| 1. |
- Berhin, Johan, et al.
(författare)
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”Den svenska skogen är underutnyttjad”
- 2023
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Ingår i: Svenska Dagbladet Debatt. - 1101-2412.
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Tidskriftsartikel (populärvet., debatt m.m.)abstract
- Forskning och nya metoder för skogsbruk visar att svensk skog kan binda mycket mer koldioxid än i dag och samtidigt ge virke med högre värden. Vi menar att svensk skog är underutnyttjad, skriver flera debattörer.
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| 2. |
- Kosunen, Timo U., et al.
(författare)
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Gastric cancers in finnish patients after cure of helicobacter pylori infection : a cohort study.
- 2011
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Ingår i: International Journal of Cancer. - : Wiley. - 0020-7136 .- 1097-0215. ; 128:2, s. 433-439
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Tidskriftsartikel (refereegranskat)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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| 3. |
- Kosunen, Timo U. U., et al.
(författare)
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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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Ingår i: Helicobacter. - : John Wiley & Sons. - 1083-4389 .- 1523-5378. ; 28:3
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Tidskriftsartikel (refereegranskat)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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| 4. |
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| 5. |
- Stevens, Richard G., et al.
(författare)
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Considerations of circadian impact for defining 'shift work' in cancer studies : IARC Working Group Report.
- 2011
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Ingår i: Occupational and Environmental Medicine. - : BMJ. - 1351-0711 .- 1470-7926. ; 68:2, s. 154-162
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Tidskriftsartikel (refereegranskat)abstract
- Based on the idea that electric light at night might account for a portion of the high and rising risk of breast cancer worldwide, it was predicted long ago that women working a non-day shift would be at higher risk compared with day-working women. This hypothesis has been extended more recently to prostate cancer. On the basis of limited human evidence and sufficient evidence in experimental animals, in 2007 the International Agency for Research on Cancer (IARC) classified 'shift work that involves circadian disruption' as a probable human carcinogen, group 2A. A limitation of the epidemiological studies carried out to date is in the definition of 'shift work.' IARC convened a workshop in April 2009 to consider how 'shift work' should be assessed and what domains of occupational history need to be quantified for more valid studies of shift work and cancer in the future. The working group identified several major domains of non-day shifts and shift schedules that should be captured in future studies: (1) shift system (start time of shift, number of hours per day, rotating or permanent, speed and direction of a rotating system, regular or irregular); (2) years on a particular non-day shift schedule (and cumulative exposure to the shift system over the subject's working life); and (3) shift intensity (time off between successive work days on the shift schedule). The group also recognised that for further domains to be identified, more research needs to be conducted on the impact of various shift schedules and routines on physiological and circadian rhythms of workers in real-world environments.
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| 6. |
- Talibov, Madar, et al.
(författare)
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Occupational exposure to solvents and acute myeloid leukemia : a population-based, case-control study in four Nordic countries
- 2014
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Ingår i: Scandinavian Journal of Work, Environment and Health. - : SCANDINAVIAN JOURNAL WORK ENVIRONMENT & HEALTH. - 0355-3140 .- 1795-990X. ; 40:5, s. 511-517
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Tidskriftsartikel (refereegranskat)abstract
- Objective The aim of the current study was to assess the relation between occupational exposure to solvents and the risk of acute myeloid leukemia (AML). Methods Altogether, this study comprises 15 332 incident cases of AML diagnosed in Finland, Norway, Sweden, and Iceland from 1961-2005 and 76 660 controls matched by year of birth, sex, and country. Occupational records were linked with Nordic Occupational Cancer Study job exposure matrix (JEM) to estimate quantitative values for 26 occupational exposure factors. Hazard ratios (HR) with 95% confidence intervals (95% CI) were estimated by using conditional logistic regression models. Results We did not observe statistically significantly increased risk for exposure to any of the solvents. HR estimates for high levels of toluene (HR 1.35, 95% CI 0.74-2.46), aromatic hydrocarbon solvents (ARHC) (HR 1.18, 95% CI 0.76-1.86), and moderate-to-high levels of trichloroethylene were slightly but non-significantly elevated. We did not observe an association between benzene exposure and AML in this study. Conclusions This study did not provide clear evidence for an association between occupational solvent exposure and AML. There was some indication for an excess risk in the groups of workers exposed to toluene, trichloroethylene, and ARHC.
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| 7. |
- Travis, Lois B., et al.
(författare)
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Cumulative absolute breast cancer risk for young women treated for Hodgkin lymphoma
- 2005
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Ingår i: Journal of the National Cancer Institute. - : Oxford University Press (OUP). - 0027-8874 .- 1460-2105. ; 97:19, s. 1428-37
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Many women develop breast cancer after treatment for Hodgkin lymphoma (HL) at a young age. We estimated this future risk, taking into account age and calendar year of HL diagnosis, HL treatment information, population breast cancer incidence rates, and competing causes of death. METHODS: Relative risks of breast cancer for categories defined by radiation dose to the chest (0, 20- < 40 Gy, or > or = 40 Gy) and use of alkylating agents (yes or no) were estimated from a case-control study conducted within an international population-based cohort of 3817 female 1-year survivors of HL diagnosed at age 30 years or younger from January 1, 1965, through December 31, 1994. To compute cumulative absolute risks of breast cancer, we used modified standardized incidence ratios to relate cohort breast cancer risks to those in the general population, enabling application of population-based breast cancer rates, and we allowed for competing risks by using population-based mortality rates in female HL survivors. RESULTS: Cumulative absolute risks of breast cancer increased with age at end of follow-up, time since HL diagnosis, and radiation dose. For an HL survivor who was treated at age 25 years with a chest radiation dose of at least 40 Gy without alkylating agents, estimated cumulative absolute risks of breast cancer by age 35, 45, and 55 years were 1.4% (95% confidence interval [CI] = 0.9% to 2.1%), 11.1% (95% CI = 7.4% to 16.3%), and 29.0% (95% CI = 20.2% to 40.1%), respectively. Cumulative absolute risks were lower in women treated with alkylating agents. CONCLUSIONS: Breast cancer projections varied considerably by type of HL therapy, time since HL diagnosis, and age at end of follow-up. These estimates are applicable to HL survivors treated with regimens of the past and can be used to counsel such patients and plan management and preventive strategies. Projections should be used with caution, however, in patients treated with more recent approaches, including limited-field radiotherapy and/or ovary-sparing chemotherapy.
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| 8. |
- Travis, Lois B, et al.
(författare)
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Lung cancer following chemotherapy and radiotherapy for Hodgkin's disease
- 2002
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Ingår i: Journal of the National Cancer Institute. - : Oxford University Press (OUP). - 0027-8874 .- 1460-2105. ; 94:3, s. 182-192
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Lung cancer is a frequent cause of death in patients cured of Hodgkin's disease, but the contributions of chemotherapy, radiotherapy, and smoking are not well described. We quantified the risk of treatment-associated lung cancer, taking into account tobacco use.METHODS: Within a population-based cohort of 19 046 Hodgkin's disease patients (diagnosed from 1965 through 1994), a case-control study of lung cancer was conducted. The cumulative amount of cytotoxic drugs, the radiation dose to the specific location in the lung where cancer developed, and tobacco use were compared for 222 patients who developed lung cancer and for 444 matched control patients. All statistical tests were two-sided.RESULTS: Treatment with alkylating agents without radiotherapy was associated with increased lung cancer risk (relative risk [RR] = 4.2; 95% confidence interval [CI] = 2.1 to 8.8), as was radiation dose of 5 Gy or more without alkylating agents (RR = 5.9; 95% CI = 2.7 to 13.5). Risk increased with both increasing number of cycles of alkylating agents and increasing radiation dose (P for trend <.001). Among patients treated with mechlorethamine, vincristine, procarbazine, and prednisone (MOPP), risk increased with cumulative amounts of mechlorethamine and procarbazine (P<.001) when evaluated separately. Statistically significantly elevated risks of lung cancer were apparent within 1-4 years after treatment with alkylating agents, whereas excess risk after radiotherapy began 5 years after treatment and persisted for more than 20 years. Risk after treatment with alkylating agents and radiotherapy together was as expected if individual excess risks were summed. Tobacco use increased lung cancer risk more than 20-fold; risks from smoking appeared to multiply risks from treatment.CONCLUSIONS: Past treatments with alkylating agents and radiation therapy for Hodgkin's disease were associated with an increased risk of lung cancer in a dose-dependent and additive fashion. The precise risk estimates, however, should be interpreted cautiously, given the possible residual and enhancing effects of tobacco.
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