Age-specific Cancer Incidence Rates Research Articles

Polygenic Risk Score, Environmental Tobacco Smoke, and Risk of Lung Adenocarcinoma in Never-Smoking Women in Taiwan

Estimating absolute risk of lung cancer for never-smoking individuals is important to inform lung cancer screening programs. To integrate data on environmental tobacco smoke (ETS), a known lung cancer risk factor, with a polygenic risk score (PRS) that captures overall genetic susceptibility, to estimate the absolute risk of lung adenocarcinoma (LUAD) among never-smokers in Taiwan. The analyses were conducted in never-smoking women in the Taiwan Genetic Epidemiology Study of Lung Adenocarcinoma, a case-control study. Participants were recruited between September 17, 2002, and March 30, 2011. Data analysis was performed from January 17 to July 15, 2022. A PRS was derived using 25 genetic variants that achieved genome-wide significance (P < 5 × 10-8) in a recent genome-wide association study, and ETS was defined as never exposed, exposed at home or at work, and exposed at home and at work. The Individualized Coherent Absolute Risk Estimator software was used to estimate the lifetime absolute risk of LUAD in never-smoking women aged 40 years over a projected 40-year span among the controls by using the relative risk estimates for the PRS and ETS exposures, as well as age-specific lung cancer incidence rates for never-smokers in Taiwan. Likelihood ratio tests were conducted to assess an additive interaction between the PRS and ETS exposure. Data were obtained on 1024 women with LUAD (mean [SD] age, 59.6 [11.4] years, 47.9% ever exposed to ETS at home, and 19.5% ever exposed to ETS at work) and 1024 controls (mean [SD] age, 58.9 [11.0] years, 37.0% ever exposed to ETS at home, and 14.3% ever exposed to ETS at work). The overall average lifetime 40-year absolute risk of LUAD estimated using PRS alone was 2.5% (range, 0.6%-10.3%) among women never exposed to ETS. When integrating both ETS and PRS data, the estimated absolute risk was 3.7% (range, 0.6%-14.5%) for women exposed to ETS at home or work and 5.3% (range, 1.2%-12.1%) for women exposed to ETS at home and work. A super-additive interaction between ETS and the PRS (P = 6.5 × 10-4 for interaction) was identified. This study found differences in absolute risk of LUAD attributed to genetic susceptibility according to levels of ETS exposure in never-smoking women. Future studies are warranted to integrate these findings in expanded risk models for LUAD.

Risk prediction models for endometrial cancer: development and validation in an international consortium.

Endometrial cancer risk stratification may help target interventions, screening, or prophylactic hysterectomy to mitigate the rising burden of this cancer. However, existing prediction models have been developed in select cohorts and have not considered genetic factors. We developed endometrial cancer risk prediction models using data on postmenopausal White women aged 45-85 years from 19 case-control studies in the Epidemiology of Endometrial Cancer Consortium (E2C2). Relative risk estimates for predictors were combined with age-specific endometrial cancer incidence rates and estimates for the underlying risk factor distribution. We externally validated the models in 3 cohorts: Nurses' Health Study (NHS), NHS II, and the Prostate, Lung, Colorectal and Ovarian (PLCO) Cancer Screening Trial. Area under the receiver operating characteristic curves for the epidemiologic model ranged from 0.64 (95% confidence interval [CI] = 0.62 to 0.67) to 0.69 (95% CI = 0.66 to 0.72). Improvements in discrimination from the addition of genetic factors were modest (no change in area under the receiver operating characteristic curves in NHS; PLCO = 0.64 to 0.66). The epidemiologic model was well calibrated in NHS II (overall expected-to-observed ratio [E/O] = 1.09, 95% CI = 0.98 to 1.22) and PLCO (overall E/O = 1.04, 95% CI = 0.95 to 1.13) but poorly calibrated in NHS (overall E/O = 0.55, 95% CI = 0.51 to 0.59). Using data from the largest, most heterogeneous study population to date (to our knowledge), prediction models based on epidemiologic factors alone successfully identified women at high risk of endometrial cancer. Genetic factors offered limited improvements in discrimination. Further work is needed to refine this tool for clinical or public health practice and expand these models to multiethnic populations.

Mathematical modeling the gene mechanism of colorectal cancer and the effect of radiation exposure.

Cancer is the result of continuous accumulation of gene mutations in normal cells. The number of mutations is different in different types of cancer and even in different patients with the same type of cancer. Therefore, studying all possible numbers of gene mutations in malignant cells is of great value for the understanding of tumorigenesis and the treatment of cancer. To this end, we applied a stochastic mathematical model considering the clonal expansion of any premalignant cells with different mutations to analyze the number of gene mutations in colorectal cancer. The age-specific colorectal cancer incidence rates from the Surveillance, Epidemiology and End Results (SEER) registry in the United States and the Life Span Study (LSS) in Nagasaki and Hiroshima, Japan are chosen to test the reasonableness of the model. Our fitting results indicate that the transformation from normal cells to malignant cells may undergo two to five driver mutations for colorectal cancer patients without radiation-exposed environment, two to four driver mutations for colorectal cancer patients with low level radiation-exposure, and two to three driver mutations for colorectal cancer patients with high level radiation-exposure. Furthermore, the net growth rate of the mutated cells with radiation-exposure was is higher than that of the mutated cells without radiation-exposure for the models with two to five driver mutations. These results suggest that radiation environment may affect the clonal expansion of cells and significantly affect the development of tumors.

Age-specific cancer incidence rates in children and adolescents in the world

Age-specific cancer incidence rates in children and adolescents in the world

ON RADIATION-INDUCED AGING: ACCELERATED OR PREMATURE AGING.

The concept of radiation-induced aging is revisited from the viewpoint of a mathematical model. The effect of radiation on carcinogenesis is treated based on the Armitage-Doll multi-stage theory. The formula obtained for cancer incidence rate indicates that radiation dose can be explained in terms of time. Radiation-induced aging for acute and chronic exposures is described using age-specific cancer incidence rates as a measure of aging. It shows that accelerated aging is related to the dose rate, whereas premature aging is related to the cumulative dose, providing a simple and natural interpretation of radiation-induced aging. The usefulness of this approach is demonstrated by applying the formula to cancer prevalence data from mice chronically exposed to low dose-rate radiation.

Abstract 2254: Risk models for lung cancer in never-smoking women in Shanghai with implications for screening

Abstract Background: The majority of female lung cancer cases in Asia are never-smokers with distinct risk factor profiles. Given the high burden of disease in this population, there is an increasing need to improve the understanding of lung cancer. Current risk models for lung cancer focus on active smokers and individuals of European ancestry. Therefore, we developed statistical models by integrating genetic and environmental risk factors to estimate absolute and population attribute risk of lung cancer among never-smoking women in Asia. Methods: We built absolute risk models for lung cancer among never-smoking women using data from 71,300 women (760 incident cases) in the Shanghai Women’s Health Study (SWHS), a population-based prospective cohort study. Relative risks were estimated using a multivariable Cox regression model with questionnaire-based risk factors. To account for missing genetic data for some subjects, we simulated genotypes for 10 common single nucleotide polymorphisms (SNP) using information on minor allele frequencies (MAF) and odds ratio estimates from previous genome-wide association studies (GWAS), conditional on family history of lung cancer. We used the iCARE tool to build two models for predicting lifetime (40 years) and 6-year absolute risk of lung cancer using age-specific lung cancer incidence rates, age-specific competing mortality rates, and risk factor distribution with: 1) questionnaire-based risk factors only and 2) questionnaire and genetic data. We then used the full absolute risk model to estimate the population attributable risk (PAR) due to modifiable risk factors, namely coal use and exposure to environmental tobacco smoke (ETS). Results: The questionnaire-based only model included family history of lung cancer, coal use, exposure to ETS, and body mass index (BMI). The full model also included data on 10 lung cancer related SNPs from our previous GWAS and had a wider spread in distribution of absolute lifetime risk (median=2.41%; range=0.43-12.36) compared to the questionnaire-based only model (median=2.72%; range=1.93-4.87). We used the full model to estimate the PAR and found that 1.74% and 6.33% of lung cancer cases could be prevented if never-smoking women in Shanghai did not use coal and were not exposed to ETS, respectively. Furthermore, we found that the full model estimated that 2.5% of the study population had a 6-year absolute risk of lung cancer higher than 1.51%, which is the suggested risk threshold for screening by existing risk models. Conclusion: We built risk models for never-smoking Asian women and estimated the contribution of coal use and ETS to the burden of lung cancer in Shanghai. This initial work shows promise for expanding and validating risk models in this population with potential translational implications, such as providing insight to identifying high risk individuals that may be eligible for lung cancer screening and primary prevention efforts. Citation Format: Batel Blechter, Parichoy Pal Choudhury, Xiao-ou Shu, Wei Zheng, Qiuyin Cai, Gong Yang, Jason Y.Y. Wong, Bu-Tian Ji, Wei Hu, Anne Rositch, Nilanjan Chatterjee, Nathaniel Rothman, Qing Lan. Risk models for lung cancer in never-smoking women in Shanghai with implications for screening [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 2254.

Fractions and trends of cancer burden attributable to population ageing in China

Objective: To analyse the fractions and trends of cancer burden attributable to population ageing, adult population size, age-specific incidence and case fatality rate in China between 1990 and 2019. Methods: We extracted data from the database of Global Disease Burden Study, including the number of cancer cases, deaths and corresponding population of 29 cancer types for Chinese adults aged 25 years and older from 1990 to 2019. Using the cancer deaths in 1990 as a reference, we employed a decomposition method to express cancer deaths as the product of four factors among men and women from 1991 to 2019. The fractions attributable to cancer deaths among total cancer deaths in that year were calculated and its time trends were assessed. Results: In 2019, we estimated that there were 2 690 000 cancer deaths among adults aged 25 and older in China. Of which, cancer deaths attributable to population ageing, adult population size, age-specific cancer incidence and case fatality rate were 740 000 (27.5% of total cancer deaths in 2019), 1 091 000 (40.6%), 198 000 (7.3%) and -728 000 (-27.1%), respectively. In 2019, lung cancer, stomach cancer, esophageal cancer, liver cancer and colorectal cancer ranked the top five cancers among population ageing attributable to cancer deaths. For 29 cancer types, the fractions of population ageing attributable to cancer deaths among total deaths of that cancer were ranged from 9.3% to 40.5%. The ageing attributable to cancer deaths and its fractions were increased rapidly since 1997, while those estimates were negative before 1997. Conclusions: The population ageing process in China was one of the major contributors to the increase in cancer burden in recent years, which has caused more cancer deaths than that by age-specific cancer incidence. Accordingly, activities toward healthy ageing would be the key to cancer prevention and control.

Age-specific lip, oral cavity and pharynx cancer incidence rate in the world

Age-specific lip, oral cavity and pharynx cancer incidence rate in the world

Global, Regional, and National Lifetime Probabilities of Developing Cancer in 2020

Background: The lifetime risk of cancer is a measure of the cumulative impact of cancer across a defined age span, and has obvious intuitive appeal. There are however few examples of its systematic use in comparative assessments of cancer-specific risk across populations. We therefore sought to estimate and interpret the lifetime and age-conditional probabilities of developing cancer at the country, world region and global level in 2020. Methods: We obtained estimates of sex- and age-specific cancer incidence rates from GLOBOCAN for 185 countries for the year 2020, alongside all-cause mortality and population data from the United Nations. Countries were categorized into quartiles of the Human Development Index (HDI) as developed by the United Nations Development Programme. The lifetime risk of cancer was estimated using the adjusted for multiple primaries (AMP) method, taking into account competing risks of death from causes other than cancer as well as average life expectancy. Findings: In 2020, the estimated global lifetime risk of cancer from birth to death was 25.1% (26.3% in men and 24.0% in women) . There were marked differences in risks between countries within world regions and by level of human development. In very high HDI, high HDI, medium HDI and low HDI countries, the lifetime risk of cancer was 38.5%, 25.4%, 11.4%, and 10.3%, respectively, with cancer risks highest in Ireland (49.7%) and lowest in Central African Republic (6.6%). There was similar heterogeneity according to cancer type by sex. Worldwide, prostate cancer and breast cancer were associated with the greatest lifetime risks among men and women, of 4.6% and 5.9% respectively. The lifetime risk of cancer decreased by age, with a remaining risk of 12.6% from the age 70 years. Interpretation: In 2020, the global lifetime risk of cancer from birth to death translates approximately 1 in 4 persons developing cancer, with men and women having similar levels of lifetime risk. The identified age-specific variations in cancer risk at the population level can provide important information to support the targeted cancer prevention and health systems planning. Funding: National Key R&D Program of China, National Natural Science Foundation of China, and Beijing Nova Program Declaration of Interest: All authors declare no competing interests.

Age-specific larynx cancer incidence rate in the world.

Age-specific larynx cancer incidence rate in the world.

Age-specific testis cancer incidence rate in the world.

Age-specific testis cancer incidence rate in the world.

Age-specific skin cancer incidence rate in the world.

Age-specific skin cancer incidence rate in the world.

Ensemble forecasting of a continuously decreasing trend in bladder cancer incidence in Taiwan

Bladder cancer is one of the most common malignancies involving the urinary system of about 1.65 million cases worldwide. To attain the 25 by 25 goal set by the World Health Organization (25% reduction in non-communicable diseases between 2015 and 2025), developing strategies to reduce cancer burdens is essential. The data of the study comprised the age-specific bladder cancer cases and total population numbers from age 25 to 85 and above from 1997 to 2016 in Taiwan. An ensemble age–period–cohort model was used to estimate bladder cancer incidence trends and forecast the trends to 2025. For men, the projected age-standardized incidence rates per 100,000 people in 2020 and 2025 are 13.0 and 10.4, respectively, with a 16.1% and 32.9% decrease projected from 2016 to 2020 and 2025, respectively. For women, the projected age-standardized incidence rates per 100,000 people in 2020 and 2025 are 4.7 and 3.7, respectively, with a 16.1% and 33.9% decrease projected from 2016 to 2020 and 2025, respectively. The age-specific bladder cancer incidence rates demonstrated a consistently downward trend after 2003 for all ages and both sexes. This study projects that the incidence rates of bladder cancer in Taiwan will continue to decrease, and more than a 25% reduction can be achieved from 2016 to 2025.

Age-specific pancreas cancer incidence rate in the world.

Age-specific pancreas cancer incidence rate in the world.

Age-specific bladder cancer incidence rate in the world.

Age-specific bladder cancer incidence rate in the world.

Age-specific prostate cancer incidence rate in the world.

Age-specific prostate cancer incidence rate in the world.

Incidence of and Trends in the Leading Cancers With Elevated Incidence Among American Indian and Alaska Native Populations, 2012-2016.

Cancer incidence varies among American Indian and Alaska Native (AI/AN) populations, as well as between AI/AN and White populations. This study examined trends for cancers with elevated incidence among AI/AN compared with non-Hispanic White populations and estimated potentially avoidable incident cases among AI/AN populations. Incident cases diagnosed during 2012–2016 were identified from population-based cancer registries and linked with the Indian Health Service patient registration databases to improve racial classification of AI/AN populations. Age-adjusted rates (per 100,000) and trends were calculated for cancers with elevated incidence among AI/AN compared with non-Hispanic White populations (rate ratio >1.0), by region. Trends were estimated using joinpoint regression analyses. Expected cancers were estimated by applying age-specific cancer incidence rates among non-Hispanic White populations to population estimates for AI/AN populations. Excess cancer cases among AI/AN populations were defined as observed minus expected cases. Liver, stomach, kidney, lung, colorectal and female breast cancers had higher incidence rate among AI/AN populations across most regions. Between 2012 and 2016, nearly 5,200 excess cancers were diagnosed among AI/AN populations, with the largest number of excess cancers (1,925) occurring in the Southern Plains region. Culturally informed efforts may reduce cancer disparities associated with these and other cancers among AI/AN populations.

Age-specific corpus uteri cancer incidence rate in the world.

Age-specific corpus uteri cancer incidence rate in the world.

Corrigendum to: Age specific colorectal cancer incidence rate in the world.

Corrigendum to: Age specific colorectal cancer incidence rate in the world.

Cervical Cancer Among Older Women: Analyses of Surveillance, Epidemiology and End Results Program Data

Objective:To describe age-specific cervical cancer incidence rates based on demographic and clinical characteristics.Methods:Women with cervical cancer in the SEER program were grouped into 3 age categories. Demographics, clinical characteristics, and incidence rates were obtained for each age group.Results:Older women (≥65 years) had higher incidence rates of cervical cancer than women <65 years with the highest rates in black women ≥75 years. Older black women had more adverse factors at diagnosis than similarly aged white and younger black women. There was a higher incidence rate of cervical cancer in women with lower socioeconomic status (SES), with the highest rates in older black women. However, the incidence rates were similar for older black women regardless of SES.Conclusion:Older black have the highest cervical cancer incidence rates, regardless of SES, suggesting an age and race disparity when compared to younger and white women.