A Web Tool for Age–Period–Cohort Analysis of Cancer Incidence and Mortality Rates

Rosenberg, Philip S.; Check, David P.; Anderson, William F.

doi:10.1158/1055-9965.epi-14-0300

Cited by 405 publications

(381 citation statements)

References 51 publications

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“…The data from the cancer register used were of good quality in terms of completeness of coverage and accuracy, which lends validity to the findings. Moreover, age‐period‐cohort analyses may have provided an assessment of the birth cohort‐specific risk with adjustment for non‐linear period effects which may be associated with artificial changes of incidence rates . A limitation is the descriptive analyses at population level without the possibility of making inferences at the individual level.…”

Section: Discussionmentioning

confidence: 99%

“…However, such random misclassification, which was independent from the cancer diagnosis, would have diluted the associations between famine exposure and cancer risks and not explained the associations identified. Moreover, the collinearity among age, period and cohort effects in age‐period‐cohort analyses needs to be considered when interpreting the results . An individual records approach would probably overcome the inherited limitations of age‐period‐cohort analysis based on surveillance data and generate more convincing evidence.…”

Section: Discussionmentioning

confidence: 99%

“…The age‐specific incidence rates of gastrointestinal cancers were calculated by sex and site for each birth cohort. We further performed age‐period‐cohort regressions on the incidence of gastrointestinal cancers by sex and site using a web tool, newly developed by the National Cancer Institute (NCI), United States . The age‐period‐cohort regression is based on a log‐linear model for the incidence rates with additive effects from age, calendar period, and birth cohort as shown in the formula below:

ρ_{p a} = α_{a} + β_{p} + γ_{c}

where

ρ_{p a}

is the expected incidence rate, and

α_{a}

β_{p}

, and

γ_{c}

indicate the effects of age, period and cohort, respectively.…”

Section: Methodsmentioning

confidence: 99%

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A possible link between famine exposure in early life and future risk of gastrointestinal cancers: Implications from age-period-cohort analysis

Xie

Lagergren

2016

Int. J. Cancer

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The Chinese famine in 1958-1962 was one of the worst in human history, but its potential influence on cancer risks is uncertain. Using cancer incidence data in Shanghai, China, during 1983-2007, we calculated age-specific incidence rates of gastrointestinal cancers in birth cohorts exposed to the Chinese famine in different periods of life and a non-exposed reference cohort. Age-period-cohort regressions estimated the overall relative risks of gastrointestinal cancers in each birth cohort. A total of 212,098 new cases of gastrointestinal cancer were identified during the study period (129,233 males and 82,865 females), among whom 18,146 had esophageal cancer, 71,011 gastric cancer, 55,864 colorectal cancer, 42,751 liver cancer, 9,382 gallbladder cancer and 14,944 had pancreatic cancer. The risk of esophageal, gastric, colorectal and liver cancers was higher in cohorts exposed to the Chinese famine in early life than in the reference cohort, except for esophageal cancer in women. The risk of esophageal, liver and colorectal cancers was particularly high in men exposed to famine during early childhood (0-9 years). There were no clear associations between famine exposure and the risk of pancreatic or gallbladder cancer. This study suggests an increased risk of esophageal, gastric, liver and colorectal cancers associated with childhood exposure to the Chinese famine. These findings indicate a need for further investigations confirming the results and identifying the underlying mechanisms.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

ρ_{p a} = α_{a} + β_{p} + γ_{c}

where

ρ_{p a}

is the expected incidence rate, and

α_{a}

β_{p}

, and

γ_{c}

indicate the effects of age, period and cohort, respectively.…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

A possible link between famine exposure in early life and future risk of gastrointestinal cancers: Implications from age-period-cohort analysis

Xie

Lagergren

2016

Int. J. Cancer

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“…[21][22][23][24] This extreme heterogeneity in estimates is likely driven by multiple factors, including different sampling protocols and HPV detection methods, which thus far rely on research-based assays that are run in multiple laboratories and likely have differing test characteristics. 16 After adjusting for age and period, OPC rates were found to increase across birth cohorts through the 1920s to the 1950s before plateauing among birth cohorts in the 1960s and 1970s. Observed data from the Surveillance, Epidemiology and End Results 18 registries (2000-2014) were used to assess whether a significant change in the slope of incidence rate trends occurred using Joinpoint software.…”

Section: Incidence and Survival Rates For Opcmentioning

confidence: 96%

“…14 We projected OPC incidence rates among white men aged 50 years for the period 2015 through 2030, when none of the vaccinated cohorts will yet age into the risk set, using a Poisson model based on observed data from SEER during 2000 through 2014. 15,16 SCREENING TOOLS AND BIOMARKERS FOR HPV-DRIVEN OPC Researchers have investigated biomarkers for HPVdriven OPC, including HPV detection in oral samples and HPV antibodies in serum/plasma (Table 1). 1) (see Supporting Information Fig.…”

Section: Incidence and Survival Rates For Opcmentioning

confidence: 99%

Screening for human papillomavirus‐driven oropharyngeal cancer: Considerations for feasibility and strategies for research

Kreimer

Shiels

Fakhry

et al. 2018

Cancer

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INTRODUCTIONOver the past 25 years, human papillomavirus (HPV) has been shown to be an important cause of oropharyngeal cancers (OPCs) in many world regions, with the great majority of HPV-driven OPC being caused by HPV type 16 (HPV-16). 1 HPV currently is overtaking tobacco exposure as the leading cause of OPC in some countries with a high human development index, including the United States and some European and Latin American countries, in which both the incidence rate of OPC and the attributable fraction (AF) of HPV are rising. 2 In the United States, the incidence of OPC currently is greater than that of cervical cancer, a consequence of the increasing incidence of OPC as well as reductions in the incidence of cervical cancer due to the success achieved by screening. 3 This shift highlights the need for parallel preventive measures. Nevertheless, arguments against additional research regarding HPV-driven OPC screening have been made and include the promise of primary prevention through HPV vaccination, 4 the currently low incidence rates, 5 and favorable outcomes with current therapy compared with non-HPV-driven head and neck cancers. 6 The lack of an identifiable clinical precursor lesion, insufficient diagnostic technology with which to detect small lesions, and the absence of de-escalated clinical management for patients with early-stage cancer or precancer are current barriers to screening for OPC. This article is not intended to address all the questions related to the validity and timeliness of screening for HPV-driven OPC but instead to raise important questions, guide discussions, highlight deficits and/or confusion in the existing literature, and propose needed steps in the research agenda. The following general aspects of a screening program are considered 7 and applied to HPV-driven OPC: 1) a sufficiently high incidence, either in the general population or an enriched high-risk population; 2) a sensitive and specific screening tool or biomarker; 3) appropriate methods for accurately diagnosing the cancer (or precancer) among individuals who screen positive; 4) effective treatment for patients with early-stage lesions; and 5) evidence of mortality and/or morbidity reductions.

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Evaluation of Sex-Specific Incidence of Melanoma

et al. 2020

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en and women develop melanoma at different rates in the US and other countries, but explanations for the observed disparities remain elusive and it is unclear to what extent the phenomena are due to innate biological differences (eg, cellular and hormonal) or different behaviors (eg, patterns of sun exposure, clothing, and sun protection). Global data on melanoma incidence for 2018 show a wide variation in the male to female incidence rate ratio (IRR); for the 30 countries with the highest melanoma incidence, 1 the male to female IRR ranged from 0.68 (95% CI, 0.63-0.73) in Denmark up to 1.35 (95% CI, 1.33-1.37) in the US white population and 1.47 (95% CI, 1.42-1.52) in Australia (Figure 1). Data from North America, Europe, Australia, and New Zealand all suggest that the incidence is generally higher in women than men up to the age of approximately 50 years, after which higher rates pre-vail in men. 2 The excess among men at older ages is most notable in the high-incidence populations of Australia and New Zealand, and data from the US suggest that the sex-specific pattern by age is similar across all histologic subtypes of melanoma. 3 Reports in the literature also point to differences between men and women with respect to the anatomic distribution of melanoma, with melanomas more likely to arise on the trunk in men and on the lower limbs in women. 4 The observed differences in anatomic distribution by sex have commonly been attributed to behavioral differences between men and women in relation to sun exposure. However, there are few data comparing incidence temporal trends across populations, with previous studies conducted either in single populations, 3,[5][6][7] at single points in time 8 or restricted to par-IMPORTANCE Men and women develop melanoma at different rates on different body sites, with variation across countries, but explanations for these disparities remain elusive. OBJECTIVE To test whether observed differences in melanoma incidence between men and women vary by population, age, or anatomic site.DESIGN Cross-sectional analysis of sex-and site-specific temporal trends in melanoma incidence over 3 decades was conducted for men and women diagnosed with invasive melanoma in the US (limited to white race), Canada, Australia, New Zealand, the UK, Sweden, Norway, and Denmark. Using cancer registry data, male to female incidence rate ratios (IRRs) were calculated overall and by anatomic site, and Joinpoint regression models were used to estimate the annual percentage rate changes in sex-and site-specific incidence in each population. Incidence rates were standardized to the

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A Web Tool for Age–Period–Cohort Analysis of Cancer Incidence and Mortality Rates

Cited by 405 publications

References 51 publications

A possible link between famine exposure in early life and future risk of gastrointestinal cancers: Implications from age-period-cohort analysis

A possible link between famine exposure in early life and future risk of gastrointestinal cancers: Implications from age-period-cohort analysis

Screening for human papillomavirus‐driven oropharyngeal cancer: Considerations for feasibility and strategies for research

Evaluation of Sex-Specific Incidence of Melanoma

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