Differences In Cancer Rates Research Articles

Early findings from the Dog Aging Project

Initial cancer findings from the Dog Aging Project reveal that there is no difference in cancer rates between purebred and mixed-breed dogs, that malignant tumours are nearly twice as common as benign tumours (rates of 29.7 per 1000 dogs, and 14.7 per 1000 dogs, respectively) and that skin tumours of the limb or foot are overwhelmingly the most common type of tumour in this cohort of American dogs. Surprisingly, owner-reported perceptions of pet health after a tumour diagnosis were still overwhelmingly positive. These findings generate more hypotheses that require testing, which will be the goal of Dog Aging Project researchers for years to come. Cancer findings from dogs will be very important in translational research to humans.

Differences in cancer rates among adults born between 1920 and 1990 in the USA: an analysis of population-based cancer registry data

Trends in cancer incidence in recent birth cohorts largely reflect changes in exposures during early life and foreshadow the future disease burden. Herein, we examined cancer incidence and mortality trends, by birth cohort, for 34 types of cancer in the USA. In this analysis, we obtained incidence data for 34 types of cancer and mortality data for 25 types of cancer for individuals aged 25-84 years for the period Jan 1, 2000, to Dec 31, 2019 from the North American Association of Central Cancer Registries and the US National Center for Health Statistics, respectively. We calculated birth cohort-specific incidence rate ratios (IRRs) and mortality rate ratios (MRRs), adjusted for age and period effects, by nominal birth cohort, separated by 5 year intervals, from 1920 to 1990. We extracted data for 23 654 000 patients diagnosed with 34 types of cancer and 7 348 137 deaths from 25 cancers for the period Jan 1, 2000, to Dec 31, 2019. We found that IRRs increased with each successive birth cohort born since approximately 1920 for eight of 34 cancers (pcohort<0·050). Notably, the incidence rate was approximately two-to-three times higher in the 1990 birth cohort than in the 1955 birth cohort for small intestine (IRR 3·56 [95% CI 2·96-4·27]), kidney and renal pelvis (2·92 [2·50-3·42]), and pancreatic (2·61 [2·22-3·07]) cancers in both male and female individuals; and for liver and intrahepatic bile duct cancer in female individuals (2·05 [1·23-3·44]). Additionally, the IRRs increased in younger cohorts, after a decline in older birth cohorts, for nine of the remaining cancers (pcohort<0·050): oestrogen-receptor-positive breast cancer, uterine corpus cancer, colorectal cancer, non-cardia gastric cancer, gallbladder and other biliary cancer, ovarian cancer, testicular cancer, anal cancer in male individuals, and Kaposi sarcoma in male individuals. Across cancer types, the incidence rate in the 1990 birth cohort ranged from 12% (IRR1990 vs 1975 1·12 [95% CI 1·03-1·21] for ovarian cancer) to 169% (IRR1990 vs 1930 2·69 [2·34-3·08] for uterine corpus cancer) higher than the rate in the birth cohort with the lowest incidence rate. The MRRs increased in successively younger birth cohorts alongside IRRs for liver and intrahepatic bile duct cancer in female individuals, uterine corpus, gallbladder and other biliary, testicular, and colorectal cancers, while MRRs declined or stabilised in younger birth cohorts for most cancers types. 17 of 34 cancers had an increasing incidence in younger birth cohorts, including nine that previously had declining incidence in older birth cohorts. These findings add to growing evidence of increased cancer risk in younger generations, highlighting the need to identify and tackle underlying risk factors. American Cancer Society.

Associations between diabetes and cancer: A 10-year national population-based retrospective cohort study

AimsTo investigate the risk of cancer in people with diabetes compared to the population without diabetes and to gain insight into the timely association between diabetes and cancer at national level. MethodsA retrospective cohort study was conducted to analyse the role of diabetes in the development of cancer, based on service utilisation and antidiabetic dispensing data of the population between 2010 and 2021. Univariate and multivariate Cox regression were used to examine how diabetes status, in relationship with age and sex are related to the time to cancer diagnosis. ResultsExamining a population of 3 681 774 individuals, people with diabetes have a consistently higher risk for cancer diagnosis for each cancer site studied. Diabetes adds the highest risk for pancreatic cancer (HR = 2.294, 99 % CI: 2.099; 2.507) and for liver cancer (HR = 1.830, 99 % CI: 1.631; 2.054); it adds the lowest – but still significant – risk for breast cancer (HR = 1.137, 99 % CI: 1.055; 1.227) and prostate cancer (HR = 1.171, 99 % CI: 1.071; 1.280).The difference in cancer rate is driven by the younger age group (40–54 years: for patients with diabetes 5.4 % vs. controls 4.4 %; 70–89 years: for patients with diabetes 12.7 % vs. controls 12.4 %). There are no consistent results whether the presence of diabetes increases the risk of cancer diagnosis differently in males and females. The cancer incidence starts to increase before the diagnosis of diabetes and peaks in the year after. By the year after the start of the inclusion date, the incidence is 114/10,000 population in the control group, vs 195/10,000 population in the group with diabetes. Following this, the incidence drops close to the control group. ConclusionsScreening activities should be revised and the guidelines on diabetes should be complemented with recommendations on cancer prevention also considering that the cancer incidence is highest around the time of the diagnosis of diabetes. For prostate cancer, our results contradict many previous studies, and further research is recommended to clarify this.

Role of sex hormones in lung cancer.

Lung cancer represents the world's leading cause of cancer deaths. Sex differences in the incidence and mortality rates for various types of lung cancers have been identified, but the biological and endocrine mechanisms implicated in these disparities have not yet been determined. While some cancers such as lung adenocarcinoma are more commonly found among women than men, others like squamous cell carcinoma display the opposite pattern or show no sex differences. Associations of tobacco product use rates, susceptibility to carcinogens, occupational exposures, and indoor and outdoor air pollution have also been linked to differential rates of lung cancer occurrence and mortality between sexes. While roles for sex hormones in other types of cancers affecting women or men have been identified and described, little is known about the influence of sex hormones in lung cancer. One potential mechanism identified to date is the synergism between estrogen and some tobacco compounds, and oncogene mutations, in inducing the expression of metabolic enzymes, leading to enhanced formation of reactive oxygen species and DNA adducts, and subsequent lung carcinogenesis. In this review, we present the literature available regarding sex differences in cancer rates, associations of male and female sex hormones with lung cancer, the influence of exogenous hormone therapy in women, and potential mechanisms mediated by male and female sex hormone receptors in lung carcinogenesis. The influence of biological sex on lung disease has recently been established, thus new research incorporating this variable will shed light on the mechanisms behind the observed disparities in lung cancer rates, and potentially lead to the development of new therapeutics to treat this devastating disease.

Abstract PS8-18: Describing the cancer spectrum in families with CHEK2 pathogenic and likely pathogenic variants by mutation type

Abstract Background: Deleterious CHEK2 variants have well-defined risks for breast and colorectal cancers. Some studies have also suggested association with a variety of other cancers, including leukemia, kidney, prostate, thyroid and gastric cancers. However, most CHEK2 studies are based on European founder mutations, and there is a lack of data on non-founder mutations. Here, we describe the cancer family histories of patients with both founder and non-founder CHEK2 mutations. Methods: This is a retrospective review of patients who underwent germline testing of 31 cancer risk genes. All pathogenic (P) and likely pathogenic (LP) variants in CHEK2 were selected from our database and categorized as founder or non-founder mutations. Personal and family histories of cancer reported by the ordering provider were recorded for each case. Cancer rates were calculated as the number of patients with a personal and/or family history of each cancer divided by the total number of patients. Ethnicities in our CHEK2+ cohort and our overall database were calculated as a percentage. Results: A total of 132 patients were found to have P/LP variants in CHEK2. This CHEK2+ cohort was largely Caucasian (79.5%), despite our overall database being ethnically diverse (56% Caucasian). Nineteen different mutations were identified, 75% of which were founder and 25% were non-founder mutations. Personal histories of cancer were identified in 7% of patients. Twenty-eight different cancers were reported in patients’ personal/family histories. The rates of select cancers in the total cohort, founder mutation group and non-founder mutation group are reported in Table 1. Discussion: These findings support previous reports that prostate, gastric and kidney cancers may be part of the CHEK2 cancer spectrum, which has typically only included breast and colorectal cancer. We also identify ovarian and pancreatic cancer as potential CHEK2-associated cancers. Cancer rates are similar between CHEK2 patients with founder and non-founder mutations. Differences in cancer rates were observed between these two groups, but this cohort was too small to determine significance. Additional studies are needed to understand the overlap of cancer risk with non-founder mutations and those well-described for founder mutations. Table 1: Select cancer rates by CHEK2 mutation typeBreast FemaleOvarianProstateColorectalPancreaticUterineGastricKidneyAll80.3%39.4%25%23.5%13.6%8.3%8.3%6.1%Founder81.8%40.4%30.3%23.2%18.2%9.1%9.1%8.1%Non-founder75.8%36.3%9.1%24.2%0%6%6%0% Citation Format: Julia G Moroney, Michele S Basiliere. Describing the cancer spectrum in families with CHEK2 pathogenic and likely pathogenic variants by mutation type [abstract]. In: Proceedings of the 2020 San Antonio Breast Cancer Virtual Symposium; 2020 Dec 8-11; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2021;81(4 Suppl):Abstract nr PS8-18.

Outcomes by Race Among Women Referred to an Academic Colposcopy Clinic with a Patient Navigation Program.

Background: Although minority women are at higher risk of cervical cancer in the United States, little is known about differences in rates of colposcopy and loop electrosurgical excision procedure (LEEP) by race once patients present for care. Materials and Methods: A prospective registry of patients presenting to an academic colposcopy clinic was queried from 2008 to 2018. Women with missing race or cytology results, prior hysterectomy, or prior history of cervical, vulvar, or vaginal cancer were excluded. Poisson and logistic regression models were performed to evaluate the associations between race and colposcopy, LEEP, and cancer rates, adjusting for referral Papanicolaou (Pap), human papillomavirus (HPV) result, year of visit, age, insurance, pregnancy, number of sexual partners, and smoking status. Results: A total of 4506 women were included (56.1% white and 43.9% non-white). Referral for high-grade cytology was more likely among white compared to non-white women (22.5% vs. 17.5%, p < 0.001), as well as positive HPV testing (white 7.8% vs. non-white 6.0%, p < 0.001). The colposcopy rate was slightly higher among black (incidence rate ratio [IRR]adjusted 1.11, 95% confidence interval [CI] 1.03-1.19, p = 0.006) and Hispanic women (IRRadjusted 1.13, 95% CI 1.06-1.21, p = 0.0003) compared to white women. Hispanic women were significantly more likely to undergo LEEP (odds ratioadjusted 1.26, 95% CI 1.01-1.58, p = 0.04). However, no significant difference in cancer, adenocarcinoma in situ, or high-grade histology was noted by race. Conclusions: Black and Hispanic women referred for abnormal Pap or HPV results underwent a greater number of colposcopies compared to white women, and Hispanic women underwent a greater number of LEEPs. Although cancer is rare in our cohort, there was no statistical difference in rate of cancer by race.

Cancer mortality rates among US and foreign-born individuals: United States 2005–2014

From 1970 to 2010 the foreign-born population in the United States has rapidly increased from 9.6 to 40.0 million individuals. Historically, differences in cancer rates have been observed between US-born and foreign-born individuals. However, comprehensive and up-to-date data on US cancer rates by birth place is lacking. To compare cancer mortality rates among foreign and US-born individuals, population-based cancer mortality data were obtained from the CDC's National Center for Health Statistics. Utilizing data recorded on death certificates, individuals were categorized as US-born or foreign-born. Annual population estimates were obtained from the American Community Survey. Age-adjusted mortality rates and rate ratios (RRs) for all cancer sites were calculated using SEER*Stat. A total of 5,670,535 deaths from malignant cancers were recorded in the US from 2005 to 2014 and 9% of deaths occurred among foreign-born individuals. Overall, foreign-born individuals had a 31% lower cancer mortality rate when compared to US-born individuals (Rate Ratio (RR): 0.69 (95% CI: 0.68–0.69)), and similar results were observed when stratifying by sex, race/ethnicity, age, and geographic region. However, foreign-born individuals did have significantly elevated cancer mortality rates for seven cancers sites, of which five were infection-related, including: nasopharynx (RR: 2.01), Kaposi Sarcoma (RR: 1.94), stomach (RR: 1.82), gallbladder (RR: 1.47), acute lymphocytic leukemia (RR: 1.27), liver and intrahepatic bile duct (RR: 1.24), and thyroid (RR: 1.22) cancers. Many of these deaths could be avoided through improved access to prevention, screening, and treatment services for immigrant populations in the US or in their country of origin.

Rural–Urban Disparities in Stage of Diagnosis Among Cancers With Preventive Opportunities

Despite having lower overall incidence rates, rural populations tend to have higher cancer mortality rates. Rural populations often have higher rates of cancers with primary and secondary prevention modalities. However, there is limited research on rural-urban differences in incidence by stage. Therefore, the objective was to assess rural-urban differences in cancer rates by stage. The North American Association of Central Cancer Registries public use data set (2009-2013) was used to calculate age-adjusted incidence rates and rate ratios (rural versus urban) for all stageable cancers, tobacco-associated cancers, human papillomavirus-associated cancers, and individual cancers with screening modalities. Analyses were performed in summer 2017 for all populations and stratified by race/ethnicity and region for localized and distant stages. For all cancers, rural populations had lower rates of localized stage cancers (rate ratio=0.95, 95% CI=0.95, 0.95) and higher rates of distant stage cancer (rate ratio=1.05, 95% CI=1.05, 1.06). Higher rates of distant stage human papillomavirus-associated, tobacco-associated, colorectal, oropharyngeal, lung, cervical cancers, and melanoma were identified in rural populations. Racial/ethnic stratifications identified higher rates of distant stage cancers in rural non-Hispanic whites, but not non-Hispanic blacks and Hispanics. Distant stage lung cancer rates were higher in all rural groups, whereas rural whites had higher distant rates of tobacco-associated, colorectal, and cervical cancers, and rural blacks had higher distant rates for human papillomavirus-associated and oral cancers. Regional stratifications showed the greatest disparity in stage at diagnosis in the South. These findings might help explain the higher rural cancer mortality rates and provide additional evidence to support targeted interventions.

Highlights of This Issue

The current opioid epidemic is an unequivocal and serious public health issue. Drug overdoses are now the leading cause of death for Americans under 50 years old, with most of the fatalities due to opioid overdoses. However, few studies have focused on the carcinogenic effects of long-term opium consumption. Moossavi and colleagues examined the association between opium consumption and pancreatic cancer incidence in a large-scale prospective cohort in Iran. This long-term case–control study confirmed opium carcinogenicity and revealed chronic opium use as a risk factor for pancreatic cancer. More studies should be organized to assess the carcinogenicity of long-term opioid use.International and ethnic differences in cancer rates exist, and they are minimally explained by genetic factors. A substantial portion of the differences in cancer rates can be explained by modifiable factors, while other factors, such as the microbiome and the metabolome, are emerging as important intermediary components in cancer prevention. To refine current concepts, researchers have started incorporating emerging technologies for measuring diet and physical activity in human populations. Questions remain regarding reported associations and the best methods to assess associations. This position paper from Mahabir and colleagues highlights the state of the science and priorities for future research.Routine testing of colorectal cancer (CRC) starting at age 50 saves lives, but local CRC screening data are not widely available. Multilevel regression post-stratification for small-area estimation with 2014 Behavioral Risk Factor Surveillance System and Census 2014 county population data revealed substantial county-level variations in the prevalence of being up-to-date with CRC screening: it ranged from 40.1% to 79.8%, with a median of 65.5%. More than 80% of 3,142 counties had &lt;70% up-to-date screening, far from the national goal of 80% by 2018. This study by Berkowitz and colleagues suggests a great need for locally targeted interventions for counties with very low CRC screening prevalence.Tobacco-specific nitrosamines (TSNAs) are carcinogens found in tobacco products. Recent evidence indicates that levels of the TSNA NNK have increased in Canadian cigarettes. The current study by Czoli and Hammond examined whether these increases translated into differences in exposure among Canadian tobacco users, using urinary metabolite measures from the Canadian Health Measures Survey. The findings indicate that exposure to the TSNA NNK among Canadian tobacco users increased considerably from 2007–09 through 2012–13, in parallel to NNK increases in the tobacco of Canadian cigarettes. The findings raise questions about the commitment of tobacco manufacturers to minimize carcinogen levels to the full extent possible.

Research Strategies for Nutritional and Physical Activity Epidemiology and Cancer Prevention.

Very large international and ethnic differences in cancer rates exist, are minimally explained by genetic factors, and show the huge potential for cancer prevention. A substantial portion of the differences in cancer rates can be explained by modifiable factors, and many important relationships have been documented between diet, physical activity, and obesity, and incidence of important cancers. Other related factors, such as the microbiome and the metabolome, are emerging as important intermediary components in cancer prevention. It is possible with the incorporation of newer technologies and studies including long follow-up and evaluation of effects across the life cycle, additional convincing results will be produced. However, several challenges exist for cancer researchers; for example, measurement of diet and physical activity, and lack of standardization of samples for microbiome collection, and validation of metabolomic studies. The United States National Cancer Institute convened the Research Strategies for Nutritional and Physical Activity Epidemiology and Cancer Prevention Workshop on June 28-29, 2016, in Rockville, Maryland, during which the experts addressed the state of the science and areas of emphasis. This current paper reflects the state of the science and priorities for future research. Cancer Epidemiol Biomarkers Prev; 27(3); 233-44. ©2017 AACR.

Comparing cancer detection rates of patients undergoing short term follow-up vs routine follow-up after benign breast biopsies, is follow-up needed?

PurposeTo compare cancer rates after benign breast biopsies between patients with short term imaging follow-up (STFU) and those with routine follow-up (RFU). Materials & methodsRetrospective review of benign stereotactic, US or DCE-MRI breast biopsies. ResultsOf 580 lesions, 192 (33%) had STFU, and 388 (67%) had RFU. For US and mammographic detected lesions, there is no difference in cancer rates between the STFU (1 cancer, n=148) and the RFU group (0 cancer, n=365) (p=0.29). There were 2 cancers in the STFU group versus 0 in the RFU DCE-MRI group (p=0.54). ConclusionOur results support RFU after benign ultrasound and stereotactic breast biopsies.

Debunking mathematically the logical fallacy that cancer risk is just “bad luck”

Tomasetti and Vogelstein recently proposed that the majority of variation in cancer risk among tissues is due to "bad luck," that is, random mutations arising during DNA replication in normal noncancerous stem cells. They generalize this finding to cancer overall, claiming that "the stochastic effects of DNA replication appear to be the major contributor to cancer in humans." We show that this conclusion results from a logical fallacy based on ignoring the influence of population heterogeneity in correlations exhibited at the level of the whole population. Because environmental and genetic factors cannot explain the huge differences in cancer rates between different organs, it is wrong to conclude that these factors play a minor role in cancer rates. In contrast, we show that one can indeed measure huge differences in cancer rates between different organs and, at the same time, observe a strong effect of environmental and genetic factors in cancer rates.

Thyroid cancer in patients with toxic nodular goiter—is the incidence increasing?

BackgroundThere has been a dramatic increase in the incidence of thyroid cancer, but it is unclear if this has occurred in patients with toxic nodular goiter (TNG). MethodsTNG was defined as one or more thyroid nodules in combination with a low serum TSH level. Patients who underwent thyroidectomy for TNG were identified from a prospectively maintained database. The rates of incidental thyroid cancer were compared over the intervals 1990 to 1999, 2000 to 2009, and 2010 to 2014. ResultsThere was no significant difference in cancer rate between the 3 time periods. Overall, 7 (4.7%) of the 148 patients had thyroid cancer; similarly, 1 (3.2%) of the 31 patients from 1990 to 1999, 3 (4.2%) of 72 patients from 2000 to 2009, and 3 (6.7%) of the 45 patients from 2010 to 2014 (P > .05) had thyroid cancer. ConclusionsNo significant increase in the rate of carcinoma was observed in patients with TNG. As a result, the risk benefit analysis should not change when considering therapeutic options for TNG.

Decision Analysis of Dutasteride Use for Patients With Negative Prostate Biopsy

To determine whether the additional benefits of improved prostate cancer detection associated with 5α-reductase inhibitors are sufficient to warrant chemoprevention in the case where the degree of prostate cancer risk reduction is deemed inadequate. We reanalyzed data from REDUCE, a randomized trial of dutasteride for prostate cancer chemoprevention in men with prior negative biopsy. We evaluated whether statistical models using prostate-specific antigen (PSA) and PSA velocity could help predict the result of repeat prostate biopsy separately for dutasteride and placebo groups. Area under the curve was evaluated by 10-fold cross-validation. PSA velocity improved discrimination at 4 years in the dutasteride group but not at 2 years nor in the placebo group. At 2 years, dutasteride improved discrimination of PSA slightly (0.616 vs. 0.603 for any grade cancer; 0.681 vs. 0.676 for high-grade disease). Between-group differences in cancer rates at 4 years were small. Clinicians who are willing to treat at least 23 patients with dutasteride for 2 years to avoid 1 prostate cancer diagnosis should offer dutasteride after initial negative biopsy. Clinicians not willing to do so might consider dutasteride for its additional benefit of reducing unnecessary biopsy, although this benefit is apparent only under very restrictive conditions. It is difficult to justify extending treatment with dutasteride for >2 years.

Abstract B17: Health disparities in brain cancer incidence

Abstract Introduction: Glioblastoma Multiforme (GBM) is a lethal and highly aggressive cancer where risk factors, other than radiation exposure, are still largely unknown. It has been reported that US black patients have lower brain cancer rates than whites, and this has been ascribed to differences in socio-economic status. No study has analyzed possible risk factors that could explain the observed differences in rates with race. Methods: All cases of pathologically confirmed GBM diagnosed between 1973 and 2010 were extracted from the Surveillance, Epidemiology and End Results (SEER) data base, and age-adjusted incidence rates x 100,000 persons were calculated according to race (blacks, whites, others), and age groups (0-19, 20-49, 50-85+ years). Survival was calculated using Cox proportional hazard models according to race. The NHANES data base was analyzed to assess time since last visit to a dentist (surveyed in 1999 through 2004), performance and frequency of a routine check-up in previous 3 years (surveyed in 1999 through 2002). Results: There were 25,101 GBM patients in the data set, 360 of which were age 0-19 years, 4,234 age 20-49 years, 20,507 age 50-85+ years. GBM incidence rate was 0.1 x 100,000 persons in the younger age group, with no differences between black and white patients. Among patients age 20-49 years the incidence rate was 1.1 x 100,000 in whites and 0.7 x 100,000 in blacks, in patients age 50-85+ years the incidence rate was 9.5 x 100,000 and 4.4 x 100,000. The ratio of the incidence in white patients/black patients was 1, 1.6 and 2.2 respectively in the three age groups, without differences across geographic areas where the diagnosis was performed. Survival was similar in the two race groups: 3 year survival was 6.5% in whites, 9% in blacks; 5year survival was 3.8% and 4.7% respectively. Cancer treatment modalities did not significantly differ between the two races. From the NHANES data base (26,958 subjects, blacks = 6,719), 65.6 % of whites had a dentist visit within the previous year versus 54.3% of blacks (p=0.001). White subjects were significantly more likely to undergo routine check up once or more a year in comparison to black subjects (81.9% vs. 68.3%; p = 0.001). Conclusions: GBM rates continue to be lower in black than white patients. The difference is largest in the older age group, suggesting a relation to the genetic background and subtype of GBM that occurs in patients older than 50 years and/or to environmental exposure. There is no geographic difference in cancer rates arguing against state specific environmental risk factors. Given the overlapping survival observed in black and white patients, it is unlikely that access to care plays a role in the differences in incidence rates. Racial differences in access to dental care and diagnostic radiation exposure should be explored in ad-hoc epidemiologic studies. Citation Format: Emanuela Taioli, Wenqi Gan, Gregory J. Riggins. Health disparities in brain cancer incidence. [abstract]. In: Proceedings of the Sixth AACR Conference: The Science of Cancer Health Disparities; Dec 6–9, 2013; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2014;23(11 Suppl):Abstract nr B17. doi:10.1158/1538-7755.DISP13-B17

Risk of Kaposi Sarcoma Among Immigrants to Sweden

Kaposi sarcoma (KS) is a locally aggressive endothelial tumour that is classified into 4 clinico-epidemiological forms: classic KS affecting lower limbs in elderly Mediterranean or East European men; endemic KS occurring in extremities among Equatorial African middle-aged men and children; iatrogenic KS involving lower limbs in immunosuppressive patients; and AIDS-associated (epidemic) KS observed among homo- and bisexual HIV-1-infected young men (1, 2). The world-wide epidemiology of KS has changed by spreading of HIV infection (1). For example, KS represented 7% of all cancers in Sub-Saharan African men in the 1960s, whereas in the 1980s the rate increased to 50%. Furthermore, the age distribution of KS has changed from elderly (in classic form) to the late thirties (in epidemic form). KS is a rare tumour in Nordic countries; the incidence is 0.1-0.2/100,000 according to the Cancer Incidence in Five Continents (CI5) report (3). According to this source, the rate in many Asian countries is <0.5/100,000, whereas African American men have a rate of 6.2/100,000. The highest rate is in men from Zimbabwe (52.2/100,000) (3). Human herpesvirus 8 (HHV-8) is the recognised cause of all forms of KS (2). There is discrepancy between the prevalence of HHV-8 and KS incidence in some populations suggesting underreporting of KS or the existance of some unknown protective factors for KS (1). Migrant studies provide data on international differences in cancer rates (4). Furthermore, studies on immigrants may provide supplementary and confirmatory data on the incidence of cancer in countries without local cancer registries. A few available studies on immigrants have focused only on classic KS (5, 6). In the present study, we report mean age at diagnosis and KS rates by site in first-generation immigrants to Sweden. (Less)

Cancer after Thyroidectomy: A Multi-Institutional Experience with 1,523 Patients

The incidence of thyroid cancer in patients treated operatively for thyroid disease has been historically low (<5%). Previous series have not specifically addressed cancer rates in both euthyroid and hyperthyroid patients. This study examined cancer frequency in patients referred for removal of benign thyroid disease in a multi-institutional series. A total of 2,551 patients underwent thyroidectomy at 3 high-volume institutions. Indeterminate/malignant fine-needle aspiration diagnosis was excluded (n = 1,028). Cancer cases were compared among 1,523 patients with Graves' disease (n = 264), nodular goiter (n = 1,095), and toxic nodular goiter (n = 164). Fisher's exact test, chi-square test, Wilcoxon rank sum, Kruskal-Wallis nonparametric t-tests, and multivariable logistic regression were used. Overall, 238 (15.6%) cancers were recorded: Graves' disease (6.1%), nodular goiter (17.5%), and toxic nodular goiter (18.3%). Cancer rates were significantly different among these groups (p < 0.01) and significantly higher in nodular goiter and toxic nodular goiter vs Graves' disease (p < 0.01); no significant differences in cancer rates were noted among institutions. Overall, 275 patients had thyroiditis (18%). There was a significant association with younger age, male sex, nodular thyroids, and cancer (p < 0.05). Presence of thyroiditis or performance of preoperative fine-needle aspiration was not associated with cancer. Mean cancer size was 1.1 cm (46% >0.5 cm; 39% >1 cm). Most patients underwent total thyroidectomy (80%). These data confirm higher than expected incidental thyroid cancer rates (15.6%) in the largest multi-institutional surgical series to date. Nodular thyroids, males, and young patients were more likely to harbor incidental carcinoma. These data support consideration of initial total thyroidectomy as the preferred approach for patients referred to the surgeon with bilateral nodular disease.

Digital versus screen film mammography: Impact on positive predictive values following transition.

12 Background: The Calgary Health Region changed from screen film mammography (SFM) to digital mammography (DM) in 2005. This retrospective study was designed to determine the effect of this conversion on positive predictive values (PPV) for cancerous and precancerous breast lesions. Methods: In the Calgary region, biopsies for mammographic calcifications are only done at Foothills Medical Centre (FMC) by a small group of mammographers employing homogeneous techniques. From FMC’s database, we reviewed core biopsy data for mammographic calcifications in the years 2002-2004 (SFM years) and 2008-2010 (DM years). Mammographic masses were excluded. We determined PPVs for each set of years for detection of cancerous lesions (PPV3for calcifications). We further calculated the PPVs of SFM and DM for detection of high-risk lesions, including ADH, ALH, LCIS, and papilloma collectively (precancerous lesions). The detection rates of benign lesions (excluding precancerous lesions) after biopsy were also determined. Statistical analysis was performed using two-tail z-tests. Results: 3,778 biopsies in 3,544 patients were reviewed. The difference in overall detection rate of cancer after biopsy for mammographic calcification between SFM (PPV3 = 24.7%) and DM (PPV3 = 23.8%) was not statistically significant (p = .53). On further analysis, the PPV for precancerous lesions increased (p &lt; .0001) in DM (11.6%) versus SFM (7.8%). No significant difference (p = .065) was found in detection of benign lesions. Conclusions: In comparing DM to SFM, we found no significant change in PPV3 with respect to calcifications. However, with DM, there was a statistically significant increase in detection of lesions considered at risk for future malignancy. Given that the natural history of these premalignant lesions is incompletely understood, the significance of this finding is in question. This potential trend could be further strengthened by determining PPV1for cancerous and precancerous lesions with respect to calcifications. [Table: see text]

Nutritional epidemiological studies in cancer prevention

It has been almost 30 years since Doll and Peto suggested that most of the differences in cancer rates could be attributed to the environment and behavioral factors including diet. Since then epidemiological studies have reported that individuals consuming large amounts of fruits and vegetables have a reduced risk of cancer. From this evidence, large randomized trials of long duration were designed to test the hypothesis that some micronutrients contained in plant foods decrease cancer risk. Despite the promising experimental and epidemiological data, most randomized controlled trials failed to confirm a protective role for single or combined elements in cancer prevention. The results from randomized trials of micronutrients for cancer prevention have been mixed. Some trials did not demonstrate chemopreventive efficacy for their primary endpoints but showed statistically significant reductions in secondary outcomes, whereas others showed unexpected harmful effects. On the basis of these findings and reflections of what went wrong it is important to find alternative approaches to move forwards in cancer prevention. Clearly, the evidence is not encouraging for further preventive trials on cancer in healthy populations. However, if we identify high-risk individuals using models that include genetic polymorphisms, or in the future, MicroRNA profiles, prevention trials could be designed to target only these groups.

Helicobacter pyloriand gastric cancer in the Middle East: A new enigma?

The Middle East is the home of ethnic groups from three main backgrounds: Semitic (Arabs and Jews), Indo-European (Persians and Kurdish) and Turkic (Turkish and Turkmens). Its geographic location, which has been under continuous influences from Asia, Europe and Africa, has made it an ideal site for epidemiological studies on Helicobacter pylori (H. pylori) infection and genotyping. The gastric cancer rate differs in this region from very high in Iran (26.1/10(5)) to low in Israel (12.5/10(5)) and very low in Egypt (3.4/10(5)). Epidemiological studies showed that the prevalence of H. pylori is almost similar in those countries with a high level of infection in childhood. Importantly, the frequency of vacA s1 and m1 regions and cagA+ genotypes were higher in non Semitic populations who inhabit the North than Semitic populations, the inhabitants of Southern parts of the Middle East. H. pylori infection prevalence, distribution pattern of virulence factors, diet and smoking could not have explained the difference in cancer rate. This reflects the multifactorial aetiology of gastric cancer and suggests that H. pylori infection does not always directly correlate with the risk for gastrointestinal disease, such as gastric cancer. Further detailed investigations and international comparative studies of each risk factor need to be performed to investigate whether this represents a true enigma.