Cancer Epidemiology</prism:publicationName><prism:publicationDate>2009-12-11</prism:publicationDate><prism:volume>34</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1877-7821(10)X0002-9</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>13</prism:startingPage><prism:endingPage>19</prism:endingPage></item><item rdf:about="http://www.cancerepidemiology.net/article/PIIS1877782109001477/abstract?rss=yes"><title>Trends in breast cancer mortality in Trinidad and Tobago—A 35-year study</title><link>http://www.cancerepidemiology.net/article/PIIS1877782109001477/abstract?rss=yes</link><description>Abstract: Background: Breast cancer is the most frequently diagnosed cancer among women worldwide. This study examines the breast cancer mortality patterns and trends in the Caribbean island state, Trinidad and Tobago for the 35-year period, 1970–2004. Methods: A retrospective analysis of the trends in breast cancer mortality from 1970 to 2004 was conducted. Crude mortality per 100,000 women, age-standardized mortality using World Standard population and age-stratified mortality were calculated and comparison was made between age groups above and below 50 years. Results: A general pattern of increase was observed in both crude and age-standardized mortality. The overall average crude mortality was 15.6 per 100,000 women (95% confidence interval (CI) 13.9–17.1) and the average age-standardized mortality was 18.0 per 100,000 women (95% CI 16.7–19.2). There was a pattern of increase in mortality with increasing age. The mortality rate was considerably higher for the age groups above 50 years than those less than 50 years of age both showing an upward trend over the 35-year period. Conclusions: Breast cancer mortality continued to increase over the 35-year period in Trinidad and Tobago. This study did not identify the exact reasons for this increasing trend. However, it is known that Trinidad and Tobago is becoming much more industrialized. It may be speculated that decrease in fertility rates, increase in the incidence of obesity and hormone utilization could have influenced this trend.</description><dc:title>Trends in breast cancer mortality in Trinidad and Tobago—A 35-year study</dc:title><dc:creator>Vijay Naraynsingh, Seetharaman Hariharan, Dilip Dan, Savrina Bhola, Satyadevi Bhola, Kerry Nagee</dc:creator><dc:identifier>10.1016/j.canep.2009.11.003</dc:identifier><dc:source>Cancer Epidemiology 34, 1 (2010)</dc:source><dc:date>2009-11-30</dc:date><prism:publicationName>Cancer Epidemiology</prism:publicationName><prism:publicationDate>2009-11-30</prism:publicationDate><prism:volume>34</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1877-7821(10)X0002-9</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>20</prism:startingPage><prism:endingPage>23</prism:endingPage></item><item rdf:about="http://www.cancerepidemiology.net/article/PIIS1877782109001830/abstract?rss=yes"><title>The incidence and survival of acute de novo leukemias in Estonia and in a well-defined region of western Sweden during 1997–2001: A survey of patients aged ≥65 years</title><link>http://www.cancerepidemiology.net/article/PIIS1877782109001830/abstract?rss=yes</link><description>Abstract: Background: In a recently published retrospective population-based study over three 5-year periods (1982–1996) we investigated the outcome for de novo acute leukemia (AL) patients aged ≥65 years at diagnosis in Estonia (a country that had been occupied by the Soviet Union over 5 decades) and in the so-called Western Swedish Health Care Region. The age-standardized yearly incidence rates regarding the total number of de novo AL was 5.3/100000 inhabitant for Estonia and 8.0 for Sweden, this difference being statistically significant merely as regards acute myeloid leukemia (AML). The relative survival for the total cohort of de novo AL as well as for de novo AML was significantly longer (p&lt;0.001) for Swedish as compared to Estonian patients. Methods: In view of the miserable outcome for the Estonian patients we decided to prospectively compare the results for incidence and outcome of de novo AL between the two countries. Results: The present report covers the first 5-year period comprising 1997–2001 and deals only with patients aged ≥65 years at diagnosis. The age-adjusted annual incidence rates for de novo AML were lower in Estonia (6.4/100000) than in Sweden (9.2/100000) but not significantly so. The present results also show that the outcome for the Estonian AML patients had improved considerably over the study period; thus, at no time point, i.e., at 1, 3 and 5 years did relative survival between the two countries differ significantly. Conclusion: Yet, as compared to the Swedish cohort relative survival for the Estonian patients did still not reach an acceptable level.</description><dc:title>The incidence and survival of acute de novo leukemias in Estonia and in a well-defined region of western Sweden during 1997–2001: A survey of patients aged ≥65 years</dc:title><dc:creator>Katrin Palk, Ene Luik, Mirja Varik, Iige Viigimaa, Krista Vaht, Hele Everaus, Lovisa Wennström, Dick Stockelberg, Soodabeh Safai-Kutti, Erik Holmberg, Jack Kutti</dc:creator><dc:identifier>10.1016/j.canep.2009.12.004</dc:identifier><dc:source>Cancer Epidemiology 34, 1 (2010)</dc:source><dc:date>2009-12-25</dc:date><prism:publicationName>Cancer Epidemiology</prism:publicationName><prism:publicationDate>2009-12-25</prism:publicationDate><prism:volume>34</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1877-7821(10)X0002-9</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>24</prism:startingPage><prism:endingPage>28</prism:endingPage></item><item rdf:about="http://www.cancerepidemiology.net/article/PIIS1877782109001921/abstract?rss=yes"><title>Spatial analysis of hepatocellular carcinoma and socioeconomic status in China from a Population-based Cancer Registry</title><link>http://www.cancerepidemiology.net/article/PIIS1877782109001921/abstract?rss=yes</link><description>Abstract: Background: Little is known about geographic variations in liver cancer at high incident regions. We aimed to identify spatial variation of hepatocellular carcinoma (HCC) at a high-risk area in China and determine its association with socioeconomic status (SES). Methods: Based on 2299 liver cancer cases diagnosed in Haimen from 2003 to 2006, we calculated age–sex standardized incidence ratios (SIRs) and used two spatial scan statistics to determine the geographic variations in HCC. Bayesian hierarchical model was used to explore the association between HCC incidence and SES. Results: Age and sex SIRs for HCC varied from 0.54 to 1.97 for 24 townships. The eastern region of Haimen was identified to have a significantly increased risk of HCC. Fitting of a Bayesian hierarchical model linking per-capita fiscal revenue with SIRs of HCC indicated that the area with a lower revenue had a significantly higher incidence of HCC [βlog(revenue)=−0.179, posterior 95% Bayesian credible interval (CI)=(−0.326, −0.04)]. Conclusions: This study demonstrated substantial geographic variation in the incidence of HCC within a high-risk region, which was associated with SES. HCC control and intervention should focus on disadvantaged areas to reduce the HCC disparities.</description><dc:title>Spatial analysis of hepatocellular carcinoma and socioeconomic status in China from a Population-based Cancer Registry</dc:title><dc:creator>Wenxiang Peng, Yue Chen, Qingwu Jiang, Yingjie Zheng</dc:creator><dc:identifier>10.1016/j.canep.2009.12.013</dc:identifier><dc:source>Cancer Epidemiology 34, 1 (2010)</dc:source><dc:date>2010-01-04</dc:date><prism:publicationName>Cancer Epidemiology</prism:publicationName><prism:publicationDate>2010-01-04</prism:publicationDate><prism:volume>34</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1877-7821(10)X0002-9</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>29</prism:startingPage><prism:endingPage>33</prism:endingPage></item><item rdf:about="http://www.cancerepidemiology.net/article/PIIS1877782109001842/abstract?rss=yes"><title>Risk factors for breast cancer in women biopsied for benign breast disease: A nested case-control study</title><link>http://www.cancerepidemiology.net/article/PIIS1877782109001842/abstract?rss=yes</link><description>Abstract: Aim: Women with a history of benign breast disease are at increased risk of subsequent breast cancer. However, few studies have examined whether established breast cancer risk factors other than histology are associated with an altered risk of breast cancer in women with benign breast disease. We used a nested case-control design within a large, multi-center cohort of women biopsied for benign breast disease (BBD) to estimate odds ratios for breast cancer in association with exposure to a range of personal and lifestyle factors. Methods: Cases were women biopsied for BBD who subsequently developed breast cancer; controls were individually matched to cases on center and age at diagnosis and were women biopsied for BBD who did not develop breast cancer in the same follow-up interval as that for the cases. After excluding women with prevalent breast cancer, 1357 records (661 case records and 696 records) were available for analysis. We used conditional logistic regression to obtain crude and multivariable-adjusted estimates of the association between specific factors and risk of breast cancer. Results: In multivariable analyses age at first live birth, number of pregnancies, and postmenopausal status were inversely associated with risk of breast cancer. The odds ratio for women with age at first birth &lt;25 years and ≥3 pregnancies, relative to nulliparous women, was 0.49, 95% confidence interval 0.13–0.79, and that for postmenopausal women relative to premenopausal women was 0.60, 95% CI 0.37–0.99. Conclusions: Further study of personal factors influencing the risk of breast cancer in women with BBD may help to identify subgroups of the population at increased risk of invasive disease.</description><dc:title>Risk factors for breast cancer in women biopsied for benign breast disease: A nested case-control study</dc:title><dc:creator>Geoffrey C. Kabat, Joan G. Jones, Neal Olson, Abdissa Negassa, Catherine Duggan, Mindy Ginsberg, Rita A. Kandel, Andrew G. Glass, Thomas E. Rohan</dc:creator><dc:identifier>10.1016/j.canep.2009.12.005</dc:identifier><dc:source>Cancer Epidemiology 34, 1 (2010)</dc:source><dc:date>2009-12-25</dc:date><prism:publicationName>Cancer Epidemiology</prism:publicationName><prism:publicationDate>2009-12-25</prism:publicationDate><prism:volume>34</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1877-7821(10)X0002-9</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>34</prism:startingPage><prism:endingPage>39</prism:endingPage></item><item rdf:about="http://www.cancerepidemiology.net/article/PIIS187778210900191X/abstract?rss=yes"><title>Micronutrient intake and risk of colon and rectal cancer in a Danish cohort</title><link>http://www.cancerepidemiology.net/article/PIIS187778210900191X/abstract?rss=yes</link><description>Abstract: Background: Micronutrients may protect against colorectal cancer. Especially folate has been considered potentially preventive. However, studies on folate and colorectal cancer have found contradicting results; dietary folate seems preventive, whereas folic acid in supplements and fortification may increase the risk. Objective: To evaluate the association between intake of vitamins C, E, folate and beta-carotene and colorectal cancer risk, focusing on possibly different effects of dietary, supplemental and total intake, and on potential effect modification by lifestyle factors. Design: In a prospective cohort study of 56,332 participants aged 50–64 years, information on diet, supplements and lifestyle was collected through questionnaires. 465 Colon and 283 rectal cancer cases were identified during follow-up. Incidence rate ratios of colon and rectal cancers related to micronutrient intake were calculated using Cox proportional hazard analyses. Results: The present study found a protective effect of dietary but not supplemental folate on colon cancer. No association with any other micronutrient was found. Rectal cancer did not seem associated with any micronutrient. For both colon and rectal cancer, we found an interaction between dietary folate and alcohol intake, with a significant, preventive effect among those consuming above 10g alcohol/day only. Conclusions: This study adds further weight to the evidence that dietary folate protects against colon cancer, and specifies that there is a source-specific effect, with no preventive effect of supplemental folic acid. Further studies should thus take source into account. Vitamins C, E and beta-carotene showed no relation with colorectal cancer.</description><dc:title>Micronutrient intake and risk of colon and rectal cancer in a Danish cohort</dc:title><dc:creator>Nina Roswall, Anja Olsen, Jane Christensen, Lars O. Dragsted, Kim Overvad, Anne Tjønneland</dc:creator><dc:identifier>10.1016/j.canep.2009.12.012</dc:identifier><dc:source>Cancer Epidemiology 34, 1 (2010)</dc:source><dc:date>2009-12-25</dc:date><prism:publicationName>Cancer Epidemiology</prism:publicationName><prism:publicationDate>2009-12-25</prism:publicationDate><prism:volume>34</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1877-7821(10)X0002-9</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>40</prism:startingPage><prism:endingPage>46</prism:endingPage></item><item rdf:about="http://www.cancerepidemiology.net/article/PIIS1877782109001933/abstract?rss=yes"><title>Cancer surveillance in Italian army peacekeeping troops deployed in Bosnia and Kosovo, 1996–2007: Preliminary results</title><link>http://www.cancerepidemiology.net/article/PIIS1877782109001933/abstract?rss=yes</link><description>Abstract: Objective: An excess of cancer cases was reported in 2000 among Italian troops involved in peacekeeping operations in Bosnia and Kosovo. A preliminary assessment of cancer risk in this cohort was done for the period 1996–2007, based on cancer surveillance activity, which was started in 2001. Methods: A retrospective cohort study was done among 27361 Italian Army soldiers deployed in Bosnia, 31052 deployed in Kosovo, and a control group of non-deployed soldiers, whose number varies from 130275 in 1996 to 40967 in 2007. Standardized incidence ratio and 95% confidence intervals (SIR [95% CI]) of the main types of tumours were computed as the ratio of the observed and expected cases. Results: 98 incident cancers were reported among soldiers deployed in Bosnia, 66 in those stationed in Kosovo and 388 in non-deployed personnel. Overall, cancer incidence was lower than expected in all groups. Annual SIR was significantly higher than expected in 2000 for Hodgkin's lymphoma only among troops deployed in Bosnia (4.34 [1.18–11.12]) and non-deployed personnel (3.48 [1.67–6.39]); and in 2001 for thyroid cancer only among troops deployed in Bosnia (5.28 [1.44–13.51]). Conclusion: Although further investigation is needed, these preliminary results give no indication of an increased risk of cancer for Italian soldiers who were stationed in Bosnia and Kosovo. The cluster of Hodgkin's lymphoma in 2000 and of thyroid cancer in 2001 were sporadic events, they did not specifically affect deployed personnel and are unlikely to be related to environmental exposures in the Balkans.</description><dc:title>Cancer surveillance in Italian army peacekeeping troops deployed in Bosnia and Kosovo, 1996–2007: Preliminary results</dc:title><dc:creator>Mario Stefano Peragallo, Florigio Lista, Giuseppe Sarnicola, Federico Marmo, Alfredo Vecchione</dc:creator><dc:identifier>10.1016/j.canep.2009.12.014</dc:identifier><dc:source>Cancer Epidemiology 34, 1 (2010)</dc:source><dc:date>2010-01-07</dc:date><prism:publicationName>Cancer Epidemiology</prism:publicationName><prism:publicationDate>2010-01-07</prism:publicationDate><prism:volume>34</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1877-7821(10)X0002-9</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>47</prism:startingPage><prism:endingPage>54</prism:endingPage></item><item rdf:about="http://www.cancerepidemiology.net/article/PIIS1877782109001829/abstract?rss=yes"><title>Occupation and risk of glioma, meningioma and acoustic neuroma: Results from a German case–control study (Interphone Study Group, Germany)</title><link>http://www.cancerepidemiology.net/article/PIIS1877782109001829/abstract?rss=yes</link><description>Abstract: Background: Several epidemiological studies have investigated the association between occupation and brain tumour risk, but results have been inconclusive. We investigated the association between six occupational categories defined a priori: chemical, metal, agricultural, construction, electrical/electronic and transport, and the risk of glioma, meningioma and acoustic neuroma. Methods: In a population-based case–control study involving a total of 844 cases and 1688 controls conducted from 2000 to 2003, detailed information on life-long job histories was collected during personal interviews and used to create job calendars for each participant. Job title, job activity, job number, and the starting and ending dates of the activity were recorded for all activities with duration of at least 1 year. Reported occupational activities were coded according to the International Standard Classification of Occupations 1988 (ISCO 88). For the analyses we focused on six a priori defined occupational sectors, namely chemical, metal, agricultural, construction, electrical/electronic and transport. Multiple conditional logistic regression analysis was used to estimate odds ratios and their 95% confidence intervals. Results: Most of the observed odds ratios were close to 1.0 for ever having worked in the six occupational sectors and risk of glioma, meningioma and acoustic neuroma. Sub-group analyses according to duration of employment resulted in two elevated odds ratios with confidence intervals excluding unity. Conclusions: We did not observe an increased risk of glioma or meningioma for occupations in the agricultural, construction, transport, chemical, electrical/electronic and metal sectors. The number of ‘significant’ odds ratios is consistent with an overall ‘null-effect’.</description><dc:title>Occupation and risk of glioma, meningioma and acoustic neuroma: Results from a German case–control study (Interphone Study Group, Germany)</dc:title><dc:creator>F. Samkange-Zeeb, B. Schlehofer, J. Schüz, K. Schlaefer, G. Berg-Beckhoff, J. Wahrendorf, M. Blettner</dc:creator><dc:identifier>10.1016/j.canep.2009.12.003</dc:identifier><dc:source>Cancer Epidemiology 34, 1 (2010)</dc:source><dc:date>2009-12-25</dc:date><prism:publicationName>Cancer Epidemiology</prism:publicationName><prism:publicationDate>2009-12-25</prism:publicationDate><prism:volume>34</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1877-7821(10)X0002-9</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>55</prism:startingPage><prism:endingPage>61</prism:endingPage></item><item rdf:about="http://www.cancerepidemiology.net/article/PIIS1877782109001866/abstract?rss=yes"><title>Second cancers following the diagnosis of Merkel cell carcinoma: A nationwide cohort study</title><link>http://www.cancerepidemiology.net/article/PIIS1877782109001866/abstract?rss=yes</link><description>Abstract: Merkel cell carcinoma (MCC) is a rare neuroendocrine carcinoma of the skin. MCCs and some other skin cancers, such as basal cell carcinomas, frequently harbour Merkel cell polyomavirus DNA. The purpose of the study was to investigate the frequency of second cancers following the diagnosis of MCC. We studied the incidence of second primary cancers after the diagnosis of MCC from the files of the Finnish Cancer Registry in 1979–2006. Among the 172 MCC patients identified a total of 34 second primary cancers were detected in 30 individuals after the diagnosis of MCC. Female MCC patients were diagnosed with 25 subsequent cancers (SIR, 2.35; 95% CI, 1.52–3.47; p&lt;0.001) and male patients with 9 cancers (SIR, 2.32, 95% CI, 1.06–4.40; p&lt;0.05). The MCC patients had an increased risk for a subsequent cancer (any site) compared to age-, gender- and calendar period-matched general population (standardized incidence ratio [SIR] 2.34; 95% confidence interval [CI], 1.62–3.27). The risks for basal cell carcinoma of the skin (O=11), SIR, 3.48; 95% CI, 1.74–6.22 and chronic lymphocytic leukemia (O=2), SIR, 17.9; 95% CI, 2.16–64.6 were significantly elevated. The SIRs for an overall second primary cancer risk did not change markedly with time since the diagnosis of MCC. We conclude that patients diagnosed with MCC have an increased risk for a second cancer. This risk may in part result from shared etiological factors between MCC and other tumour types, such as immunosuppression or possibly Merkel cell polyomavirus infection.</description><dc:title>Second cancers following the diagnosis of Merkel cell carcinoma: A nationwide cohort study</dc:title><dc:creator>Virve Koljonen, Heli Kukko, Erkki Tukiainen, Tom Böhling, Risto Sankila, Heikki Joensuu, Eero Pukkala</dc:creator><dc:identifier>10.1016/j.canep.2009.12.007</dc:identifier><dc:source>Cancer Epidemiology 34, 1 (2010)</dc:source><dc:date>2009-12-25</dc:date><prism:publicationName>Cancer Epidemiology</prism:publicationName><prism:publicationDate>2009-12-25</prism:publicationDate><prism:volume>34</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1877-7821(10)X0002-9</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>62</prism:startingPage><prism:endingPage>65</prism:endingPage></item><item rdf:about="http://www.cancerepidemiology.net/article/PIIS1877782109001854/abstract?rss=yes"><title>Genetic polymorphism of glutathione S-transferase T1 and the risk of colorectal cancer: A meta-analysis</title><link>http://www.cancerepidemiology.net/article/PIIS1877782109001854/abstract?rss=yes</link><description>Abstract: Background: Studies investigating the association between genetic polymorphism of glutathione S-transferase T1 (GSTT1) and risk of colorectal cancer have reported conflicting results. In order to clarify the effect of GSTT1 polymorphism on the risk of developing colorectal cancer, we carried out a meta-analysis using published data to obtain more precise estimates of risk. Methods: Electronic searches of PubMed and EMBASE were conducted to select studies for this meta-analysis. Papers were included if they were observational studies investigating the association between GSTT1 polymorphism and colorectal cancer risk. The principal outcome measure was the odds ratio (OR) with 95% confidence interval (CI) for the risk of colorectal cancer associated with GSTT1 null genotype. Results: We identified 30 eligible studies, which included 7635 cases and 12,911 controls. The combined results based on all studies showed that there was a statistically significant link between GSTT1 null genotype and colorectal cancer risk (OR=1.20, 95% CI=1.03–1.40). In the analysis of ethnic groups, we observed distinct differences associated with GSTT1 null genotype, the pooled odds ratios for the GSTT1 polymorphism were 1.32 in Caucasians (95% CI=1.09–1.58) and 1.03 in Asians (95% CI=0.81–1.32). As far as concerned the interaction between GSTT1 genotype and colorectal cancer risk in relation to smoking history, there was no increase in risk for smokers or nonsmokers with the GSTT1 null genotype (smokers: OR=1.13, 95% CI=0.80–1.60, nonsmokers: OR=0.99, 95% CI=0.71–1.38). When stratifying by the location of colorectal cancer, we found that there was a statistically significant link in rectal cancer (OR=1.50, 95% CI=1.09–2.07), but not in colon cancer (OR=1.33, 95% CI=0.94–1.88). No associations could be detected between null GSTT1 polymorphism and age, sex, tumor stage and differentiation. Conclusion: Our current study demonstrates that GSTT1 null genotype is associated with an increased risk of colorectal cancer, specifically, among Caucasians.</description><dc:title>Genetic polymorphism of glutathione S-transferase T1 and the risk of colorectal cancer: A meta-analysis</dc:title><dc:creator>Hongwei Wan, Yong Zhou, Ping Yang, Bo Chen, Guiqing Jia, Xiaoting Wu</dc:creator><dc:identifier>10.1016/j.canep.2009.12.006</dc:identifier><dc:source>Cancer Epidemiology 34, 1 (2010)</dc:source><dc:date>2009-12-25</dc:date><prism:publicationName>Cancer Epidemiology</prism:publicationName><prism:publicationDate>2009-12-25</prism:publicationDate><prism:volume>34</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1877-7821(10)X0002-9</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>66</prism:startingPage><prism:endingPage>72</prism:endingPage></item><item rdf:about="http://www.cancerepidemiology.net/article/PIIS1877782109001805/abstract?rss=yes"><title>Breast cancer screening among Asian immigrant women in Canada</title><link>http://www.cancerepidemiology.net/article/PIIS1877782109001805/abstract?rss=yes</link><description>Abstract: Objective: The objective of this study was to examine the pattern of breast cancer screening among Asian immigrant women aged 50–69 years and compare it with corresponding non-immigrant women in Canada. Methods: Data from the Canadian Community Health Survey cycle 2.1 (2003) were utilized. Self-reported screening histories were used as outcome variables: socioeconomic status and medical histories were used as predictive variables. Analyses were weighted to represent the target population. Multivariate logistic regression analyses were performed to compare the screening pattern among Asian immigrant women and corresponding non-immigrant Canadians. Results: In total, 508 Asian immigrant women were included in this study. The results suggest that 71% and 60% of Asian immigrant women reported ever having had and recent mammogram use, respectively, while the corresponding figures for non-immigrant women were 89% and 72%. The observed differences were statistically significant and could not be explained by confounding factors. The ability to speak one of the two official languages is an important barrier to mammography screening among Asian immigrant women. Conclusion: The findings show lower rates of mammography screening among Asian immigrant women in Canada. If breast screening is to remain a health policy objective in Canada, targeted efforts to increase the recruitment of Asian immigrant women need to be developed or strengthened.</description><dc:title>Breast cancer screening among Asian immigrant women in Canada</dc:title><dc:creator>Zhuoyu Sun, Hui Xiong, Anne Kearney, Jin Zhang, Wei Liu, Guowei Huang, Peizhong Peter Wang</dc:creator><dc:identifier>10.1016/j.canep.2009.12.001</dc:identifier><dc:source>Cancer Epidemiology 34, 1 (2010)</dc:source><dc:date>2009-12-17</dc:date><prism:publicationName>Cancer Epidemiology</prism:publicationName><prism:publicationDate>2009-12-17</prism:publicationDate><prism:volume>34</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1877-7821(10)X0002-9</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>73</prism:startingPage><prism:endingPage>78</prism:endingPage></item><item rdf:about="http://www.cancerepidemiology.net/article/PIIS1877782109001817/abstract?rss=yes"><title>Characterizing the range of simulated prostate abnormalities palpable by digital rectal examination</title><link>http://www.cancerepidemiology.net/article/PIIS1877782109001817/abstract?rss=yes</link><description>Abstract: Background: Although the digital rectal exam (DRE) is a common method of screening for prostate cancer and other abnormalities, the limits of ability to perform this hands-on exam are unknown. Perceptible limits are a function of the size, depth, and hardness of abnormalities within a given prostate stiffness. Methods: To better understand the perceptible limits of the DRE, we conducted a psychophysical study with 18 participants using a custom-built apparatus to simulate prostate tissue and abnormalities of varying size, depth, and hardness. Utilizing a modified version of the psychophysical method of constant stimuli, we uncovered thresholds of absolute detection and variance in ability between examiners. Results: Within silicone-elastomers that mimic normal prostate tissue (21kPa), abnormalities of 4mm diameter (20mm3 volume) and greater were consistently detectable (above 75% of the time) but only at a depth of 5mm. Abnormalities located in simulated tissue of greater stiffness (82kPa) had to be twice that volume (5mm diameter, 40mm3 volume) to be detectable at the same rate. Conclusions: This study finds that the size and depth of abnormalities most influence detectability, while the relative stiffness between abnormalities and substrate also affects detectability for some size/depth combinations. While limits identified here are obtained for idealized substrates, this work is useful for informing the development of training and allowing clinicians to set expectations on performance.</description><dc:title>Characterizing the range of simulated prostate abnormalities palpable by digital rectal examination</dc:title><dc:creator>Leigh A. Baumgart, Gregory J. Gerling, Ellen J. Bass</dc:creator><dc:identifier>10.1016/j.canep.2009.12.002</dc:identifier><dc:source>Cancer Epidemiology 34, 1 (2010)</dc:source><dc:date>2009-12-25</dc:date><prism:publicationName>Cancer Epidemiology</prism:publicationName><prism:publicationDate>2009-12-25</prism:publicationDate><prism:volume>34</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1877-7821(10)X0002-9</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>79</prism:startingPage><prism:endingPage>84</prism:endingPage></item><item rdf:about="http://www.cancerepidemiology.net/article/PIIS1877782109001465/abstract?rss=yes"><title>Breast cancer risk and common single nucleotide polymorphisms in homologous recombination DNA repair pathway genes XRCC2, XRCC3, NBS1 and RAD51</title><link>http://www.cancerepidemiology.net/article/PIIS1877782109001465/abstract?rss=yes</link><description>Abstract: The possible role for DNA repair deficiencies in cancer development, namely in breast cancer has been the subject of increasing interest since it has been reported that breast cancer patients might be deficient in the repair of DNA damage. Exposure to ionizing radiation has been pointed out as a risk factor for breast cancer, and the type of DNA lesions induced by this carcinogen can be repaired by homologous recombination DNA repair (HRR) pathway. To evaluate the potential modifying role of some single nucleotide polymorphisms (SNP) in HRR involved genes on the individual susceptibility to breast cancer we carried out a hospital based case–control study in a Caucasian Portuguese population (289 histological confirmed breast cancer patients and 548 control individuals). We genotyped 4 SNPs in 4 different HRR pathway genes, XRCC2 (Ex3+442G&gt;A, R188H, rs3218536), XRCC3 (Ex8-5C&gt;T, T241M, rs861539), NBS1 (Ex5-32C&gt;G, E185Q, rs1805794) and RAD51 5′UTR (Ex1-59G&gt;T, rs1801321), tagging 41 SNPs in these genes. The frequency of the different polymorphisms in the Portuguese control population is similar to the ones reported for other Caucasian populations, and the deviation of the Hardy–Weinberg equilibrium was only observed for the XRCC2 (Ex3+442G&gt;A, R188H, rs3218536) polymorphism in the control population. The results obtained, after logistic regression analysis, did not reveal a major role of these polymorphisms on breast cancer susceptibility. However, when the population was stratified according to breast feeding (women that breast fed and women that never breast fed) it is observed, in women that never breast fed, that the heterozygous individuals for the XRCC2 (Ex3+442G&gt;A, R188H, rs3218536) polymorphism have a decreased risk for breast cancer [adjusted OR=0.45; 95% CI=0.22–0.92] (P=0.03). Additionally, after stratification according to menopausal status, our results suggest that post-menopausal women carrying at least one variant allele for the XRCC3 (Ex8-5C&gt;T, T241M, rs861539) polymorphism have a lower risk for breast cancer [adjusted OR=0.67; 95% CI, 0.47–0.94] (P=0.03). Most of the studies suggest that breastfeeding may be responsible for 2/3 of the estimate reduction of breast cancer. The longer the duration of breastfeeding the lower the potential risk associated with breast cancer. Therefore, in our study the potential protective role of the variant allele of XRCC2 (Ex3+442G&gt;A, R188H, rs3218536), in never breast fed women, might be related with a more efficient DNA repair activity.</description><dc:title>Breast cancer risk and common single nucleotide polymorphisms in homologous recombination DNA repair pathway genes XRCC2, XRCC3, NBS1 and RAD51</dc:title><dc:creator>Susana N. Silva, Marta Tomar, Claudia Paulo, Bruno Costa Gomes, Ana Paula Azevedo, Valdemar Teixeira, Julieta Esperança Pina, José Rueff, Jorge Francisco Gaspar</dc:creator><dc:identifier>10.1016/j.canep.2009.11.002</dc:identifier><dc:source>Cancer Epidemiology 34, 1 (2010)</dc:source><dc:date>2009-11-30</dc:date><prism:publicationName>Cancer Epidemiology</prism:publicationName><prism:publicationDate>2009-11-30</prism:publicationDate><prism:volume>34</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1877-7821(10)X0002-9</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>85</prism:startingPage><prism:endingPage>92</prism:endingPage></item><item rdf:about="http://www.cancerepidemiology.net/article/PIIS187778210900188X/abstract?rss=yes"><title>The MLH1 −93 promoter variant influences gene expression</title><link>http://www.cancerepidemiology.net/article/PIIS187778210900188X/abstract?rss=yes</link><description>Abstract: The −93 SNP of MLH1 gene is associated with MLH1 gene methylation in endometrial and colorectal cancers. We undertook luciferase reporter assay and electrophoretic mobility shift assay (EMSA) to test whether the −93 SNP affects the MLH1 gene expression. The luciferase activity for −93A plasmid is significantly lower than −93G plasmid. In EMSA experiments, the −93A and −93G probes have different binding affinity to nuclear proteins of JEG3 cells. Our data indicate that −93 SNP affects MLH1 gene expression by altering protein binding to the promoter of MLH1 gene.</description><dc:title>The MLH1 −93 promoter variant influences gene expression</dc:title><dc:creator>Manxue Mei, Dong Liu, Shuo Dong, Sigurdur Ingvarsson, Paul J. Goodfellow, Huiping Chen</dc:creator><dc:identifier>10.1016/j.canep.2009.12.009</dc:identifier><dc:source>Cancer Epidemiology 34, 1 (2010)</dc:source><dc:date>2009-12-25</dc:date><prism:publicationName>Cancer Epidemiology</prism:publicationName><prism:publicationDate>2009-12-25</prism:publicationDate><prism:volume>34</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1877-7821(10)X0002-9</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>93</prism:startingPage><prism:endingPage>95</prism:endingPage></item><item rdf:about="http://www.cancerepidemiology.net/article/PIIS1877782109001763/abstract?rss=yes"><title>Efficacy of genotype notification to Japanese smokers on smoking cessation—An intervention study at workplace</title><link>http://www.cancerepidemiology.net/article/PIIS1877782109001763/abstract?rss=yes</link><description>Abstract: Objectives: It is well-known that smoking causes many diseases including cancers. Informing smokers of their genotypes associated with the vulnerability to the harms of smoking may be effective measures for smoking cessation. The present study examined the effects of genotype notification of an oncogene (L-myc) genotype to smokers on their behavior to quit smoking. Methods: Subjects were 562 employees of a bank who answered to be a smoker for a questionnaire used at annual health checkup at workplace from July to December 2002. Those enrolled on August, October, and December were allocated into the genotype notification group (intervention group), and the rest into the controls. Among 286 smokers allocated into the intervention group, 257 participants (89.9%) agreed to genotype testing. One year after the enrollment, a follow-up questionnaire survey was conducted for all smokers including controls. Results: Those who stated to have quitted smoking were 22 (8.0%) among the 276 controls and 15 (5.8%) among the 257 genotype notified participants, providing that the odds ratio (OR) of cessation for the intervention was 0.64 (95% confidence interval, 0.32–1.28). No psychological problems associated with genotype notification were observed. Conclusion: The present study did not show positive effects of genotype notification on smoking cessation rate. To elevate the cessation rate, methods to explain and notify genotypes should be improved.</description><dc:title>Efficacy of genotype notification to Japanese smokers on smoking cessation—An intervention study at workplace</dc:title><dc:creator>Asahi Hishida, Tetsuro Terazawa, Toshiko Mamiya, Hidemi Ito, Keitaro Matsuo, Kazuo Tajima, Nobuyuki Hamajima</dc:creator><dc:identifier>10.1016/j.canep.2009.11.008</dc:identifier><dc:source>Cancer Epidemiology 34, 1 (2010)</dc:source><dc:date>2009-12-11</dc:date><prism:publicationName>Cancer Epidemiology</prism:publicationName><prism:publicationDate>2009-12-11</prism:publicationDate><prism:volume>34</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1877-7821(10)X0002-9</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>96</prism:startingPage><prism:endingPage>100</prism:endingPage></item><item rdf:about="http://www.cancerepidemiology.net/article/PIIS1877782109001945/abstract?rss=yes"><title>Unchanging clinico-epidemiological profile of lung cancer in North India over three decades</title><link>http://www.cancerepidemiology.net/article/PIIS1877782109001945/abstract?rss=yes</link><description>Abstract: Objective: In the recent past, adenocarcinoma has become the commonest histological type of lung cancer (LC) in the developed countries. The present study was conducted to assess the change in epidemiology of LC, if any, in North India. Methods: Prospectively collected data on 250 newly diagnosed LC patients presenting to a tertiary care institute was analyzed. Results were compared with the previously published data from this center. Results: No significant differences were observed in the demographical, histological or smoking profiles of LC patients compared to those seen three decades earlier. The mean [standard deviation] age was 57.9 [±11.3] years (previously 54.3 years). Male to female ratio was 4.43:1 (previously 4.48:1; p=0.952) while the smoker to non-smoker ratio was 2.67:1 (previously 2.68:1; p=0.980). The commonest histological types were squamous cell (34.8%), adenocarcinoma (26.0%) and small cell (18.4%) while previously these were 34.3%, 25.9% and 20.3%, respectively; p=0.916. However, in the present study, significant differences were observed between smokers and non-smokers in relation to distribution of gender, histology and disease stage. Conclusions: There has been no significant change in the epidemiology of LC in North India over the past three decades. An absence of change in the smoking pattern of the population could be a possible reason.</description><dc:title>Unchanging clinico-epidemiological profile of lung cancer in North India over three decades</dc:title><dc:creator>Navneet Singh, Ashutosh N. Aggarwal, Dheeraj Gupta, Digambar Behera, Surinder K. Jindal</dc:creator><dc:identifier>10.1016/j.canep.2009.12.015</dc:identifier><dc:source>Cancer Epidemiology 34, 1 (2010)</dc:source><dc:date>2010-01-06</dc:date><prism:publicationName>Cancer Epidemiology</prism:publicationName><prism:publicationDate>2010-01-06</prism:publicationDate><prism:volume>34</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1877-7821(10)X0002-9</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>101</prism:startingPage><prism:endingPage>104</prism:endingPage></item><item rdf:about="http://www.cancerepidemiology.net/article/PIIS1877782109001489/abstract?rss=yes"><title>Why is the incidence of childhood cancer lower in rural India?</title><link>http://www.cancerepidemiology.net/article/PIIS1877782109001489/abstract?rss=yes</link><description>I welcome the recent publication on cancer incidence and survival patterns in India from a population-based cancer registry (PBCR) with predominantly rural coverage . As more than 70% of the Indian population lives in rural areas, such studies are necessary to provide a more accurate estimation of disease burden in the country.</description><dc:title>Why is the incidence of childhood cancer lower in rural India?</dc:title><dc:creator>Ramandeep S. Arora</dc:creator><dc:identifier>10.1016/j.canep.2009.11.004</dc:identifier><dc:source>Cancer Epidemiology 34, 1 (2010)</dc:source><dc:date>2009-11-30</dc:date><prism:publicationName>Cancer Epidemiology</prism:publicationName><prism:publicationDate>2009-11-30</prism:publicationDate><prism:volume>34</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1877-7821(10)X0002-9</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>105</prism:startingPage><prism:endingPage>106</prism:endingPage></item><item rdf:about="http://www.cancerepidemiology.net/article/PIIS1877782109001738/abstract?rss=yes"><title>Under-diagnosis and under-ascertainment of cases may be the reasons for low childhood cancer incidence in rural India</title><link>http://www.cancerepidemiology.net/article/PIIS1877782109001738/abstract?rss=yes</link><description>Abstract: Cancer statistics from India revealed that childhood cancer incidence is lesser in rural than urban India. This might be due to under-diagnosis or under-ascertainment of cases or could even be true. With registries able to explicitly measure and appropriately streamline the ascertainment of cases to comply with acceptable standards, it is under-diagnosis that is variable and highly influenced by development of or accessibility to specialized centres in or around the registry area. This is reflected implicitly by marked variation in incidence between different populations in India: weighted age standardized rates of all childhood cancers together was the highest (108 per million) in metropolitan areas, followed by other urban (86) and rural (53) areas in that order. A childhood cancer registry focusing on pertinent data collection and specific epidemiological studies is desirable to explain the variations in incidence and outcome of childhood cancers in India.</description><dc:title>Under-diagnosis and under-ascertainment of cases may be the reasons for low childhood cancer incidence in rural India</dc:title><dc:creator>Rajaraman Swaminathan, Rengaswamy Sankaranarayanan, on behalf of other authors</dc:creator><dc:identifier>10.1016/j.canep.2009.11.006</dc:identifier><dc:source>Cancer Epidemiology 34, 1 (2010)</dc:source><dc:date>2009-12-07</dc:date><prism:publicationName>Cancer Epidemiology</prism:publicationName><prism:publicationDate>2009-12-07</prism:publicationDate><prism:volume>34</prism:volume><prism:number>1</prism:number><prism:issueIdentifier>S1877-7821(10)X0002-9</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>107</prism:startingPage><prism:endingPage>108</prism:endingPage></item></rdf:RDF>