Cancer incidence and incidence rates in Japan in 2000: Estimates based on data from 11 population-based cancer registries.
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Biomedical subjects
Publications and source records attributed to Tomotaka Sobue.
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Fifty single-nucleotide polymorphisms (SNPs) associated with amino acid changes in 36 genes involved in diverse DNA repair pathways were assessed for associations with risk for small cell lung carcinoma (SCLC) by a case-control study consisting of 211 SCLC cases and 685 controls. An SNP, Val83Met, in the MTH1 (microtT homolog 1) gene encoding a triphosphatase that hydrolyzes pro-mutagenic oxidized nucleoside triphosphates, such as 8-hydroxy-dGTP and 2-hydroxy-dATP, showed the strongest and a significant association with SCLC risk [odds ratio (OR)=1.6, 95% confidence interval (CI): 1.2-2.2, P=0.004], while three other SNPs in the TP53, BLM and SNM1 genes, respectively, also showed marginal associations (0.05<P<0.1). Another SNP, which causes a nucleotide change in the 5'-UTR of MTH1 transcripts leading to alternative translation initiation, was additionally examined and the SNP also showed a significant association (OR=1.7, 95% CI: 1.2-2.3, P=0.002). The two SNPs in the MTH1 gene were in linkage disequilibrium, and the OR for carrying a copy of the haplotype consisting of both the risky SNP alleles was 2.0 (95% CI: 1.2-3.2, P=0.002). The present results indicate that inter-individual differences in MTH1 activities due to SNPs are involved in susceptibility to SCLC.
BACKGROUND: The Research Center for Cancer Prevention and Screening program is a one-arm prospective study designed to evaluate the effect of multiple modalities for cancer screening. Basic programs consist of screening tests for cancer of the lung, esophagus, stomach, colon, rectum, liver, gall bladder, pancreas and kidneys, in addition to prostate cancer screening for males and breast, cervical, endometrial and ovarian cancer screenings for females. OBJECTIVE: To investigate the possibility of overdiagnosis, we compared the observed numbers with expected numbers based on the model. METHODS: We calculated the expected number of cancers on the basis of negative or positive history of screening tests within the previous year, based on assumed sensitivity and sojourn time. Observed numbers of screen-detected cases for stomach, colorectal, lung, prostate and breast cancer were compared with expected numbers. RESULTS: From February 2004 to January 2005, 3786 participants were enrolled in our study. The overall cancer detection rate was 5.8% (119/2061) for males and 4.1% (71/1725) for females. No statistically significant difference was found between observed and expected cases for colorectal cancer screening, gastric cancer screening for females and lung cancer screening for males. Observed numbers of breast, prostate and lung cancer for females exceeded those expected (P < 0.05). CONCLUSIONS: Although cancer screening programs in the present study increased the detection of potentially curable cancers, these modalities, particularly lung, breast and prostate screening, might detect cancers which would not necessarily be clinically significant. We should therefore weigh up benefit and harm for such cancer screening programs.
We investigated the degree of generalizability of relative risk (RR) estimates for a sample from a well-defined population to a general population using actual data. A total of 45,452 men aged 40-69 years who completed a self-administered questionnaire were followed from 1990-1994 to the end of 1999-2000 in the Japan Public Health Center-based Prospective Study. We considered those who responded to the self-administered questionnaire (45,452 men) as representing the general population (population), and those who underwent a health check-up as representing a sample from a well- defined population (sample) (12,162 men). Exposure distributions, mortality rates, and the confounder-adjusted RRs of all-cause mortality according to cigarette smoking or body mass index (BMI) were compared between the sample and the population using empirical sampling distributions from the population. The sample had significantly different prevalences of exposures and lower mortality rates than the population. Adjusted RRs were significantly higher in current smokers (RR = 1.83) and in subjects who smoked > or =40 cigarettes per day (RR = 2.67) in the sample than the respective values in the corresponding categories (RR = 1.48 and 1.62, respectively) of the population. The adjusted RR of those with the lowest BMI in the sample (RR = 1.30) were also significantly lower than those of the corresponding category in the population (RR = 2.06). Our results suggest that even for RRs, the extrapolation of estimates for a sample from a well-defined population to a general population may not be possible.
To evaluate recent improvements in lung cancer screening, we compared the results of recently conducted lung cancer screening with those of a previous screening. This study compared the survival of lung cancer patients detected by lung cancer screening conducted between 1976 and 1984 (early period) with that conducted between 1989 and 1997 (late period). Two hundred seventy-six patients with lung cancer were detected in the early period and 541 patients with lung cancer were detected in the late period. The median survival time (late : 49.8 vs. early : 27.8 months) and the 5-year survival rate (late : 47.8 vs. early : 34.8%) of the patients with lung cancer detected in the late period were significantly better than those in the early period (p = 0.0054). Among patients undergoing resection, the proportion of pathological stage I patients in the late period was significantly higher than that in the early period (late : 60.8 vs. early : 54.9%, p = 0.005). Multivariate analysis showed that the screening time period was a significant prognostic factor (hazard ratio = 0.685, 95% confidence interval : 0.563-0.832, p = 0.0002). These results were consistent with the findings of case-control studies of lung cancer screening programs in the late period recently conducted in Japan, which also showed a greater efficacy for screening than for previous case-control studies in the early period.
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Although a link between female hormonal factors and the risk of lung cancer has been suggested, few studies have examined this association in detail. We investigated the associations between reproductive factors, hormone use and the risk of lung cancer in a population-based prospective study. Self-administered questionnaires were distributed to 44,677 lifelong never-smoking women in 1990-1994 to assess menstrual and reproductive factors and hormone use. After 8-12 years of follow-up, 153 lung cancer cases were diagnosed. Relative risk (RR) and 95% confidence intervals (CI) were calculated using the Cox proportional hazards model. Age at menopause, age at menarche, number of children, age at first live birth, breast feeding and use of hormones were not associated with a risk of lung cancer, either overall or among postmenopausal women or women with natural menopause. Compared to women with both late age at menarche (> or =16) and early age at menopause (< or =50), those with either early age at menarche or late age at menopause had a >2-fold, significant increase in the risk of lung cancer. Induced menopausal women with experience of hormone replacement therapy had a significantly elevated risk compared to naturally menopausal women without female hormone use, with an RR of 2.40 (95% CI 1.07-5.40). These findings suggest that both endogenous and extraneous estrogen may be involved in the etiology of lung cancer.
BACKGROUND: The present study aimed to elucidate the changing patterns of smoking among successive birth cohorts in Japan. METHODS: Birth-cohort-specific smoking prevalence was estimated for birth cohorts born from 1900 to 1952, using data pooled from four prospective studies (242,330 men and 274,075 women), and for birth cohorts born from 1925 to 1977, using National Nutrition Survey data. RESULTS: For men, two peaks were observed in smoking prevalence, in the 1925 and late-1950s birth cohorts, while a trough was observed for the 1938 birth cohort. For women, ever smoking prevalence was lowest among the 1930s birth cohorts. After the female 1940s birth cohorts, no peak was observed until the end of our observations, the 1970s birth cohorts. Although Japanese women have historically tended to start smoking at later ages, recently, smoking habits have widely expanded among females in young birth cohorts. CONCLUSIONS: Smoking trends in Japanese men and women vary by birth cohorts. Smoking cessation should continue to be strongly promoted among men, although the younger generation has widely adopted a nonsmoking lifestyle. For women, efforts for preventing the onset of smoking, while necessary among the younger generation, should even be enhanced among middle-aged women.
The epidemiologic evidence that dietary fiber protects against colorectal cancer is equivocal. No large-scale clinical study of the administration of Lactobacillus casei has been reported. We examined whether dietary fiber and L. casei prevented the occurrence of colorectal tumors. Subjects were 398 men and women presently free from tumor who had had at least 2 colorectal tumors removed. Subjects were randomly assigned to 4 groups administered wheat bran, L. casei, both or neither. The primary end point was the presence or absence of new colorectal tumor(s) diagnosed by colonoscopy after 2 and 4 years. Among 380 subjects who completed the study, 95, 96, 96 and 93 were assigned to the wheat bran, L. casei, both and no treatment groups, respectively. Multivariate adjusted ORs for occurrence of tumors were 1.31 (95% CI 0.87-1.98) in the wheat bran group and 0.76 (0.50-1.15) in the L. casei group compared to the control group. There was a significantly higher number of large tumors after 4 years in the wheat bran group. The occurrence rate of tumors with a grade of moderate atypia or higher was significantly lower in the group administered L. casei. No significant difference in the development of new colorectal tumors was observed with administration of either wheat bran or L. casei. However, our results suggest that L. casei prevented atypia of colorectal tumors.
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Single nucleotide polymorphisms (SNPs) were searched for in 36 genes involved in diverse DNA repair pathways, and 50 nonsynonymous (associated with amino acid changes) SNPs identified were assessed for associations with lung cancer risk by a case-control study consisting of 752 adenocarcinoma cases, 250 squamous cell carcinoma cases and 685 controls. An SNP, Arg72Pro, of the TP53 gene encoding a DNA damage response protein showed the strongest association with squamous cell carcinoma risk (OR Pro/Pro vs. Arg/Arg = 2.2), while 2 other SNPs, Phe257Ser of the REV gene encoding a translesion DNA polymerase and Ile658Val of the LIG4 gene encoding a DNA double-strand break repair protein, also showed associations (OR Ser/Ser vs. Phe/Phe = 2.0 and OR Ile/Val vs. Ile/Ile = 0.4, respectively). An SNP, Thr706Ala, in the POLI gene encoding another translesion DNA polymerase was associated with adenocarcinoma and squamous cell carcinoma risk, particularly in individuals of ages < 61 years (OR Ala/Ala + Ala/Thr vs. Thr/Thr = 1.5 and 2.4, respectively). POLI is the human counterpart of PolI, a strong candidate for the Par2 (pulmonary adenoma resistance 2) gene responsible for adenoma/adenocarcinoma susceptibility in mice. The present results suggest that these 4 SNPs function as genetic factors underlying lung cancer susceptibility by modulating activities to maintain the genome integrity of each individual.
To examine the hypothesis that tobacco smoke is associated with the risk of female breast cancer, we estimated the relative risks of active and passive smoke in middle-aged Japanese women in a population-based prospective study. The cohort consisted of residents in 4 public health center areas, aged 40 to 59 years. A self-administered questionnaire survey was conducted in 1990. This analysis included 21,805 subjects, 180 of whom had developed breast cancer by December 31, 1999. When the reference was defined as never-active smokers without passive smoking, adjusted relative risks (RRs) were 1.9 (95% confidence interval [CI] = 1.0-3.6) in current active smokers, 1.2 (95% CI = 0.4-4.0) in ex-active smokers and 1.2 (95% CI = 0.8-1.6) in never-active smokers with passive smoking. The elevated risk for ever-smokers was clearly observed in premenopausal women at baseline (RR = 3.9, 95% CI = 1.5-9.9) but not in postmenopausal women (RR = 1.1, 95% CI = 0.5-2.5). In never-active smokers, the adjusted RR for passive smoking, residential or occupational/public tobacco smoke exposure was 1.1 (95% CI = 0.8-1.6). In premenopausal women, passive smoking increased the risk (RR = 2.6; 95% CI = 1.3-5.2) but not in postmenopausal women (RR = 0.7; 95% CI = 0.4-1.0). We conclude that tobacco smoking increases the risk of female breast cancer in premenopausal women.
BACKGROUND: An association between coffee drinking and reduced risk of liver cancer has been suggested by animal studies, but epidemiologic evidence of such an association in a high-risk population is lacking. We conducted a large-scale population-based cohort study of the association between coffee drinking and hepatocellular carcinoma (HCC) in a Japanese population. METHODS: Newly diagnosed case patients (250 men and 84 women) with HCC were identified from a 10-year follow-up of the Japan Public Health Center-based Prospective Study, which consists of 90,452 middle-aged and elderly Japanese subjects (43,109 men and 47,343 women). Case patients were grouped according to coffee intake and were stratified by hepatitis virus infection, sex, age, diet, lifestyle factors, and previous history of liver disease. Multivariable-adjusted hazard ratios (HR) and 95% confidence intervals (CIs) for HCC were calculated with Cox proportional-hazards modeling. All statistical tests were two-sided. RESULTS: Subjects (men and women combined) who consumed coffee on a daily or almost daily basis had a lower HCC risk than those who almost never drank coffee (HR = 0.49 [95% CI = 0.36 to 0.66]); risk decreased with the amount of coffee consumed (compared with nondrinkers, the HR for 1-2 cups per day = 0.52 [95% CI = 0.38 to 0.73]; for 3-4 cups per day = 0.48 [95% CI = 0.28 to 0.83]; for > or =5 cups per day = 0.24 [95% CI = 0.08 to 0.77], P(trend) < .001). The risk of liver cancer in almost never drinkers in this population was 547.2 cases per 100,000 people over 10 years, but it was 214.6 cases per 100 000 people with drinking coffee on a daily basis. The inverse association persisted when the participants were stratified by lifestyle factors. Similar associations were observed when the analysis was restricted to hepatitis C virus-positive patients (all daily drinkers compared with nondrinkers: HR =0.57 [95% CI = 0.37 to 0.86]), to hepatitis B virus-positive patients (HR = 0.60 [95% CI = 0.31 to 1.18]) and to subjects with no past history of chronic liver disease (HR = 0.45 [95% CI = 0.30 to 0.67]). CONCLUSIONS: In the Japanese population, habitual coffee drinking may be associated with reduced risk of HCC.
Basic information on the association between lifestyle factors and candidate genes is valuable for genetic-environmental study. We screened the association of habitual smoking or drinking with polymorphism in 40 candidate genes for a total of 153 single nucleotide polymorphisms (SNPs) using a sample of 339 middle-aged, randomly selected Japanese men. Smoking and drinking statuses were elicited during questionnaire-based interviews. Genes were selected based on their possible involvement in genetic-environmental, life-style interactions and constitute the genes expressing xenobiotic metabolism enzymes, DNA repair enzymes, and other stress-related proteins. The P values of odds ratios to habitual smoking for CYP17A1, ESR1, EPHX1, GSTT2, ALDH2, NOS2A, OGG1, and SLC6A4 and those of odds ratios to habitual drinking for CYP1B1, ESR1, HSD17B3, GSTM3, COMT, ADH1C, ALDH2, NOS3, and NUDT1 were under 0.05. These variables were included in a stepwise logistic analysis in order to develop a predictive model for smoking or drinking behavior. In the final model, the only significant variables selected for smoking were OGG1, SLC6A4, EPHX1, ESR1, and CYP17A1, and for drinking, ALDH2 and NUDT1. The findings of the present study suggest that polymorphism in associated candidate genes plays a role in the habitual use of tobacco and alcohol among Japanese men.
BACKGROUND: Trends in lung cancer mortality among young adults, which are important for projecting future trends, have not been explored previously in Japan. METHODS: Using data from the National Vital Statistics between 1958 and 2003, we compiled lung cancer mortality by sex and 5-year birth cohort among young adults aged 20-49. RESULTS: Mortality among those aged 20-29 has consistently decreased regardless of sex. There were birth cohort effects in mortality from lung cancer, although these were less evident among women than among men. Both men and women born in the 1930s had lower mortality rates, while those born after 1940 had higher lung cancer mortality rates. Mortality rates appear to be declining for male birth cohorts born after 1950 and female birth cohorts after 1960, although these trends may not be stable due to the small number of deaths in these cohorts. CONCLUSION: Lung cancer mortality trends appear to be decreasing among young adults. This might be associated with the lower mortality of birth cohorts after 1950 for men and the 1960s birth cohorts for women. Careful monitoring is needed to confirm continuation of these declining trends.
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Cigarette smoking is an established risk factor for lung cancer. However, the magnitude of the relative risk (RR) on lung cancer mortality in relation to cigarette smoking is reported to be lower in Japan than in Western countries. We investigated whether this discrepancy could be explained by differences in the exposure to cigarettes smoked, by differences in sensitivity to smoking, or by differences in lung cancer mortality among non-smokers. We examined the 10-year follow-up data on 88,153 participants in a Japanese population-based prospective study conducted in three prefectures. Data used as a Western counterpart was retrieved from a published report of the US Cancer Prevention Study (CPS)-II. Although there was a significant increased risk of lung cancer death among current smokers compared with non-smokers, the observed RR in the Three-Prefecture Study were much lower than RR reported in the CPS-II. Lung cancer mortality of our Japanese sample was lower among current smokers and higher among non-smokers regardless of age and sex. Current smokers in our sample had initiated smoking at an older age and smoked fewer cigarettes per day for shorter durations than those in the CPS-II sample. The Poisson regression model (controlling for age, number of cigarettes smoked per day and duration of smoking) showed that male current smokers in our sample had a lower risk of lung cancer compared with those in the CPS-II sample (rate ratio 0.34 [95%CI 0.27-0.43]). These findings might explain why Japanese risks of lung cancer are lower than those observed in Western countries.