| 21. |
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| 22. |
- Kharazmi, Elham, et al.
(author)
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Familial Risk of Small Intestinal Carcinoid and Adenocarcinoma
- 2013
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In: Clinical Gastroenterology and Hepatology. - : Elsevier BV. - 1542-7714 .- 1542-3565. ; 11:8, s. 944-949
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Journal article (peer-reviewed)abstract
- BACKGROUND & AIMS: Small intestinal cancer (SIC) is rare, and its etiology is poorly understood. We compared clusters of families with SICs of different histologic subtypes. METHODS: By using the nationwide family cancer data sets of Sweden and Finland, we identified a cohort of 9964 first-degree relatives of 1799 patients with SIC, diagnosed from 1961 through 2009. Data were collected from time periods as long as 47 years (mean, 35.4 y), and cancer incidence was determined. Standardized incidence ratios (SIRs) were calculated and stratified by sex, age, time period, and cancer type, using the incidence rates for the entire national population as the reference. RESULTS: Among the 1799 SIC cases, 1.1% had a sibling with SIC, so the SIR was 11.8 (95% confidence interval [CI], 7.2-18.2); 1.1% had a parent or child with SIC (SIR, 3.5; 95% CI, 2.0-5.6). The SIR of concordant carcinoid histology of SIC among siblings was 28.4 (95% CI, 14.7-49.6; n = 12) and in parent-child pairs was 9.9 (95% CI, 5.4-16.6; n = 14). The familial risk of concordant histologic subtypes increased for siblings diagnosed with adenocarcinoma, but only 2 familial cases were identified. In family members of patients with SIC of the adenocarcinoma subtype, risks of colorectal and bladder cancer were modestly but significantly increased compared with the general population. Family members of patients with SIC of the carcinoid subtype had an increased risk for kidney cancer and polycythemia vera. CONCLUSIONS: Based on data from our population-based study, first-degree relatives of patients with small intestinal carcinoid tumors have developed these tumors with high incidence. Because of the rareness of this tumor, the absolute risk remains moderate even within families. Gastroenterologists could inform patients with small intestinal carcinoids about the familial risk and encourage counseling for their first-degree relatives. Studies are needed to identify genetic factors that affect susceptibility to SIC.
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| 23. |
- Kharazmi, Elham, et al.
(author)
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Familial risks for childhood acute lymphocytic leukaemia in Sweden and Finland: far exceeding the effects of known germline variants
- 2012
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In: British Journal of Haematology. - : Wiley. - 0007-1048. ; 159:5, s. 585-588
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Journal article (peer-reviewed)abstract
- Despite recent successes in the identification of genetic susceptibility loci, no familial risk has been demonstrated for childhood acute lymphoblastic leukaemia (ALL). We identified 3994 childhood ALL cases from two cancer registries; family members were obtained from population registers. The standardized incidence ratio for familial risk in singleton siblings and twins was 3.2 (95% confidence interval 1.55.9) and 162.6 (70.2320.4), respectively. The present data constitute the first demonstration of familial risk for singleton siblings; the high risk for twins is believed to result from shared prenatal blood circulation. The data suggest that currently unidentified genetic loci underlie these observed familial effects.
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| 24. |
- Kharazmi, Elham, et al.
(author)
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Risk of familial classical Hodgkin lymphoma by relationship, histology, age, and sex: A joint study from five Nordic countries.
- 2015
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In: Blood. - : American Society of Hematology. - 1528-0020 .- 0006-4971. ; 126:17, s. 1990-1995
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Journal article (peer-reviewed)abstract
- The rarity of familial Hodgkin lymphoma (HL) has hampered detailed analyses of familial clustering. We aimed to provide the familial risk of HL by relationship, histology, age at diagnosis and sex. A cohort of 57,475 first-degree relatives of 13,922 HL patients, diagnosed between 1955 and 2009, in five European countries was followed for HL incidence. Standardized incidence ratios (SIRs) were calculated using histology-, age-, sex-, period-, and country-specific incidence rates as the reference. The lifetime cumulative risks (CR) were also calculated. The overall CR of HL in first-degree relatives of a patient with HL was 0.6%, which represents a 3-fold (SIR=3.3, 95%CI=2.8-3.9) increased risk over the general population risk. The risk in siblings (6.0-fold; 4.8-7.4) was significantly higher than in parents/children (2.1-fold; 1.6-2.6). Very high lifetime risk of HL was found for those with multiple affected first-degree relatives (13-fold; 2.8-39) and for same-sex twins (57-fold; 21-125). We found high familial risks between some concordant histological subtypes of HL [lymphocyte-rich (81-fold, 30-177) and nodular sclerosis (4.6-fold, 2.9-7.0)] and also between some discordant subtypes. The familial risk in sisters (9.4-fold; 5.9-14) was higher than in brothers (4.5-fold; 2.9-6.7) or unlike-sex siblings (5.9-fold; 4.3-8.1). The lifetime risk of HL was higher when first-degree relatives were diagnosed at early ages (before age 30). This study provides tangible absolute risk estimates for relatives of HL patients, which can be used as a sex-, age-, and family history-based risk calculator for classical Hodgkin lymphoma by oncologists and genetic counselors.
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| 25. |
- Koivisto-Korander, Riitta, et al.
(author)
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Second primary malignancies among women with uterine sarcoma
- 2012
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In: Gynecologic Oncology. - : Elsevier BV. - 1095-6859 .- 0090-8258. ; 126:1, s. 30-35
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Journal article (peer-reviewed)abstract
- Objective. Uterine sarcomas (US) are rare malignancies with unclear aetiology. Studies on uterine sarcomas in the setting of second primary malignant tumours can provide clues to aetiology and identify side effects of different treatments. Methods. A cohort of 8606 cases of US was extracted from the data from 13 cancer registries and followed for second primary cancers within the period 1943-2000. Standardized incidence ratios (SIRs) were calculated, and Poisson regression analyses were performed. Results. There were 499 cancer cases observed after a first diagnosis of US (SIR 1.26, 95%CI 1.16-1.38). SIRs were elevated for cancers of the mouth and pharynx (2.16, 95%CI 1.15-3.69), colorectum (1.60, 95%CI 1.28-1.98), lung (1.73, 95%CI 1.27-2.29), breast (1.25, 95%CI 1.05-1.49), urinary bladder (1.74, 95%CI 1.02-2.79), kidney (2.00, 95%CI 1.24-3.06), thyroid gland (2.74, 95%CI 1.42-4.79), and soft tissue sarcoma (5.23, 95%CI 2.51-9.62). The risk of breast cancer increased along with increasing age of US diagnosis (p trend 0.040). The risk of kidney cancer increased along with decreasing age of US diagnosis (p trend 0.004) and short time since the US diagnosis (p trend 0.018). Conclusions. Our study demonstrated increased risk of certain cancers following a diagnosis of US. The elevated risk for breast cancer may indicate shared hormonal aetiology, while the increased risk of colorectal and bladder cancers after US may be caused by radiation therapy of US. The clustering of smoking-related cancers after US is worth exploring in the future. (c) 2012 Elsevier Inc. All rights reserved.
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| 26. |
- Koljonen, Virve, et al.
(author)
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Joint occurrence of Merkel cell carcinoma and non-Hodgkin lymphomas in four Nordic countries
- 2015
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In: Leukemia & Lymphoma. - : Informa UK Limited. - 1042-8194 .- 1029-2403. ; 56:12, s. 3315-3319
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Journal article (peer-reviewed)abstract
- The objective of this study was to assess the reciprocal association between non-Hodgkin lymphoma (NHL) and Merkel cell carcinoma (MCC) using the data of four Nordic Cancer Registries. Data for this study were drawn from the Danish, Finnish, Norwegian, and Swedish cancer registries. Standardized incidence ratios (SIRs) for MCC among NHL patients, and for NHL among MCC patients, were calculated. There were 109 838 individuals with NHL and 1411 individuals with MCC, of which 28 had joint occurrence of NHL and MCC. In 18 cases, NHL was diagnosed first, and in 10 cases, MCC was diagnosed first. The SIR for MCC after NHL was 4.34 (95% confidence interval 2.57-6.85). The SIR for NHL after MCC was 3.13 (1.50-5.77). Although the absolute frequency of joint occurrence of MCC and NHL is low, individuals suffering from one of the cancer forms have an increased risk of the other.
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| 27. |
- Korhonen, Pasi, et al.
(author)
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Entacapone and prostate cancer risk in patients with Parkinson's disease
- 2015
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In: Movement Disorders. - Hoboken, USA : Wiley-Blackwell. - 0885-3185 .- 1531-8257. ; 30:5, s. 724-728
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Journal article (peer-reviewed)abstract
- Background: The association between Parkinson’s disease (PD) and prostate cancer, both common in elderly men, is disputable. In the STRIDE-PD study, prostate cancer developed in 9 patients (3.7%) receiving levodopa/carbidopa with entacapone, a catechol-O-methyltransferase inhibitor, versus 2 cases (0.9%) without entacapone. The current pharmacoepidemiological study aimed to determine whether entacapone increases prostate cancer incidence or mortality in PD patients and whether cumulative exposure affects these rates.Methods: We performed a retrospective cohort study using population-wide health care registers with patientlevel linkage. Prostate cancer incidence and mortality were modeled by Cox’s proportional hazards models.Results and Conclusions: Use of entacapone with Ldopa/dopa decarboxylase inhibitor caused no increased risk of prostate cancer incidence (hazard ratio [HR]: 1.05; 95% confidence interval: 0.76-1.44) or mortality (0.93; 0.43-1.98). The HR for cumulative entacapone use of >360 days versus never-use was 0.82 (0.56-1.18) for prostate cancer incidence and 1.27 (0.60-2.72) for prostate cancer mortality.
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| 28. |
- Kosunen, Timo U., et al.
(author)
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Gastric cancers in finnish patients after cure of helicobacter pylori infection : a cohort study.
- 2011
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In: International Journal of Cancer. - : Wiley. - 0020-7136 .- 1097-0215. ; 128:2, s. 433-439
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Journal article (peer-reviewed)abstract
- Helicobacter pylori infection is associated with gastric cancer. A total of 97% of the infected subjects have elevated levels of H. pylori antibodies. The antibody titers have been shown to decline rapidly (40-60% within 4-12 months) only after successful eradication therapy. We allocated 26,700 consecutive patients tested during 1986-1998 for H. pylori antibodies to three subcohorts: seropositive patients with rapidly falling antibody titers (Hp+CURED, n=3,650), seropositive patients where no serological information indicating cure was obtained (Hp+NoInfo, n=11,638) and seronegative patients (Hp-, n=11,422). In the subcohorts, the standardised incidence ratios (SIRs) with 95% confidence intervals (CI) were defined for subsequent cancers of stomach, pancreas, colon, rectum, breast and prostate separately and for all cancers except stomach combined. The mean follow-up time was 10.1 years and the number of gastric cancers 72. For the Hp+CURED, the SIR for gastric cancers for the first five follow-up years was 1.62 but decreased from the sixth follow-up year thereon to 0.14 (CI: 0.00-0.75). Likewise, the risk ratio (RR), defined in a Poisson regression analysis using the Hp+NoInfo group as the reference, decreased from 1.60 to 0.13 (CI: 0.02-1.00, p = 0.049). The SIR for Hp- was not significantly higher than that for Hp+NoInfo for any of the cancers analysed. To conclude, cured H. pylori infection led to a significantly decreased incidence of gastric cancers from the sixth follow-up year. Advanced atrophic gastritis would be a plausible contributor to the elevated SIR in elderly Hp- patients.
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| 29. |
- Kosunen, Timo U. U., et al.
(author)
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Incidence of gastrointestinal malignancies increases in persons received eradication therapy for Helicobacter pylori : A cohort study
- 2023
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In: Helicobacter. - : John Wiley & Sons. - 1083-4389 .- 1523-5378. ; 28:3
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Journal article (peer-reviewed)abstract
- Background: Long-term Helicobacter pylori infection increases the risk of gastric malignancies. Since the symptoms for H. pylori gastritis, as well as for several malignancies, may be nonexisting or highly unspecific, even H. pylori-positive subjects with underlying malignancies may receive eradication therapy. The aim was to assess the incidence of gastrointestinal and various other malignancies in individuals after eradication therapy for H. pylori infection.Materials and Methods: A cohort of 217,554 subjects (120,344 women and 97,210 men), who had purchased specific combinations of drugs for H. pylori eradication therapy in 1994-2004, was identified by the Finnish National Prescription Registry and followed for cancer incidence until the end of 2008 (1.89 million person-years at risk).Results: A total of 22,398 malignancies were identified in the cohort. In both genders, for the first 6 months after drug prescription, the standardized incidence ratios (SIRs) were between 5 and 32 for gastric, colorectal, and pancreatic cancers, and 2 and 3 for several other malignancies. Although later on the SIRs of most malignancies fell rapidly, those of gastric noncardia and lung cancers remained elevated up to 5 years of follow-up. The only SIRs below unity were seen in men for gastric cancers (cardia 0.61, 95% CI: 0.37-0.95; intestinal noncardia 0.74, 95% CI: 0.56-0.97) during the post-therapy period covering years 5-15.Conclusion: Incidence levels significantly above the population rates were detected for many malignancies. Although eradication of H. pylori may have a long-lasting protective effect against gastric cancer, H. pylori therapy may postpone the detection of malignancies possibly underlying unspecific gastrointestinal symptoms. Therefore, it should be emphasized that the diagnostic work-up for malignancies should not be stopped in case of detection and treatment of H. pylori infection.
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| 30. |
- Laukkanen, Päivi, et al.
(author)
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Time trends in incidence and prevalence of human papillomavirus type 6, 11 and 16 infections in Finland.
- 2003
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In: Journal of General Virology. - : Microbiology Society. - 1465-2099 .- 0022-1317. ; 84:Pt 8, s. 2105-2109
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Journal article (peer-reviewed)abstract
- Human papillomavirus (HPV) type 16 is the major cause of cervical carcinoma, the incidence of which is decreasing in western countries. In Finland the incidence is, however, increasing in women aged <40 years, but possible underlying changes in HPV-16 epidemiology are unknown. To assess incidence trends of HPV infections, paired sera from a random sample of 8000 women with two pregnancies/sera within 5 years, taken from the serum bank of the Finnish Maternity Cohort (1983–98), were analysed for HPV-6, -11 and -16 antibodies. For 23–31-year-old women, HPV-16 incidence increased over the period 1983–97. HPV-16 seroprevalence increased from 17 % in 1983–85 to 24 % in 1995–97, but HPV-6 and HPV-11 prevalence was stable at 9–12 % throughout the study period. Epidemic spread of the oncogenic HPV-16, but not the non-oncogenic HPV-types, throughout the 1980s and 1990s preceded an increase in the incidence of cervical carcinoma in fertile-aged Finnish women.
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