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Background: Previous prospective studies of associations between circulating inflammation-related molecules and pancreatic cancer risk have included limited numbers of markers. Methods: We conducted a case–cohort study nested within the Japan Public Health Center-based Prospective Study Cohort II. We selected a random subcohort (n = 774) from a total of 23,335 participants aged 40 to 69 years who returned a questionnaire and provided blood samples at baseline. During the follow-up period from 1993 to 2010, we identified 111 newly diagnosed pancreatic cancer cases, including one case within the subcohort. Plasma concentrations of 62 inflammatory markers of chemokines, cytokines, and growth factors were measured by a Luminex fluorescent bead-based assay. Cox regression models were applied to estimate HR and 95% confidence intervals (CI) for pancreatic cancer risk for quartiles of marker levels adjusted for potential confounders. Results: The HR (95% CI) for the highest versus the lowest category of C–C motif ligand chemokine 8/monocyte chemoattractant protein 2 (CCL8/MCP2) was 2.03 (1.05–3.93; Ptrend = 0.048). After we corrected for multiple comparisons, none of the examined biomarkers were associated with pancreatic cancer risk at P-value Conclusions: We found no significant associations between 62 inflammatory markers and pancreatic cancer risk. Impact: The suggestive association with circulating levels of leukocyte recruiting cytokine CCL8/MCP2 may warrant further investigation.

The association between alcohol intake and stomach cancer risk remains controversial. We undertook a pooled analysis of data from six large‐scale Japanese cohort studies with 256 478 participants on this topic. Alcohol intake as ethanol was estimated using a validated questionnaire. The participants were followed for incidence of stomach cancer. We calculated study‐specific hazard ratios (HRs) and 95% confidence intervals (CIs) for stomach cancer according to alcohol intake using a Cox regression model. Summary HRs were estimated by pooling the study‐specific HRs using a random‐effects model. During 4 265 551 person‐years of follow‐up, 8586 stomach cancer cases were identified. In men, the multivariate‐adjusted HRs (95% CIs) of stomach cancer were 1.00 (0.87‐1.15) for occasional drinkers, and 1.00 (0.91‐1.11) for, Alcohol intake increased stomach cancer risk in men, and heavy drinkers showed a greater point estimate of risk for proximal cancer than for distal cancer.

Evidence is limited regarding the association between low-carbohydrate diet (LCD) score and mortality among Asians, a population that consumes a large amount of carbohydrates.The present study examined the association between low-carbohydrate diet (LCD) score (based on percentage of energy as carbohydrate, fat, and protein) and the risk of total and cause-specific mortality among Asians.This study was a prospective cohort study in Japan with follow-up for a median of 16.9 years involving 43008 men and 50646 women aged 45-75 years. Association of LCD score, LCD score based on animal sources of protein and fat, and LCD score based on plant sources of protein and fat with risk of mortality was assessed using Cox proportional hazards model.A U-shaped association was observed between LCD score and total mortality: the multivariable-adjusted hazard ratios (HRs) (95% CI) of total mortality for lowest through highest scores were 1.00, 0.95 (0.91, 1.01), 0.93 (0.88, 0.98), 0.93 (0.88, 0.98), and 1.01 (0.95, 1.07) (P-non-linearity0.01). A similar association was found for mortality from cardiovascular disease (CVD) and heart disease. LCD score based on carbohydrate, animal protein, and animal fat also showed a U-shaped association for total mortality (P-non-linearity0.01). In contrast, LCD score based on carbohydrate, plant protein, and plant fat was linearly associated with lower total (HR, 0.89; 95% CI: 0.83, 0.94 for highest versus lowest quintile), CVD [0.82 (0.73, 0.92)], heart disease [0.83 (0.71, 0.98)], and cerebrovascular disease [0.75 (0.62, 0.91) mortality.Both LCD with high animal protein and fat and high-carbohydrate diet with low animal protein and fat were associated with higher risk of mortality. Meanwhile, LCD high in plant-based sources of protein and fat was associated with a lower risk of total and CVD mortality.

Summary Background WHO has launched an initiative aiming to eliminate cervical cancer as a public health problem. Elimination is a long-term target that needs long-lasting commitment. To support local authorities in implementing human papillomavirus (HPV) vaccination, we provide regional and country-specific estimates of cervical cancer burden and the projected impact of HPV vaccination among today's young girls who could develop cervical cancer if not vaccinated. Methods The expected number of cervical cancer cases in the absence of vaccination among girls born between 2005 and 2014 was quantified by combining age-specific incidence rates from GLOBOCAN 2018 and cohort-specific mortality rates by age from UN demographic projections. Preventable cancers were estimated on the basis of HPV prevalence reduction attributable to vaccination and the relative contribution of each HPV type to cervical cancer incidence. We assessed the number of cervical cancer cases preventable through vaccines targeting HPV types 16 and 18, with and without cross-protection, and through vaccines targeting HPV types 16, 18, 31, 33, 45, 52, and 58. Findings Globally, without vaccination, the burden of cervical cancer in these birth cohorts is expected to reach 11·6 million (95% uncertainty interval 11·4–12·0) cases by 2094. Approximately 75% of the burden will be concentrated in 25 countries mostly located in Africa and Asia, where the future number of cases is expected to increase manyfold, reaching 5·6 million (5·4–6·0) cases in Africa and 4·5 million (4·4–4·6) cases in Asia. Worldwide immunisation with an HPV vaccine targeted to HPV types 16 and 18, with cross-protection against HPV types 31, 33, and 45, could prevent about 8·7 million (8·5–9·0) cases. Interpretation Detailed estimates of the increasing burden of cervical cancer and projected impact of HPV vaccination is of immediate relevance to public health decision makers. Shifting the focus of projections towards recently born girls who could develop cervical cancer if not vaccinated is fundamental to overcome stakeholders' hesitancy towards HPV vaccination. Funding Bill & Melinda Gates Foundation, Canadian Institutes of Health Research.

Background: Alcohol use is causally linked to multiple cancers. We present global, regional, and national estimates of alcohol-attributable cancer burden in 2020 to inform alcohol policy and cancer control across different settings globally. Methods: In this population-based study, population attributable fractions (PAFs) calculated using a theoretical minimum-risk exposure of lifetime abstention and 2010 alcohol consumption estimates from the Global Information System on Alcohol and Health (assuming a 10-year latency period between alcohol consumption and cancer diagnosis), combined with corresponding relative risk estimates from systematic literature reviews as part of the WCRF Continuous Update Project, were applied to cancer incidence data from GLOBOCAN 2020 to estimate new cancer cases attributable to alcohol. We also calculated the contribution of moderate (60 g per day) drinking to the total alcohol-attributable cancer burden, as well as the contribution by 10 g per day increment (up to a maximum of 150 g). 95% uncertainty intervals (UIs) were estimated using a Monte Carlo-like approach. Findings: Globally, an estimated 741 300 (95% UI 558 500–951 200), or 4·1% (3·1–5·3), of all new cases of cancer in 2020 were attributable to alcohol consumption. Males accounted for 568 700 (76·7%; 95% UI 422 500–731 100) of total alcohol-attributable cancer cases, and cancers of the oesophagus (189 700 cases [110 900–274 600]), liver (154 700 cases [43 700–281 500]), and breast (98 300 cases [68 200–130 500]) contributed the most cases. PAFs were lowest in northern Africa (0·3% [95% UI 0·1–3·3]) and western Asia (0·7% [0·5–1·2]), and highest in eastern Asia (5·7% [3·6–7·9]) and central and eastern Europe (5·6% [4·6–6·6]). The largest burden of alcohol-attributable cancers was represented by heavy drinking (346 400 [46·7%; 95% UI 227 900–489 400] cases) and risky drinking (291 800 [39·4%; 227 700–333 100] cases), whereas moderate drinking contributed 103 100 (13·9%; 82 600–207 200) cases, and drinking up to 10 g per day contributed 41 300 (35 400–145 800) cases. Interpretation: Our findings highlight the need for effective policy and interventions to increase awareness of cancer risks associated with alcohol use and decrease overall alcohol consumption to prevent the burden of alcohol-attributable cancers. Funding: None.

The association of fermented soy products, separately from total soy products, with cardiovascular disease (CVD) and total cancer has not been reported. We examined this association in a population-based prospective cohort study in Japan. We studied 79,648 participants (42,788 women; 36,860 men) aged 45–74 years without a history of cancer, myocardial infarction, or stroke. Participants completed a food frequency questionnaire (1995–1998) and were followed to 2009–2012. Cox proportional hazards regression analysis was used to calculate the hazard ratios (HR) and 95% confidence intervals (CI) of incidence of CVD and total cancer according to quartiles of total soy products, nonfermented soy products, fermented soy products, miso soup, natto, total isoflavones from soy products, isoflavones from nonfermented soy products, and isoflavones from fermented soy products. In women, we observed a significant inverse association between fermented soy product intake and the risk of CVD (multivariate HR in the highest compared with the lowest quartile of fermented soy product intake: 0.80; 95% CI: 0.68, 0.95; P for trend = 0.010), and also found significant inverse associations for natto and isoflavones among fermented soy products. In site-specific analysis, we observed a similar, significant inverse association between fermented soy product intake and the risk of stroke in women. We found no significant association between any soy product and risk of CVD in men or total cancer in both sexes. Intake of fermented soy products such as natto was inversely associated with the risk of CVD in women.

Background: Metabolic syndrome (MetS) is a systemic inflammatory state. Low physical activity (PA) could modify this patho-physiology or act as an independent contributor to inflammation. Previous studies of both conditions have identified altered levels of inflammation- and immune-related proteins based on limited sets of candidate markers. Methods: We investigated associations of MetS and low PA with circulating inflammation markers in a stratified random sample of Japanese adults (N = 774, mean age 60.7 years) within the Japan Public Health Center-based Prospective Study (JPHC) Cohort II. AHA/NHLBI criteria were used to define MetS (19%) and the bottom quartile of PA was considered low. 110 circulating biomarkers, including cytokines, chemokines, and soluble receptors were measured by multiplex bead-based and proximity-extension assays. Associations of MetS and low PA with marker quantiles were adjusted for each other and for age, sex, study site, cigarette smoking, alcohol consumption, and blood sample fasting state by ordinal logistic regression. P values were corrected for FDR. Results: MetS was significantly associated with levels of six markers: IL18R1 [odds ratio 2.37; 95% confidence interval (CI), 1.45–3.87], CRP (2.07; 95% CI, 1.48–2.90), SAP (2.08; 95% CI, 1.47–2.95), CCL19/MIP3β (2.06; 95% CI, 1.48–2.88), CXCL12/SDF1α+β (0.48; 95% CI, 0.32–0.65), and CCL28 (0.44; 95% CI, 0.27–0.71). Low PA had no significant marker associations. Conclusions: Positively associated markers with MetS are mostly Th1 immune response–related and acute phase proteins, whereas negatively associated markers are generally Th2-related. Impact: MetS is associated with a broad range of alterations in immune and inflammatory biomarkers that may contribute to risks of various chronic diseases, independent of low PA.

Background: Here, we explore the association between excess weight during early to mid-adulthood and survival in patients diagnosed with breast and colorectal cancer, using a pooled analysis of five cohort studies and study participants from 11 countries. Methods: Participant-level body mass index (BMI) trajectories were estimated by fitting a growth curve model using over 2 million repeated BMI measurements from close to 600,000 cohort participants. Cumulative measures of excess weight were derived. Data from over 23,000 patients with breast and colorectal cancer were subsequently analyzed using time-to-event models for death with the date of diagnosis as start of follow-up. Study-specific results were combined through a random effect meta-analysis. Results: We found a significant dose–response relationship (P trend = 0.013) between the average BMI during early and mid-adulthood and death from breast cancer, with a pooled HR of 1.31 (1.07–1.60) and the time to death shortened by 16% for average BMI above 25 kg/m2 compared with average BMI less than or equal to 22.5 kg/m2, respectively. Similar results were found for categories of cumulative time spent with excess weight. There was no association between excess body fatness during early to mid-adulthood and death in patients with colorectal cancer. Conclusions: Excess body fatness during early to mid-adulthood is associated not only with an increased risk of developing cancer, but also with a lower survival in patients with breast cancer. Impact: Our results emphasize the importance of public health policies aimed at reducing overweight during adulthood and inform future studies on the relationship between excess weight and cancer outcomes.

Obesity, often assessed at one point in time, is an established risk factor of several types of cancer, however, associations with cumulative exposure to obesity across the life course are not well understood. We investigated the relationship between combined measures of duration and intensity of premenopausal overweight and obesity and the incidence of postmenopausal breast, endometrial, and colorectal cancers in Icelandic women. Body mass index (BMI) trajectories between ages 20 and 50 of 88,809 women from the Cancer Detection Clinic Cohort were predicted using growth curve models. Indicators of overweight and obesity duration and intensity were computed and their association with risk of postmenopausal breast, endometrial, and colorectal cancers was examined using multivariate Cox models for subjects followed-up beyond the age of 50 (n = 67,488). During a mean follow-up of 17 years, incident events of 3,016 postmenopausal breast, 410 endometrial and 987 colorectal cancers were ascertained. Each 0.1 kg/m2 per year increase in BMI between ages 20 and 50 was positively associated with risks of postmenopausal breast, endometrium and colorectal cancers with hazard ratios equal to 1.09 (95% Confidence Interval (CI):1.04-1.13), 1.31 (95% CI: 1.18-1.44) and 1.10 (95% CI: 1.00-1.21), respectively. Compared to women who were never obese, cumulative BMI × years of obesity were linearly positively associated with risk of endometrial cancer, whereas the association with breast cancer was initially positive, but leveled off with increasing cumulative BMI × years. Cumulative exposure to obesity may provide additional insights into the etiology of cancer and should be considered in future studies that assess obesity-cancer relationships.

Background: Circulating inflammation proteins may be important mediators or markers of carcinogenic mechanisms. There have been few studies with limited numbers of analytes in patients with upper gastrointestinal (GI) tract tumors. We therefore evaluated risk associations of gastric and esophageal cancers with prediagnostic levels of a wide range of these molecules. Methods: We performed a case–cohort analysis within the Japan Public Health Center–Based Prospective Study Cohort II, including incident cases of gastric (n = 446) and esophageal (n = 68) cancers and a random subcohort (n = 774). A total of 64 biomarkers were measured in baseline plasma using Luminex bead-based assays. The median time between blood collection and diagnosis was 8.1 years for gastric cancer and 9.4 years for esophageal cancer. HRs for association with each marker were adjusted for potential confounders using Cox regression. Results: In separate models, sEGFR and TSLP were nominally associated with gastric cancer risk, and CRP, CXCL11/ITAC, and CCL15/MIP1D were associated with esophageal cancer. However, no association satisfied statistical significance after FDR correction. Associations did not differ by time from blood collection to cancer ( Conclusions: Our study failed to identify associations of circulating inflammation markers with risk of upper GI tract tumors. Impact: To date, this is the largest assessment of inflammation-related proteins with gastric and esophageal cancer risks. However, the evaluated molecules may not fully represent the complex inflammation processes preceding malignant transformation. Further investigation of other markers in prospective studies is warranted, as demonstration of associations may have important implications for prevention and treatment of these cancers.

Gastric cancer is preceded by a chronic inflammatory process. Circulating levels of inflammation-related markers may reveal molecular pathways contributing to cancer development. Our study evaluated risk associations of gastric cancer with a wide range of systemic soluble inflammation and immune-response proteins. We performed a case-cohort analysis within the JPHC Study II, including a subcohort of 410 participants selected randomly within defined age and sex groups, and 414 individuals with incident gastric cancer. Ninety-two biomarkers were measured in baseline plasma using proximity extension assays. Gastric cancer multivariable hazard ratios were calculated for two to four quantiles used as ordinal variables of each biomarker by Cox proportional hazards regression models with age as the time metric. Of 73 evaluable biomarkers, three (CCL11, CCL20 and IL17C) were associated with increased gastric cancer risk and two (CCL23 and MMP1) with reduced cancer risk (Ptrends

We sought to understand the role of stage at diagnosis in observed age disparities in colon cancer survival among people aged 50 to 99 years using population-based cancer registry data from seven high-income countries: Australia, Canada, Denmark, Ireland, New Zealand, Norway and the United Kingdom. We used colon cancer incidence data for the period 2010 to 2014. We estimated the 3-year net survival, as well as the 3-year net survival conditional on surviving at least 6 months and 1 year after diagnosis, by country and stage at diagnosis (categorised as localised, regional or distant) using flexible parametric excess hazard regression models. In all countries, increasing age was associated with lower net survival. For example, 3-year net survival (95% confidence interval) was 81% (80-82) for 50 to 64 year olds and 58% (56-60) for 85 to 99 year olds in Australia, and 74% (73-74) and 39% (39-40) in the United Kingdom, respectively. Those with distant stage colon cancer had the largest difference in colon cancer survival between the youngest and the oldest patients. Excess mortality for the oldest patients with localised or regional cancers was observed during the first 6 months after diagnosis. Older patients diagnosed with localised (and in some countries regional) stage colon cancer who survived 6 months after diagnosis experienced the same survival as their younger counterparts. Further studies examining other prognostic clinical factors such as comorbidities and treatment, and socioeconomic factors are warranted to gain further understanding of the age disparities in colon cancer survival.

Objective We described the role of patient-related and clinical factors on age disparities in colon cancer survival among patients aged 50–99 using New Zealand population-based cancer registry data linked to hospitalisation data. Method We included 21,270 new colon cancer cases diagnosed between 1 January 2006 and 31 July 2017, followed up to end 2019. We modelled the effect of age at diagnosis, sex, ethnicity, deprivation, comorbidity, and emergency presentation on colon cancer survival by stage at diagnosis using flexible excess hazard regression models. Results The excess mortality in older patients was minimal for localised cancers, maximal during the first six months for regional cancers, the first eighteen months for distant cancers, and over the three years for missing stages. The age pattern of the excess mortality hazard varied according to sex for distant cancers, emergency presentation for regional and distant cancers, and comorbidity for cancer with missing stages. Ethnicity and deprivation did not influence age disparities in colon cancer survival. Conclusion Factors reflecting timeliness of cancer diagnosis most affected age-related disparities in colon cancer survival, probably by impacting treatment strategy. Because of the high risk of poor outcomes related to treatment in older patients, efforts made to improve earlier diagnosis in older patients are likely to help reduce age disparities in colon cancer survival in New Zealand.

ObjectiveWe described the role of patient-related and clinical factors on age disparities in colon cancer survival among patients aged 50-99 using New Zealand population-based cancer registry data linked to hospitalization data.DesignWe included new colon cancer cases diagnosed between 1 January 2006 and 31 July 2017, followed up to 31 December 2019. We linked these cases to hospitalisation data for the five years before the cancer diagnosis. We modelled the effect of age at diagnosis, sex, deprivation, comorbidity, and route to diagnosis on colon cancer survival by stage at diagnosis (localized, regional, distant, missing).ResultsNet survival decreased as the age at diagnosis increased, notably in advanced stages and missing stage. The excess mortality in older patients was minimal for localised cancers, maximal during the first six months for regional cancers, the first 18 months for distant cancers, and over the three years for missing stages. The age pattern of the excess mortality hazard varied according to sex for distant cancers, the route to diagnosis for regional and distant cancers, and comorbidity for cancer with missing stages.ConclusionThe present population-based study shows that factors reflecting timeliness of cancer diagnosis most affected the difference in survival between middle-aged and older patients, probably by impacting treatment strategy. Because of the high risk of poor outcomes related to treatment in older patients, efforts made to improve earlier diagnosis in older patients are likely to help reduce age disparities in colon cancer survival in New Zealand.

To elucidate the individual impacts of insulin and blood glucose on cancer risk, we investigated the association of plasma C-peptide, a surrogated marker of insulin and glycated albumin (GA), a more stable marker of blood glucose, with all-site and site-specific cancer risk by mutually accounting for their confounding effects. The study was prospectively conducted with nearly 4,000 cancer cases arising in our population-based cohort of 33,736 subjects who answered the baseline questionnaire and supplied blood samples. After exclusion of subjects with apparent DM, analysis was done in 3,036 cancer cases and 3,667 subcohort subjects. Among men and women combined, highest levels of C-peptide were statistically significantly associated with an increased risk of all-site [Hazard ratio (HR): 1.21; 95% confidence interval: 1.02-1.42], colon [1.73; 1.20-2.47], liver [3.23; 1.76-5.91], kidney, renal pelvis and ureter cancers [2.47; 1.07-5.69], compared to the respective lowest levels, after adjustment for GA levels. Among these C-peptide-related cancers, colon and liver cancers also showed an increased risk associated with elevated GA levels independently of C-peptide levels. The corresponding HRs for colon and liver cancers compared to the highest and lowest GA levels were 1.43 [1.02-2.00] and 2.02 [1.15-3.55], respectively. Effect modification by gender was only evident for the association between C-peptide and colon cancer (p for interaction = 0.04). Higher insulin levels, independently of higher blood glucose levels, may be relevant to DM-related carcinogenesis for several cancer sites. Examination of circulating insulin levels is a plausible option in evaluating cancer risk even in individuals who have not developed DM.

Blood levels of inflammation-related markers may reveal molecular pathways contributing to carcinogenesis. To date, prospective associations with colorectal cancer (CRC) risk have been based on few studies with limited sets of analytes. We conducted a case-cohort study within the Japan Public Health Center-based Prospective Study Cohort II, comparing 457 incident CRC cases during median 18 years follow-up with a random subcohort of 774 individuals. Baseline plasma levels of 62 cytokines, soluble receptors, acute-phase proteins, and growth factor markers were measured using Luminex bead-based assays. We estimated hazard ratios (HRs) associating each marker with CRC risk by Cox proportional hazards models adjusted for potential confounders. Subanalyses compared cases by years after blood draw (

Although the impact of tobacco consumption on the occurrence of lung cancer is well-established, risk estimation could be improved by risk prediction models that consider various smoking habits, such as quantity, duration, and time since quitting. We constructed a risk prediction model using a population of 59 161 individuals from the Japan Public Health Center (JPHC) Study Cohort II. A parametric survival model was used to assess the impact of age, gender, and smoking-related factors (cumulative smoking intensity measured in pack-years, age at initiation, and time since cessation). Ten-year cumulative probability of lung cancer occurrence estimates were calculated with consideration of the competing risk of death from other causes. Finally, the model was externally validated using 47 501 individuals from JPHC Study Cohort I. A total of 1210 cases of lung cancer occurred during 986 408 person-years of follow-up. We found a dose-dependent effect of tobacco consumption with hazard ratios for current smokers ranging from 3.78 (2.00-7.16) for cumulative consumption ≤15 pack-years to 15.80 (9.67-25.79) for >75 pack-years. Risk decreased with time since cessation. Ten-year cumulative probability of lung cancer occurrence estimates ranged from 0.04% to 11.14% in men and 0.07% to 6.55% in women. The model showed good predictive performance regarding discrimination (cross-validated c-index = 0.793) and calibration (cross-validated χ2 = 6.60; P-value = .58). The model still showed good discrimination in the external validation population (c-index = 0.772). In conclusion, we developed a prediction model to estimate the probability of developing lung cancer based on age, gender, and tobacco consumption. This model appears useful in encouraging high-risk individuals to quit smoking and undergo increased surveillance.

Background We examined the associations of alcohol consumption and liver holidays with all-cause mortality and with mortality due to cancer, heart disease, cerebrovascular disease, respiratory disease, and injury using a large-scale prospective study in Japan. Methods We followed 102,849 Japanese who were aged between 40 and 69 years at baseline for 18.2 years on average, during which 15,203 deaths were reported. Associations between alcohol intake and mortality risk were assessed using a Cox proportional hazards model, with analysis by the number of liver holidays (in which a person abstains from drinking for several days a week). Results A J-shaped association was observed between alcohol intake and total mortality in men (nondrinkers: reference; occasional drinkers: hazard ratio [HR] 0.74; 95% confidence interval [CI], 0.68-0.80; 1-149 g/week: HR 0.76; 95% CI, 0.71-0.81; 150-299 g/week: HR 0.75; 95% CI, 0.70-0.80; 300-449 g/week: HR 0.84; 95% CI, 0.78-0.91; 450-599 g/week: HR 0.92; 95% CI, 0.83-1.01; and ≥600 g/week: HR 1.19; 95% CI, 1.07-1.32) and in women (nondrinkers: reference; occasional: HR 0.75; 95% CI, 0.70-0.82; 1-149 g/week: HR 0.80; 95% CI, 0.73-0.88; 150-299 g/week: HR 0.91; 95% CI, 0.74-1.13; 300-449 g/week: HR 1.04; 95% CI, 0.73-1.48; and ≥450 g/week: HR 1.59; 95% CI, 1.07-2.38). In current drinkers, alcohol consumption was associated with a linear, positive increase in mortality risk from all causes, cancer, and cerebrovascular disease in both men and women, but not heart disease in men. Taking of liver holidays was associated with a lower risk of cancer and cerebrovascular disease mortality in men. Conclusions Alcohol intake showed J-shaped associations with the risk of total mortality and three leading causes of death. However, heavy drinking increases the risk of mortality, which highlights the necessity of drinking in moderation coupled with liver holidays.

Lifetime cumulative incidence and mortality risk for gastric cancer was estimated by risk classifications, which will be useful for designing individually tailored prevention strategy., Objective To estimate cumulative incidence and mortality risk for gastric cancer by risk category. Methods Risk was classified into four types according to the presence/absence of Helicobacter pylori infection and chronic atrophic gastritis: in order of lowest to highest risk, Group A: H. pylori(−) and atrophic gastritis(−); Group B: H. pylori(+) and atrophic gastritis(−); Group C:H. pylori(+) and atrophic gastritis(+); and, Group D: H. pylori(−) and atrophic gastritis(+). We used vital statistics for the crude all-cause and crude gastric cancer mortality rates in 2011 and data from population-based cancer registries (the Monitoring of Cancer Incidence in Japan) for gastric cancer incidence in 2011. For relative risk and prevalence, we used the results of a meta-analysis integrating previous studies and data from the Japan Public Health Center-based Prospective Study for the Next Generation, respectively (baseline survey 2011–16). We calculated the crude incidence and mortality rates and estimated the cumulative risk using a life-table method. Results The estimated lifetime cumulative incidence risk was 11.4% for men and 5.7% for women. The estimated risk for Groups A, B, C and D was 2.4%, 10.8%, 26.7% and 35.5% for men, and 1.2%, 5.5%, 13.5% and 18.0% for women, respectively. Similarly, the estimated lifetime cumulative mortality risk was 3.9% for men and 1.8% for women. The estimated risk of mortality for Groups A, B, C and D was 0.8%, 3.6%, 9.0% and 12.0% for men, and 0.4%, 1.7%, 4.2% and 5.7% for women, respectively. Conclusions Our results may be useful for designing individually tailored prevention programs.

Background: Randomized controlled studies have investigated the short-term effect of soy product intake on blood pressure (BP) in normotensive people. To our knowledge, no prospective studies exist on the effect of habitual intake of fermented soy products, separate from total soy products, on BP in the general population.Objective: We examined the association between the habitual intake of soy products, including fermented soy products, and the development of high BP during a 5-y period among participants in a population-based prospective cohort study in Japan.Methods: The study included normotensive participants aged 40-69 y at baseline (926 men and 3239 women) who completed 2 questionnaires and whose BP was measured at the baseline survey between 1993 and 1994 and the 5-y follow-up in the Japan Public Health Center-Based Prospective Study Cohort II. The intake of soy products was assessed with a food-frequency questionnaire. High BP was defined as systolic blood pressure ≥130 mm Hg, diastolic blood pressure ≥85 mm Hg, or antihypertensive medication use. ORs and 95% CIs of high BP by frequency of soy products (miso, natto, and tofu) consumption, intake of total and fermented soy products, and intake of isoflavones from total and fermented soy products were estimated with the use of multiple logistic regression analysis.Results: Multivariable-adjusted ORs of high BP for the highest compared with the lowest tertile of total and fermented soy product intake were 1.03 (95% CI: 0.84, 1.25; P-trend = 0.786) and 0.72 (95% CI: 0.56, 0.92; P-trend = 0.009), respectively. The frequency of nonfermented soy product (tofu) intake was not associated with the development of high BP (P-trend = 0.597).Conclusions: The intake of fermented soy products, but not total or nonfermented soy products, was inversely associated with developing high BP in men and women with normal BP.

Objective To investigate the association between serum total cholesterol (TC) and suicide using a large general population cohort with long follow-up times. Method Analyses included 16 341 men and 28 905 women aged 40–69 from the Japan Public Health Center-based Prospective Study followed from 1990 to 2012. TC levels were defined per clinical guidelines: low (

Importance Epidemiological evidence regarding the long-term effects of higher dietary protein intake on mortality outcomes in the general population is not clear. Objective To evaluate the associations between animal and plant protein intake and all-cause and cause-specific mortality. Design, Setting, and Participants This prospective cohort study included 70 696 participants in the Japan Public Health Center–based Prospective Cohort who were aged 45 to 74 years and had no history of cancer, cerebrovascular disease, or ischemic heart disease at study baseline. Data were collected from January 1, 1995, through December 31, 1999, with follow-up completed December 31, 2016, during which 12 381 total deaths were documented. Dietary intake information was collected through a validated food frequency questionnaire and used to estimate protein intake in all participants. Participants were grouped into quintile categories based on their protein intake, expressed as a percentage of total energy. Data were analyzed from July 18, 2017, through April 10, 2019. Main Outcomes and Measures Hazard ratios (HRs) and 95% CIs for all-cause and cause-specific mortality were estimated using Cox proportional hazards regression models with adjustment for potential confounding factors. Results Among the 70 696 participants, 32 201 (45.5%) were men (mean [SD] age, 55.6 [7.6] years) and 38 495 (54.5%) were women (mean [SD] age, 55.8 [7.7] years). Intake of animal protein showed no clear association with total or cause-specific mortality. In contrast, intake of plant protein was associated with lower total mortality, with multivariable-adjusted HRs of 0.89 (95% CI, 0.83-0.95) for quintile 2; 0.88 (95% CI, 0.82-0.95) for quintile 3; 0.84 (95% CI, 0.77-0.92) for quintile 4; and 0.87 (95% CI, 0.78-0.96) for quintile 5, with quintile 1 as the reference category (P = .01 for trend). For cause-specific mortality, this association with plant protein intake was evident for cardiovascular disease (CVD)–related mortality (HRs, 0.84 [95% CI, 0.73-0.96] to 0.70 [95% CI, 0.59-0.83];P = .002 for trend). Isocaloric substitution of 3% energy from plant protein for red meat protein was associated with lower total (HR, 0.66; 95% CI, 0.55-0.80), cancer-related (HR, 0.61; 95% CI, 0.45-0.82), and CVD-related (HR, 0.58; 95% CI, 0.39-0.86) mortality; substitution for processed meat protein was associated with lower total (HR, 0.54; 95% CI, 0.38-0.75) and cancer-related (HR, 0.50; 95% CI, 0.30-0.85) mortality. Conclusions and Relevance In this large prospective study, higher plant protein intake was associated with lower total and CVD-related mortality. Although animal protein intake was not associated with mortality outcomes, replacement of red meat protein or processed meat protein with plant protein was associated with lower total, cancer-related, and CVD-related mortality.

Esophageal squamous cell carcinoma (ESCC) is the predominant histologic subtype of esophageal cancer worldwide. Measurements of circulating inflammation-related biomarkers may inform etiology or provide noninvasive signatures for early diagnosis. We therefore examined levels of inflammation molecules for associations with ESCC risk. Using a case-cohort study designed within the Japan Public Health Center-based Prospective Study, we measured baseline plasma levels of 92 biomarkers using a multiplex assay in a subcohort of 410 randomly selected participants and 66 participants with incident ESCC (including four cases that occurred in the subcohort). ESCC hazard ratios (HRs) were calculated for 2-4 quantiles of each biomarker by Cox proportional hazards regression models with age as the time metric, adjusted for sex, smoking and alcohol use. Twenty analytes were undetectable in nearly all samples. Of the remaining 72, 12 biomarkers (FGF19, ST1A1, STAMBP, AXIN1, CASP8, NT3, CD6, CDCP1, CD5, SLAMF1, OPG and CSF1) were associated with increased ESCC risk (ptrend

Background:The impact of overweight duration and intensity during adulthood on the prognosis after a cancer diagnosis remains largely unknown. We investigated this association in Swedish women with breast and colorectal cancer.Methods:A cohort of 47,051 women from the Swedish Lifestyle and Health Study was included, of whom 1,241 developed postmenopausal breast (mean age at diagnosis, 57.5 years) and 259 colorectal (mean age at diagnosis, 59.1 years) cancer. Trajectories of body mass index (BMI) between ages 20 and 50 years were estimated for the full cohort using a quadratic growth model and studied in relation to risk of death from any cause using multivariate Cox regression models among cancer survivors.Results:Compared with patients with cancer who were never overweight (BMI < 25) during early adulthood (ages 20–50 years), the risk of early death from breast cancer increased by 3% [hazard ratio (HR) = 1.03; 95% confidence interval (CI), 1.01–1.05] and from colorectal cancer by 4% (HR = 1.04; 95% CI, 1.01–1.06) for every year lived with overweight. A higher intensity of overweight (i.e., a combination of duration and degree of overweight—a concept comparable to pack-years of cigarette smoking) further increased the risk of dying in this population. Although risks were slightly more pronounced for women diagnosed with late-stage breast cancer, no clear association was found for colorectal cancer.Conclusions:Our results suggest that adulthood overweight duration and intensity have a long-lasting influence on breast and colorectal cancer survival.Impact:Our study highlights the need for effective prevention of overweight and obesity starting at an early age.

Cytochrome P450 (CYP) 1A1 and glutathione S-transferases (GST) M1 and T1 are major enzymes in the carcinogen metabolizing pathway. We examined the association between single nucleotide polymorphisms (SNPs) of CYP1A1 (rs4646421, rs4646422 and rs1048943), GSTM1 and GSTT1 and gastric cancer risk in Japan. This is a nested case-control study (457 cases and 457 matched controls) of our population-based cohort involving 36,745 subjects who answered a baseline questionnaire and supplied blood samples. The odds ratios (ORs) and their corresponding 95% confidence intervals (CIs) were calculated using conditional logistic regression models. We found that CYP1A1 (rs4646422) variant allele was associated with a statistically significant increased risk of gastric cancer compared with the homozygous wild-type genotype (OR = 1.65; 95% CI = 1.17-2.32). GSTM1 null, GSTT1 null and GSTM1/T1 both or either null genotypes were associated with increased risk, but not statistically significantly. Combination of the CYP1A1 (rs4646422) variant allele and GSTM1/T1 both or either null genotypes was associated with a statistically significant increased risk compared with the combination of the CYP1A1 homozygous wild-type genotype and the GSTM1/T1 both active genotypes. In addition, compared with CYP1A1 (rs4646422) homozygous wild-type genotypes in those who were never-smokers, CYP1A1 variant alleles in those who smoked ≥30 pack-years were associated with an increased risk; neither gene-gene nor gene-environment interactions were significant. The CYP1A1 (rs4646422) polymorphism might be involved in gastric carcinogenesis among the Japanese population.

Aims Coping strategies may be significantly associated with health outcomes. This is the first study to investigate the association between baseline coping strategies and cardiovascular disease (CVD) incidence and mortality in a general population cohort. Methods and results The Japan Public Health Center-based prospective Study asked questions on coping in its third follow-up survey (2000–04). Analyses on CVD incidence and mortality included 57 017 subjects aged 50–79 without a history of CVD and who provided complete answers on approach- and avoidance-oriented coping behaviours and strategies. Cox regression models, adjusted for confounders, were used to determine hazard ratios (HRs) according to coping style. Mean follow-up time was 7.9 years for incidence and 8.0 years for mortality. The premorbid use of an approach-oriented coping strategy was inversely associated with incidence of stroke (HR = 0.85; 95% CI, 0.73–1.00) and CVD mortality (HR = 0.74; 95% CI, 0.55–0.99). Stroke subtype analyses revealed an inverse association between the approach-oriented coping strategy and incidence of ischaemic stroke (HR = 0.79; 95% CI, 0.64–0.98) and a positive association between the combined coping strategy and incidence of intra-parenchymal haemorrhage (HR = 2.03; 95% CI, 1.01–4.10). Utilizing an avoidance coping strategy was associated with increased mortality from ischaemic heart disease (IHD) only in hypertensive individuals (HR = 3.46; 95% CI, 1.07–11.18). The coping behaviours fantasizing and positive reappraisal were associated with increased risk of CVD incidence (HR = 1.24; 95% CI, 1.03–1.50) and reduced risk of IHD mortality (HR = 0.63; 95% CI, 0.40–0.99), respectively. Conclusion An approach-oriented coping strategy, i.e. proactively dealing with sources of stress, may be associated with significantly reduced stroke incidence and CVD mortality in a Japanese population-based cohort.

Although the countries of Sub-Sharan Africa represent among the most rapidly growing and aging populations worldwide, no previous studies have examined the cancer patterns in older adults in the region as a means to inform cancer policies. Using data from Cancer Incidence in Five Continents, we describe recent patterns and trends in incidence rates for the major cancer sites in adults aged ≥60 years and in people aged 0-59 for comparison in four selected population-based cancer registries in Kenya (Nairobi), the Republic of South Africa (Eastern Cape Province), Uganda (Kyadondo country), and Zimbabwe (Harare blacks). Over the period 2008-2012, almost 9,000 new cancer cases were registered in older adults in the four populations, representing one-third of all cancer cases. Prostate and esophageal cancers were the leading cancer sites in older males, while breast, cervical and esophageal cancers were the most common among older females. Among younger people, Kaposi sarcoma and non-Hodgkin lymphoma were common. Over the past 20 years, incidence rates among older adults have increased in both sexes in Uganda and Zimbabwe while rates have stabilized among the younger age group. Among older adults, the largest rate increase was observed for breast cancer (estimated annual percentage change: 5% in each country) in females and for prostate cancer (6-7%) in males. Due to the specific needs of older adults, tailored considerations should be given to geriatric oncology when developing, funding and implementing national and regional cancer programmes.

Background The aim of the study was to investigate trends in cancer prognosis by examining the relationship between period of diagnosis and probability of death from cancer in a population-based cohort. Methods Within a cohort of Japanese men and women aged 40–69 years and free of prior diagnosis of cancer and cardiovascular disease at baseline, data from 4403 patients diagnosed with cancer between 1990 and 2006 and followed up until 2012 were analyzed using survival regression models to assess the presence of an effect of the period of diagnosis (before 1998 versus after 1998) on the risk of dying from cancer. Results We noted a significant decrease in risk of dying from cancer among individuals diagnosed after 1998 with lung cancer (hazard ratio [HR] = 0.676 [0.571–0.800]) or colorectal cancer (HR = 0.801 [0.661–0.970]). A decrease in the estimated five-year probability of death from cancer was also noted between the first (before 1998) and the second (after 1998) period of diagnosis for lung and colorectal cancers (e.g., 85.4% vs. 73.3% for lung cancer and 44.6% vs. 37.7% for colorectal cancer, respectively, for stage III in men aged 60 at diagnosis). Conclusions This study presented the first scientific evidence of improvement in prognosis for lung and colorectal cancer patients in a population-based cohort in Japan. Our results suggest that recent advances in cancer treatment could have influenced cancer survival differently among lung, colorectal and gastric cancers.

Summary Background & aims Cruciferous vegetables contain isothiocyanates, which effectively reduce inflammation and oxidative stress related to chronic diseases, inhibit the bioactivation of procarcinogens, and enhance the excretion of carcinogens. However, at present, no large cohort studies have investigated the effect of cruciferous vegetable on mortality. We aimed to examine the association between cruciferous vegetable intake and all-cause mortality, namely cancer, heart disease, cerebrovascular disease, and injuries, in a large cohort study conducted between 1990 and 1993, in Japan. Methods The analysis included 88,184 participants (age: 45–74 years) with no history of cancer, myocardial infarction, and stroke. Participants were tracked for a median of 16.9 years, during which 15,349 deaths were occurred. The association between cruciferous vegetable intake and risk of all-cause and cause-specific mortality was determined by Cox proportional hazard regression analysis to calculate the hazard ratios (HRs) and 95% confidence intervals (CIs), after adjustment for potential confounding factors. Results An inverse association was found between cruciferous vegetable intake and total mortality in both gender. HRs (95% CI) for all-cause mortality in the highest compared to the lowest quintile were 0.86 (0.80, 0.93) for men (P = 0.0002 for trend) and 0.89 (0.81, 0.98) for women (P = 0.03 for trend). Cruciferous vegetable intake was associated with lower cancer mortality in men, as well as with heart disease-, cerebrovascular disease-, and injury-related mortality in women. Conclusions This prospective study suggests that a higher cruciferous vegetables intake is associated with reduced risk of all-cause mortality.

Purpose Cross-sectional studies have shown an association between different coping styles and suicidal behavior. It is unknown whether there is any prospective association between coping behaviors and suicide in the general population. Methods The study population consisted of participants of the Japanese Public Health Center-based Prospective Study. In the 10-year follow-up questionnaire, subjects aged 50–79 years were asked how they handle daily problems. Coping behaviors were used to determine two coping strategies (approach coping and avoidance coping). Of 99,439 subjects that returned the 10-year follow-up questionnaire, 70,213 subjects provided complete answers on coping and were included in our analyses. Cox regression models, adjusted for confounders, were used to determine the risk of committing suicide according to coping style. Mean follow-up time was 8.8 years. Results Two coping behaviors were significantly associated with suicide over time: planning (hazard ratio [HR], 0.64; 95% confidence interval [CI], 0.41–0.98) and self-blame (HR, 2.20; 95% CI, 1.29–3.76). Of the coping strategies, only the avoidance coping strategy was significantly associated with suicide (HR, 2.45; 95% CI, 1.24–4.85). Conclusions For the first time, two coping behaviors and one coping strategy have been shown to have a significant prospective association with suicide in a general population.

Introduction/Background After stroke, standing balance is usually described as a predictor of functional recovery. Regarding literature, various type of physical therapy (PT) is used to improve balance. The aim of this meta-analysis is to evaluate the effects of PT directly focused on balance training (DFBT) and theses of PT indirectly focused on balance training (IFBT) on balance after stroke. Material and method Randomised controlled trials (RCT), without language restriction, until October 2015, assessing the Berg Balance Scale (BBS), the Postural Assessment Scale for Stroke, the posturographic parameters in static condition and measures of independence in activities of daily living were included. Two independent authors (AH and JDM) led this selection following the Cochrane recommendations (Hugues et al., 2017). Results One hundred and ninety-three parallel and crossover RCT from 9337 records were included, involving 8018 subjects [study sample: mean 41.5 (SD 49.7) subjects, age: pooled mean 61.7 (pooled SD 12.78) years]. A significant difference in favor of PT compared to no treatment was immediately found after the intervention for the BBS (DFBT: 7 studies, mean difference [MD] 1.38; 95% confidence interval [CI] [0.71; 2.05]. IFBT: 18 studies, MD 1.88; 95% CI [1.31; 2.45]). Only IFBT PT is more effective than sham treatment or usual care immediately after the intervention for the BBS (DFBT: 1 study, MD 5.33; 95% CI [−4.68; 15.34]. IFBT: 26 studies, MD 1.85; 95% CI [0.67; 3.03]). Conclusion These results show immediately after the intervention: –that balance can be improved by PT aiming directly or indirectly at the recovery of balance compared to no treatment; –an improvement of balance by PT indirectly focused on the recovery of balance compared to sham treatment or usual care.

Introduction/Background Several studies highlight that the physical therapy (PT) timing is important in rehabilitation process from physical disability after stroke. The purpose of this meta-analysis was to investigate the effect of all PT on balance after stroke and to evaluate whether changes are related to stroke stage of recovering [acute and subacute (ASS) or chronic stage (CS)]. Material and method Randomised controlled trials (RCT), without language restriction, until October 2015, assessing the Berg Balance Scale (BBS), the Postural Assessment Scale for Stroke, the posturographic parameters in static condition and measures of independence in activities of daily living were included. Two independent authors (AH and JDM) led this selection following the Cochrane recommendations (Hugues et al., 2017). Results One hundred and ninety-three parallel and crossover RCT from 9337 records were included, involving 8018 subjects [study sample: mean 41.5 (SD 49.7) subjects, age: pooled mean 61.7 (pooled SD 12.78) years]. A significant difference in favor of PT compared to no treatment was immediately found after the intervention for the BBS at ASS and CS (ASS: 11 studies, mean difference (MD) 3.14; 95% confidence interval (CI) [2.21; 4.06]. CS: 12 studies, MD 1.31; 95% CI [0.79; 1.82]. Mixed: 2 studies, MD 0.89; 95% CI [−0.63; 2.40]). Only at CS, PT is more effective than sham treatment or usual care immediately after the intervention for the BBS (ASS: 12 studies, MD 2.21; 95% CI [−0.37; 4.78]. CS: 13 studies, MD 2.50; 95% CI [1.00; 3.99]. Mixed: 2 studies, MD −1.17; 95% CI [−2.94; 0.60]). Conclusion These results show immediately after the intervention: –that balance can be improved by PT compared to no treatment whatever the stage of stroke; –an improvement of balance by PT compared to sham treatment or usual care at chronic stage.

Diabetes mellitus constitutes a major disease burden globally, and the prevalence of diabetes continues to increase worldwide. We aimed to estimate the burden of cancer associated with type 2 diabetes mellitus in Japan between 2010 and 2030. In this study, we estimated the population attributable fraction of cancer risk associated with type 2 diabetes in 2010 and 2030 using the prevalence estimates of type 2 diabetes in Japan from 1990 to 2030, summary hazard ratios of diabetes and cancer risk from a pooled analysis of eight large‐scale Japanese cohort studies, observed incidence/mortality of cancer in 2010 and predicted incidence/mortality for 2030 derived from the age–period–cohort model. Our results showed that between 2010 and 2030, the total numbers of cancer incidence and mortality were predicted to increase by 38.9% and 10.5% in adults aged above 20 years, respectively. In the number of excess incident cancer cases associated with type 2 diabetes, an increase of 26.5% in men and 53.2% in women is expected between 2010 and 2030. The age‐specific analysis showed that the population attributable fraction of cancer will increase in adults aged >60 years over time, but will not change in adults aged 20–59 years. In conclusion, this study suggests a modest but steady increase in cancers associated with type 2 diabetes., This study provides the first comprehensive evidence on the current and future burden of cancer associated with type 2 diabetes mellitus. Between 2010 and 2030, the incident cancer cases associated with type 2 diabetes were found to increase constantly over time, particularly in liver, pancreas and colon in Japan. Given the prolonged life expectancy in Japan, increase in people living with type 2 diabetes and subsequent cancer will be a public health issue in the years to come.

Background Psychological stress is a modifiable risk factor for health outcomes and can be managed through coping mechanisms. Biological and behavioral hypotheses have been proposed to explain the association between stress coping strategies and cancer outcomes. Methods The Japan Public Health Center-based study asked questions on coping behaviors in its 10-year follow-up survey. 55,130 subjects aged 50–79 without a history of cancer diagnosis and who provided complete answers on coping were included in analyses on cancer incidence and mortality. Hazard Ratios (HR) according to coping style were determined using Cox regression models adjusted for known confounders for cancer. Results Mean follow-up time was 9.5 years for cancer incidence and 9.8 years for cancer mortality. The utilization of the approach-oriented coping strategy (HR = 0.85, 95% CI: 0.72–0.99) and a behavior of positive reappraisal (HR = 0.84, 95% CI: 0.72–0.97) was associated with a reduced risk of cancer mortality. The approach-oriented coping strategy was further associated with localized cancer incidence (HR = 1.13, 95% CI: 1.01–1.27) and screening-detected cancers (HR = 1.35, 95% CI: 1.15–1.58). The avoidance oriented coping strategy was inversely associated with cancer incidence (HR = 0.69, 95% CI: 0.50–0.94) only after excluding events occurring in the first three years of follow-up. Conclusion The results of this study may favor the behavioral hypothesis to explain associations between premorbid coping styles and cancer outcomes.

Although a growing body of evidence suggests a link between diabetes and cancer, it is not clear whether diabetes independently increases the risk of cancer. We conducted a comprehensive assessment of the association between pre-existing diabetes and total and site-specific cancer risk based on a pooled analysis of eight cohort studies in Japan (>330 000 subjects). We estimated a summary hazard ratio by pooling study-specific hazard ratios for total and site-specific cancer by using a random-effects model. A statistically increased risk was observed for cancers at specific sites, such as colon (hazard ratio; HR = 1.40), liver (HR = 1.97), pancreas (HR = 1.85) and bile duct (HR = 1.66; men only). Increased risk was also suggested for other sites, and diabetes mellitus was associated with an overall 20% increased risk in total cancer incidence in the Japanese population. The association between these two diseases has important implications for reiterating the importance of controlling lifestyle factors and may suggest a possible strategy for cancer screening among patients with diabetes. Studies continuously investigating the risk factors for diabetes are also important.

Objective The present work aims to provide 10-year estimates of the probability of cancer occurrence in the Japanese population based on age, sex, and the pattern of adherence to five healthy lifestyle habits. Methods The study population consisted of 74,935 participants in the Japan Public Health Center-Based Prospective Study (aged 45 to 74 years) who answered a 5-year follow-up questionnaire about various lifestyle habits between 1995 and 1999. The relationship between five previously identified healthy lifestyle habits (never smoking, moderate or no alcohol consumption, adequate physical activity, moderate salt intake, and appropriate body mass index) and cancer occurrence was assessed using a sex-specific parametric survival model. Results Compared to individuals not adhering to any of the five habits, never-smoking men had a nearly 30% reduction in the 10-year probability of cancer occurrence (e.g., 20.5% vs. 28.7% at age 70), and never-smoking women had a 16% reduction (e.g., 10.5% vs. 12.5% at age 70). Adherence to all five habits was estimated to reduce the 10-year probability of cancer occurrence by 1/2 in men and 1/3 in women. Conclusion By quantifying the impact of lifestyle habits on the probability of cancer occurrence, this study emphasizes the importance of lifestyle improvement.

BackgroundAge is an important prognostic factor for lung cancer. However, no studies have investigated the age difference in lung cancer survival per se. We, therefore, described the role of patient-related and clinical factors on the age pattern in lung cancer excess mortality hazard by stage at diagnosis in New Zealand.MethodsWe extracted 22 487 new lung cancer cases aged 50-99 (median age = 71, 47.1% females) diagnosed between 1 January 2006 and 31 July 2017 from the New Zealand population-based cancer registry and followed up to December 2019. We modelled the effect of age at diagnosis, sex, ethnicity, deprivation, comorbidity, and emergency presentation on the excess mortality hazard by stage at diagnosis, and we derived corresponding lung cancer net survival.ResultsThe age difference in net survival was particularly marked for localised and regional lung cancers, with a sharp decline in survival from the age of 70. No identified factors influenced age disparities in patients with localised cancer. However, for other stages, females had a greater age difference in survival between middle-aged and older patients with lung cancer than males. Comorbidity and emergency presentation played a minor role. Ethnicity and deprivation did not influence age disparities in lung cancer survival.ConclusionSex and stage at diagnosis were the most important factors of age disparities in lung cancer survival in New Zealand.Key messagesWhat is the key question?How do patient-related and clinical factors influence age pattern in lung cancer survival?What is the bottom line?Age disparities in lung cancer survival were strongest for females and non-advanced disease. Deprivation, ethnicity, comorbidity, and emergency presentation did not influence age disparities.Why read on?Our findings reinforce the call for a better representation of older adults in clinical trials and a wider use of geriatric assessment to identify patients who will benefit treatment.