Age-incidence relationships are informative of carcinogenic mechanisms. These have been previously assessed for cervical squamous cell carcinoma (SCC) but not for adenocarcinoma. The aim was to assess by means of age-, period- and cohort-specific analyses and Poisson regression modelling whether the two types of cervical cancer show an age-incidence maximum at a relatively young age, as shown in cross-sectional analyses. The Swedish Family-Cancer Database was used to analyse age-incidence relationships in cervical SCC and adenocarcinoma diagnosed in years 1958-1996, including a total of 15,118 and 1866 cases, respectively. Area of residence and socio-economic status were included in analyses because they were risk factors of cervical cancer. The analysis of cervical SCC confirmed an incidence maximum at ages 35-39 years. The data for adenocarcinoma also suggested a similar early age maximum but the curves differed extensively by birth cohort. The incidence of adenocarcinoma increased substantially at young age groups towards the end of follow-up. Endometrial adenocarcinoma and vaginal and vulvar SCC, which share some risk factors with cervical cancer, did not show an early age incidence maximum. The results also showed that there was a decrease in the incidence of cervical SCC around year 1960, almost 10 years before the organized population screening, probably due to introduced opportunistic pap testing. The benefits of the organized screening were observed as a further decline in the incidence rates. The unique age-incidence relationships in cervical cancer call for biological explanations.
BACKGROUND: Familial breast cancers are known to be of early onset. This article provides differences in the age of onset of breast cancer and death by breast cancer between women with and without a family history. METHODS: The Swedish Family-Cancer Database was used to estimate the cumulative risk of breast cancer and death by breast cancer according to family history with a stratified Cox model. Family history was defined separately for affected mother or sister considering their diagnostic ages. RESULTS: The age to reach the same cumulative incidence as women without family history decreased with decreasing diagnostic age of the affected relative. Women with a maternal history reached the risk of women lacking a family history at the age of 50 years between 12.3 (mother affected 82 years) earlier. The trend for breast cancer mortality was essentially similar. CONCLUSIONS: Women with mother or sister affected by breast cancer are diagnosed and die at earlier ages than do women without family history. The differences depend on the diagnostic age of the affected relative. The present data may provide a rationale to derive recommendations for the starting age of screening in women with affected family members.
The goal of this study was to test whether there is genetic anticipation in Hodgkin's disease (HD) and non-Hodgkin's lymphoma (NHL). We analyzed 102 parent-child pairs with HD or NHL, based upon the Swedish Cancer Database. We identified 18 sib-pairs (2 HD and 16 NHL) and 102 parent-child pairs (13 HD/HD, 56 NHL/NHL, 25 HD/NHL, and 8 NHL/HD). The mean anticipation score was 27.6 years for all 102 parent-child pairs. The anticipation means were 13.8, 28.4, 19.8 and 35.8 years for these pair-type groups, respectively. These differences between the age of onset for each affected parent-child pair type were statistically significant. The anticipation level was more pronounced among the NHUNHL pairs than in the HD/HD pairs (difference = 12.6 years, p = 0.0003). These results allow us to conclude with confidence that there is an apparent genetic anticipation in familial HD and NHL in the Swedish population.
We used the nationwide Swedish Family-Cancer Database to analyse the association of histology-specific brain tumours with other cancers in family members. Among 0-68-year-old offspring, 9414 patients with brain tumours were identified from 1961 to 2000, of whom, 3387 parents were diagnosed with any primary neoplasm. Astrocytoma, meningioma and neurinoma were the main histological types. Increased standardised incidence ratios (SIRs) were found for brain tumours in association with cancers at sites that are known features in recognised syndromes, such as haemangioblastoma and renal cancer in von Hippel-Lindau disease. In addition, an association between astrocytoma and melanoma was recognised. Among as yet unknown clustering, neurinoma was associated with testicular cancer and myeloma; meningioma was associated with cervical cancer; astrocytoma was associated with prostate cancer; ependymoma was associated with breast cancer. Although some of these may feature a true tumour cluster, they need to be confirmed in another setting.
Children whose twins have had leukaemia have a higher risk of contracting acute lymphoblastic leukaemia (ALL), confirming a prenatal origin of the disease. This association was not true when considering other types of affected first-degree relatives. Children whose fathers were diagnosed with testicular cancer have a higher risk of ALL.
The cumulative risk of non-Hodgkin lymphoma (NHL) in Sweden by age 80 years has increased to 1.1 in women and 1.6% in men in 2011. Increased risk of NHL associated with personal histories of some autoimmune diseases (ADs) is known. It is unclear whether there are other NHL-related ADs and whether this association holds across different sex, age and year of diagnosis, or NHL histological subtypes.
Over an average of 9.4-year (maximum 47 years) follow-up of 878 161 patients diagnosed in 1964-2010 with 33 different ADs, 3096 subsequent NHL were diagnosed (data: Swedish Cancer Registry).
Of 33 studied ADs, 21 showed significantly increased risk of NHL; 6 of them tended to increase the risk and none significantly decreased it. The overall standardized incidence ratio (SIR) for NHL after ADs was 1.6 [novel findings: immune thrombocytopenic purpura (ITP) = 7.5, polymyositis/dermatomyositis = 4.1, primary biliary cirrhosis = 3.9, myasthenia gravis = 2.2, Behcet = 1.7, rheumatoid fever = 1.7, ulcerative colitis = 1.5, polymyalgia rheumatica = 1.4, and chronic rheumatic heart disease = 1.4; confirmatory findings: autoimmune hemolytic anemia = 27.2, Sj?gren = 4.9, Celiac = 4.8, systemic lupus erythematosus = 4.4, polyarteritis nodosa = 2.9, discoid lupus erythematosus = 2.7, sarcoidosis = 2.6, Crohn = 2.1, systemic sclerosis = 2.1, rheumatoid arthritis = 2.0, and Hashimoto/hypothyroidism and psoriasis = 1.4]. SIR for NHL diagnosis before age 60 (2.2) was significantly higher than that in older ages (age =60: 1.5). The SIRs in women or men and in period 1993-2010 or 1964-1992 were similar. Risk of all common NHL histology subtypes significantly increased after ADs (cutaneous/peripheral T cell and anaplastic large T and null cell = 2.2; small B-cell lymphocytic = 1.7; diffuse large B cell = 1.6; follicular and mantel cell = 1.3).
Many of 33 studied ADs (except for ankylosing spondylitis, diabetes type I graves/hyperthyroidism, multiple sclerosis, chorea minor, and pernicious anemia), especially when diagnosed at younger ages, were associated with higher risk of NHL. However, the absolute risk of NHL in many ADs is still small.
We used the Swedish Family-Cancer Database to analyse the effects of birth order and family size on the risk of common cancers among offspring born over the period 1958-96. Some 1.38 million offspring up to age 55 years with 50.6 million person-years were included. Poisson regression analysis included age at diagnosis, birth cohort, socio-economic status and region of residence as other explanatory variables. The only significant associations were an increasing risk for breast cancer by birth order and a decreasing risk for melanoma by birth order and, particularly, by family size. When details of the women's own reproductive history were included in analysis, birth orders 5-17 showed a relative risk of 1.41. The effects on breast cancer may be mediated through increasing birth weight by birth order. For melanoma, socio-economic factors may be involved, such as limited affordability of sun tourism in large families. Testis cancer showed no significant effect and prostate cancer was excluded from analysis because of the small number of cases.
To assess whether occupational exposure to aromatic hydrocarbons increases carcinogenic risk.
We followed cancer incidence among 3,922 male and 1,379 female workers monitored for exposure to styrene, toluene, or xylene. The follow-up after the first personal measurement comprised 66,500 person-years at risk over the period 1973-1992. We computed the indirectly standardized incidence ratios (SIR) with 95% confidence interval (CI) with regard to age-, gender-, and period-specific incidence rates of cancer in the Finnish general population.
The overall rate of cancer incidence for the total cohort was fairly similar to that of the general population. The risk for nervous system tumors was increased at 10 years after the first personal measurement (SIR 2.80, CI 1.03-6.08). For styrene there was an excess risk for rectal cancer (SIR 3.11, CI 1.14-6.77), and risks for pancreatic and nervous system tumors were increased nonsignificantly. For toluene and xylene, no clear increase in cancer risk was found.
The data are not supportive of an overall increase in the cancer risk for these solvents, even though we cannot rule out site-specific associations with the rectum, pancreas, and nervous system. There is supporting evidence in the epidemiology literature for pancreatic cancer risk and heavy exposure to styrene. More studies are warranted on solvents, with detailed information on lifetime exposures and habits being collected whenever possible.
Epidemiologic studies and long-term carcinogenicity studies in experimental animals suggest that some halogenated hydrocarbons are carcinogenic. To investigate whether exposure to trichloroethylene, tetrachloroethylene, or 1,1,1-trichloroethane increases carcinogenic risk, a cohort of 2050 male and 1924 female workers monitored for occupational exposure to these agents was followed up for cancer incidence in 1967 to 1992. The overall cancer incidence within the cohort was similar to that of the Finnish population. There was an excess of cancers of the cervix uteri and lymphohematopoietic tissues, however. Excess of pancreatic cancer and non-Hodgkin lymphoma was seen after 10 years from the first personal measurement. Among those exposed to trichloroethylene, the overall cancer incidence was increased for a follow-up period of more than 20 years. There was an excess of cancers of the stomach, liver, prostate, and lymphohematopoietic tissues combined. Workers exposed to 1,1,1-trichloroethane had increased risk of multiple myeloma and cancer of the nervous system. The study provides support to the hypothesis that trichloroethylene and other halogenated hydrocarbons are carcinogenic for the liver and lymphohematopoietic tissues, especially for non-Hodgkin lymphoma. The study also documents excess of cancers of the stomach, pancreas, cervix uteri, prostate, and the nervous system among workers exposed to solvents.