It is not clear whether screening for breast cancer works as public health policy and whether early indicators of effect predict an ultimate reduction in mortality. The malignant potentials of 248 breast cancers detected by the screening service in Finland were compared with those of 490 control cancers diagnosed before the screening service was established. Aggressiveness was assessed by DNA flow cytometry and clinical status by cancer size and node involvement. After the first screening round, the results of DNA flow cytometry were the same in cancers diagnosed by screening and in controls; these findings are consistent with the hypothesis that the biological aggressiveness of breast cancer remains constant as the cancer progresses. The proportion of patients with node-negative and small T1 cancers after the first screening was higher among the screened population than among controls, indicating earliness of diagnosis among those screened. Cancers diagnosed in the first round had a low malignant potential, as indicated by the DNA flow-cytometry and by clinical stage. Lower aggressiveness of cancers found by screening than of control cancers would indicate overdiagnosis or length-biased sampling, but not earliness of diagnosis. Screening with mammography is practised as a public-health policy in Finland. The results predict that the mortality reduction found in randomised trials can be repeated with a screening service.
Alcohol intake may be associated with cancer risk, but epidemiologic evidence for prostate cancer is inconsistent. We aimed to prospectively investigate the association between midlife alcohol intake and drinking patterns with future prostate cancer risk and mortality in a population-based cohort of Finnish twins.
Data were drawn from the Older Finnish Twin Cohort and included 11,372 twins followed from 1981 to 2012. Alcohol consumption was assessed by questionnaires administered at two time points over follow-up. Over the study period, 601 incident cases of prostate cancer and 110 deaths from prostate cancer occurred. Cox regression was used to evaluate associations between weekly alcohol intake and binge drinking patterns with prostate cancer risk and prostate cancer-specific mortality. Within-pair co-twin analyses were performed to control for potential confounding by shared genetic and early environmental factors.
Compared to light drinkers (=3 drinks/week; non-abstainers), heavy drinkers (>14 drinks/week) were at a 1.46-fold higher risk (HR 1.46; 95 % CI 1.12, 1.91) of prostate cancer, adjusting for important confounders. Among current drinkers, binge drinkers were at a significantly increased risk of prostate cancer (HR 1.28; 95 % CI 1.06, 1.55) compared to non-binge drinkers. Abstainers were at a 1.90-fold higher risk (HR 1.90; 95 % CI 1.04, 3.47) of prostate cancer-specific mortality compared to light drinkers, but no other significant associations for mortality were found. Co-twin analyses suggested that alcohol consumption may be associated with prostate cancer risk independent of early environmental and genetic factors.
Heavy regular alcohol consumption and binge drinking patterns may be associated with increased prostate cancer risk, while abstinence may be associated with increased risk of prostate cancer-specific mortality compared to light alcohol consumption.
Cites: Adv Exp Med Biol. 2015;815:59-7025427901
Cites: Am J Epidemiol. 2002 Dec 1;156(11):985-9312446254
Cites: Br J Cancer. 2015 Feb 3;112(3):580-9325422909
Cites: Eur J Cancer Prev. 2012 Jul;21(4):350-922095143
Cites: Nutr Cancer. 2006;56(1):50-617176217
Cites: Int J Cancer. 2006 Sep 15;119(6):1501-416615108
Cites: Hum Hered. 1978;28(4):241-54566252
Cites: Epidemiol Rev. 2001;23(1):110-411588834
Cites: Urology. 2004 Oct;64(4):717-2215491708
Cites: Am J Epidemiol. 2010 Oct 1;172(7):773-8020813803
We evaluated the risk of angiosarcoma after radiotherapy among all patients with cancers of breast, cervix uteri, corpus uteri, lung, ovary, prostate, or rectum, and lymphoma diagnosed in Finland during 1953-2003, identified from the Finnish Cancer Registry. Only angiosarcomas of the trunk were considered, this being the target of radiotherapy for the first cancer. In the follow-up of 1.8 million person-years at risk, 19 angiosarcomas developed, all after breast and gynaecological cancer. Excess of angiosarcomas over national incidence rates were observed after radiotherapy without chemotherapy (standardised incidence ratio (SIR) 6.0, 95% confidence interval (CI) 2.7-11), after both radiotherapy and chemotherapy (SIR 100, 95% CI 12-360), and after other treatments (SIR 3.6, 95% CI 1.6-7.1). In the regression analysis however, the adjusted rate ratio for radiotherapy was 1.0 (95% CI 0.23-4.4). Although an increased risk of angiosarcoma among cancer patients is evident, especially with breast and gynaecological cancer, the excess does not appear to be strongly related to radiotherapy.
We assessed the levels of arsenic in drilled wells in Finland and studied the association of arsenic exposure with the risk of bladder and kidney cancers. The study persons were selected from a register-based cohort of all Finns who had lived at an address outside the municipal drinking-water system during 1967-1980 (n = 144,627). The final study population consisted of 61 bladder cancer cases and 49 kidney cancer cases diagnosed between 1981 and 1995, as well as an age- and sex-balanced random sample of 275 subjects (reference cohort). Water samples were obtained from the wells used by the study population at least during 1967-1980. The total arsenic concentrations in the wells of the reference cohort were low (median = 0.1 microg/L; maximum = 64 microg/L), and 1% exceeded 10 microg/L. Arsenic exposure was estimated as arsenic concentration in the well, daily dose, and cumulative dose of arsenic. None of the exposure indicators was statistically significantly associated with the risk of kidney cancer. Bladder cancer tended to be associated with arsenic concentration and daily dose during the third to ninth years prior to the cancer diagnosis; the risk ratios for arsenic concentration categories 0.1-0.5 and [Greater/equal to] 0.5 microg/L relative to the category with
Cites: J Natl Cancer Inst. 1968 Mar;40(3):453-635644201
Cites: Mutat Res. 1997 Jun;386(3):263-779219564
Cites: Lancet. 1988 Feb 20;1(8582):414-52893213
Cites: Am J Epidemiol. 1989 Dec;130(6):1123-322589305
Cites: Ind Health. 1990;28(2):53-622376527
Cites: Cancer Res. 1990 Sep 1;50(17):5470-42386951
Identification of human papillomavirus type 16 (HPV16) as the major risk factor for cervical neoplasia, and mass production of DNA free HPV capsids have paved the way to preventive vaccination trials. Design of such trials requires reliable attack rate data.
Determination of (1) HPV16 and (2) cervical neoplasia attack rates in primiparous women. Estimation of actuarial sample sizes for HPV16 vaccination phase IV trials.
A longitudinal cohort study.
Population based Finnish Maternity Cohort (FMC) and Finnish Cancer Registry (FCR) were linked for the identification of two cohorts of primiparous women: (1) a random subsample of the FMC: 1656 women with two pregnancies between 1983-9 or 1990-6 and living in the Helsinki metropolitan area, and (2) all 72,791 primiparous women living in the same area during 1983-94. Attack rate for persistent HPV16 infection (1) was estimated in 1279 seronegative women by proportion of seroconversions between the first and the second pregnancy. Comparable 10 year cumulative incidence rate (CR) of cervical intraepithelial neoplasia grade III and cervical cancer (CIN III+) (2) was estimated based on cases registered at the FCR during 1991-4.
The HPV16 attack rates were 13.8% (
Cites: N Engl J Med. 1998 Feb 12;338(7):423-89459645
Cites: BMJ. 1997 Sep 13;315(7109):646-99310566
Cites: Lancet. 1987 May 30;1(8544):1247-92884378
Cites: Postgrad Med J. 1987;63 Suppl 2:73-813317362
Cites: Stat Med. 1988 Dec;7(12):1279-883231951
Cites: Sex Transm Dis. 1990 Jan-Mar;17(1):15-92154865
Cites: Int J Cancer. 1993 Apr 1;53(6):919-238386137
Cites: Int J Cancer. 1993 Jun 19;54(4):594-6068514451
Cites: J Natl Cancer Inst. 1994 Apr 6;86(7):494-98133532
Cites: Lancet. 1994 Jun 4;343(8910):1383-57910881
Cites: Curr Top Microbiol Immunol. 1994;186:55-818205846
Cites: Acta Oncol. 1994;33(4):365-98018367
Cites: Int J Cancer. 1995 Jan 27;60(3):377-827530234
Cites: J Gen Virol. 1995 Mar;76 ( Pt 3):529-397897345
Alcohol intake is causally associated with cancers of the larynx, oral cavity, pharynx, oesophagus and liver. In all five Nordic countries, alcohol consumption increased substantially between 1965 (6.5 litres per adult per year) and 1975 (10 litres), but remained at about 10 litres between 1975 and 1985. The daily consumption of men during the period was substantially higher than that of women, and that of both men and women was higher in Denmark than in the other Nordic countries. In about 2000, an annual total of almost 1,300 cancer cases (1,000 in men and 300 in women) would be avoided if alcohol drinking were eliminated. This corresponds to about 29% of all alcohol-related cancers, i.e. in the oesophagus (37%), oral cavity and pharynx (33%), larynx (29%) and liver (15%). About 2% of all cancers in men and 1% in women in the Nordic countries around the year 2000 will be caused by the drinking habits of the respective populations.
Air pollutants arising from traffic clustering and industrial production include a number of chemical compounds that at high doses are carcinogenic in animal models and in some instances also in humans. Direct epidemiological evidence for a carcinogenic effect of air pollution in humans is, however, weak, and most of the available studies are limited by lack of adequate control of confounding factors and other methodological drawbacks. Limited evidence exists for a link between urban air pollution and lung cancer, with reported relative risks of 1.0-1.5. About one-third of the population of the Nordic countries, corresponding to 7.3 million people, lives in urban areas. If there is an excess risk associated with air pollution, the annual number of lung cancer cases around the year 2000 in the Nordic countries would range from 0 (no excess risk) to 1,800 (relative risk, 1.5). As the existence of a causal link between air pollution and cancer is not uncorroborated, measures for avoiding cancer from this source cannot be recommended.
A number of chemicals encountered predominantly in occupational settings have been causally linked with cancer in humans; furthermore, several industrial processes and occupations have been associated convincingly with increased rates of cancer, although the specific carcinogens remain to be identified. The tissues affected are mainly the epithelial lining of the respiratory organs (nasal cavity, paranasal sinuses, larynx and lung), and urinary tract (renal parenchyma, renal pelvis and urinary bladder), the mesothelial linings, the bone marrow and the liver. During the period 1970-84, almost 4 million people (3.7 million men and 0.2 million women) in the Nordic countries were potentially exposed to above-average levels of one or more verified industrial carcinogens. It is expected that these exposures will result in a total of about 1,900 new cases of cancer every year in the Nordic countries around the year 2000, with 1,890 among men and fewer than 25 among women. The proportions that could be avoided if industrial carcinogens were eliminated would be 70% of mesotheliomas, 20% of cancers of the nasal cavity and sinuses, 12% of lung cancers, 5% of laryngeal cancers, 2% of urinary bladder cancers, 1% of the leukaemias, and 1% of renal cancers. Overall, it is estimated that verified industrial carcinogens will account for approximately 3% of all cancers in men and less than 0.1% of all cancers in women in the Nordic countries around the year 2000. No attempt was made to estimate the potential effects of suspected carcinogens in the workplace.
Exposure to solar and ionizing radiation increases the risk for cancer in humans. Some 5% of solar radiation is within the ultraviolet spectrum and may cause both malignant melanoma and non-melanocytic skin cancer; the latter is regarded as a benign disease and is accordingly not included in our estimation of avoidable cancers. Under the assumption that the rate of occurrence of malignant melanoma of the buttocks of both men and women and of the scalp of women would apply to all parts of the body in people completely unexposed to solar radiation, it was estimated that approximately 95% of all malignant melanomas arising in the Nordic populations around the year 2000 will be due to exposure to natural ultraviolet radiation, equivalent to an annual number of about 4700 cases, with 2100 in men and 2600 in women, or some 4% of all cancers notified. Exposure to ionizing radiation in the Nordic countries occurs at an average effective dose per capita per year of about 3 mSv (Iceland, 1.1 mSv) from natural sources, and about 1 mSv from man-made sources. While the natural sources are primarily radon in indoor air, natural radionuclides in food, cosmic radiation and gamma radiation from soil and building materials, the man-made sources are dominated by the diagnostic and therapeutic use of ionizing radiation. On the basis of measured levels of radon in Nordic dwellings and associated risk estimates for lung cancer derived from well-conducted epidemiological studies, we estimated that about 180 cases of lung cancer (1% of all lung cancer cases) per year could be avoided in the Nordic countries around the year 2000 if indoor exposure to radon were eliminated, and that an additional 720 cases (6%) could be avoided annually if either radon or tobacco smoking were eliminated. Similarly, it was estimated that the exposure of the Nordic populations to natural sources of ionizing radiation other than radon and to medical sources will each give rise to an annual total of 2120 cancers at various sites. For all types of ionizing radiation, the annual total will be 4420 cancer cases, or 3.9% of all cancers arising in the Nordic populations, with 3.4% in men and 4.4% in women.