| 61. |
- Andersson, Kristin, et al.
(författare)
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Prospective study of genital human papillomaviruses and nonmelanoma skin cancer.
- 2013
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Ingår i: International Journal of Cancer. - : Wiley. - 0020-7136 .- 1097-0215. ; 133:8, s. 1840-1845
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Tidskriftsartikel (refereegranskat)abstract
- Genital high-risk human papillomaviruses (HPVs) cause cervical cancer and are also found in a small proportion of nonmelanoma skin cancers (NMSCs). We used cancer registry linkages to follow the 856,000 serum donors included in the Southern Sweden Microbiology Biobank or the Janus Biobank in Norway, for incident skin cancers occurring up to 30 years after serum donation. Serum samples taken before diagnosis of squamous cell carcinoma (SCC) (N = 633), basal cell carcinoma (BCC) (N = 1990) or other NMSC (N = 153) and matched samples from control donors were tested for antibodies to the genital HPV types 16 and 18. Both HPV 16 and 18 were associated with increased risk for SCC [odds ratio (OR) 1.6, 95% confidence interval (CI) 1.1-2.6 and OR 1.7, 95% CI 1.1-2.5, respectively] and other NMSC (OR 2.3, 95% CI 1.0-5.2 and OR 3.5, 95% CI 1.4-8.7, respectively), but not for BCC. Tumor blocks from HPV16 or 18 seropositive cases were tested with real-time polymerase chain reaction for presence of HPV16 or 18 DNA. No HPV18 DNA was found and only four of 79 SCC cases (two of which were from the perineum/perianal area), one of 221 BCC cases and zero of five cases with other NMSC contained HPV16 DNA. In conclusion, we found prospective evidence that HPV16 and 18 antibodies associate with SCC and other NMSC risk, but not with BCC risk. As only a small proportion of seropositive subjects had evidence of the corresponding HPV DNA in the tumor, most of this excess risk is likely to be due to confounders associated with genital HPV infection.
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| 62. |
- Andersson, Ulrika, et al.
(författare)
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MNS16A minisatellite genotypes in relation to risk of glioma and meningioma and to glioblastoma outcome.
- 2009
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Ingår i: International journal of cancer. Journal international du cancer. - : Wiley. - 1097-0215 .- 0020-7136. ; 125:4, s. 968-972
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Tidskriftsartikel (refereegranskat)abstract
- The human telomerase reverse transcriptase (hTERT) gene is upregulated in a majority of malignant tumours. A variable tandem repeat, MNS16A, has been reported to be of functional significance for hTERT expression. Published data on the clinical relevance of MNS16A variants in brain tumours have been contradictory. The present population-based study in the Nordic countries and the United Kingdom evaluated brain-tumour risk and survival in relation to MNS16A minisatellite variants in 648 glioma cases, 473 meningioma cases and 1,359 age, sex and geographically matched controls. By PCR-based genotyping all study subjects with fragments of 240 or 271 bp were judged as having short (S) alleles and subjects with 299 or 331 bp fragments as having long (L) alleles. Relative risk of glioma or meningioma was estimated with logistic regression adjusting for age, sex and country. Overall survival was analysed using Kaplan-Meier estimates and equality of survival distributions using the log-rank test and Cox proportional hazard ratios. The MNS16A genotype was not associated with risk of occurrence of glioma, glioblastoma (GBM) or meningioma. For GBM there were median survivals of 15.3, 11.0 and 10.7 months for the LL, LS and SS genotypes, respectively; the hazard ratio for having the LS genotype compared with the LL was significantly increased HR 2.44 (1.56-3.82) and having the SS genotype versus the LL was nonsignificantly increased HR 1.46 (0.81-2.61). When comparing the LL versus having one of the potentially functional variants LS and SS, the HR was 2.10 (1.41-3.1). However, functionality was not supported as there was no trend towards increasing HR with number of S alleles. Collected data from our and previous studies regarding both risk and survival for the MNS16A genotypes are contradictory and warrant further investigations.
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| 63. |
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| 64. |
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| 65. |
- Ankerst, Jaro, et al.
(författare)
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Cross‐reacting tstas in adeno 7 and 12 tumors demonstrated by 51CR‐Cytotoxicity and isograft rejection tests
- 1969
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Ingår i: International Journal of Cancer. - : Wiley. - 0020-7136 .- 1097-0215. ; 4:3, s. 279-287
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Tidskriftsartikel (refereegranskat)abstract
- Antisera of mice hyperimmunized against syngeneic X‐irradiated adeno 12 tumor cells were tested for complement‐dependent cytotoxicity against an adeno 7 and an adeno 12 hamster tumor by a 51Cr‐cytotoxic test, developed to work on non‐lymphoid target cells. Significant isotope release above the level of release obtained after exposure to control sera was recorded with both tumors. There was no similar release from BHK‐C13 control hamster cells. The cytotoxic effect on hamster adeno 7 tumor cells was confirmed by the colony inhibition technique. Furthermore, it was demonstrated by transplantation tests in mice that the hamster adeno 7 tumor cells were immunogenic, causing an isograft immunity to adeno 12 tumors similar to that induced by adeno 12 hamster and mouse tumor cells.
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| 66. |
- Ankerst, Jaro, et al.
(författare)
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Demonstration of two group‐specific TSTAs in adenovirus‐induced tumors
- 1970
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Ingår i: International Journal of Cancer. - : Wiley. - 0020-7136 .- 1097-0215. ; 6:1, s. 84-92
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Tidskriftsartikel (refereegranskat)abstract
- Infection of mice and rats with any one of five tested human adenovirus types belonging to groups A and B (types 3, 7, 12, 18 and 31) induced an immunity to the TSTAs of type 12 tumors as detected by the colony inhibition (CI) test. No immunity was found against an adenovirus type 1 tumor. Two adenovirus types belonging to group C (types 1 and 5) were similarly tested and found to induce a clear‐cut immunity to the adenovirus type 1 tumor but not to tumors induced by adenovirus of groups A and B. The only tested virus type of group D (type 4) did not induce any clear‐cut immunity to either adenovirus 12 tumors or the adenovirus 1 tumor. Immunization of rats with rat adenovirus 12 tumor cells induced a cellular immunity to adenovirus 12 mouse tumor cells but not to a mouse polyoma tumor. Adenovirus 1 rat tumor cells induced no such immunity. Immunization of rats with syngenic adenovirus 12 tumor cells induced a cellular immunity to adenovirus 12 rat and mouse tumors and an adenovirus 7 hamster tumor, but not to an adenovirus 1 rat tumor or BHK‐C13 control hamster cells. The result of a tumor prevention experiment is consistent with the existence of a common TSTA induced by types 7 and 12 and a different TSTA induced by type 5 virus. It is concluded that the highly oncogenic group A and the weakly oncogenic group B adeno virus types all induce a common TSTA. Another TSTA is induced by the group C viruses, while no evidence has been obtained for the existence of any TSTA induced by a group D virus type.
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| 67. |
- Ankerst, Jaro, et al.
(författare)
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Effect of selenium on the induction of breast fibroadenomas by adenovirus type 9 and 1,2‐dimethylhydrazine‐induced bowel carcinogenesis in rats
- 1982
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Ingår i: International Journal of Cancer. - : Wiley. - 0020-7136 .- 1097-0215. ; 29:6, s. 707-710
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Tidskriftsartikel (refereegranskat)abstract
- Selenium in its organic and inorganic forms has been shown to inhibit the development of chemically induced, spontaneous and transplanted tumors. The present investigation was performed to study the effect of selenium (4 μg per ml of drinking water) on tumorigenesis of adenovirus‐type‐9‐induced breast fibroadenomas and on 1,2‐dimethylhydrazine‐induced bowel carcinogenesis in WF rats. It was found that identical treatment with Se under identical conditions and with no obvious toxic effects on the rats (I) resulted in inhibition of DMH‐induced large‐bowel carcinogenesis; (2) facilitated induction of small‐bowel cancer by the same carcinogen in the same animals, and (3) greatly facilitated induction of breast fibroadenoma by adenovirus type 9 in the same strain of rats. The effect of Se treatment on DMH‐induced largebowel carcinogenesis confirms previous findings and proves that the opposite effect on fibroadenoma development is not due to differences in e.g. effective dose, animal strains or condition of the animals. It is not yet clear through which mechanisms Se exerts these effects.
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| 68. |
- Ankerst, J., et al.
(författare)
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Induction of mammary fibroadenomas in rats by adenovirus type 9
- 1974
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Ingår i: International Journal of Cancer. - : Wiley. - 0020-7136 .- 1097-0215. ; 13:3, s. 286-290
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Tidskriftsartikel (refereegranskat)abstract
- After inoculation of adenovirus type 9 into newborn Wistar/Furth rats, seven out of seven females developed one or several mammary fibroadenomas within 14–25 weeks after virus inoculation. No tumours were observed in male rats inoculated with the same virus or in untreated controls. Neonatal inoculations of adenovirus type 5, produced on the same HeLa cells, gave negative results in both sexes. The results indicate that benign mammary tumours can be induced in rats by a virus and that mammary fibroadenomas are induced by adenovirus type 9, previously known to be capable of transforming cells in vitro but not of inducing tumours in vivo.
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| 69. |
- Ankerst, Jaro, et al.
(författare)
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Inhibitory effects of BCG on adenovirus tumorigenesis : Dependence on administration schedule
- 1972
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Ingår i: International Journal of Cancer. - : Wiley. - 0020-7136 .- 1097-0215. ; 10:2, s. 351-356
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Tidskriftsartikel (refereegranskat)abstract
- The cumulative incidence of tumours was registered in CBA mice inoculated with adenovirus type 12 when newborn and treated with BCG in different ways during the latency period. A single subcutaneous dose of BCG at 3–4 weeks of age had a preventive effect, while no prevention could be recorded after a single BCG dose at 9 weeks of age or eight BCG injections at intervals of 1 week. Sera obtained during the latency period were tested for capacity to block lymph‐node cell‐mediated tumour immunity. Blocking activity was detectable in pooled serum of the mice which had been infected with BCG at 9 weeks of age, already at 10 weeks, i.e. 1 to 2 weeks before the appearance of palpable tumours. Blocking activity could not be demonstrated in a serum pool from control mice until 14 weeks after virus inoculation, at which time sera from mice inoculated with BCG at the age of 3 weeks were still negative. The results indicate that the effect of BCG upon tumour development is dependent upon the point of time of BCG treatment and further suggest that BCG treatment initiated at a stage when serum blocking activity is already present can further stimulate the production of blocking factors and tentatively promote tumour development.
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| 70. |
- Araghi, Marzieh, et al.
(författare)
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Use of moist oral snuff (snus) and pancreatic cancer : Pooled analysis of nine prospective observational studies
- 2017
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Ingår i: International Journal of Cancer. - : Wiley. - 0020-7136 .- 1097-0215. ; 141:4, s. 687-693
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Tidskriftsartikel (refereegranskat)abstract
- While smoking is a well-established risk factor for pancreatic cancer, the effect of smokeless tobacco is less well understood. We used pooled individual data from the Swedish Collaboration on Health Effects of Snus Use to assess the association between Swedish snus use and the risk of pancreatic cancer. A total of 424,152 male participants from nine cohort studies were followed up for risk of pancreatic cancer through linkage to health registers. We used shared frailty models with random effects at the study level, to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) adjusted for confounding factors. During 9,276,054 person-years of observation, 1,447 men developed pancreatic cancer. Compared to never-snus use, current snus use was not associated with risk of pancreatic cancer (HR 0.96, 95% CI 0.83-1.11) after adjustment for smoking. Swedish snus use does not appear to be implicated in the development of pancreatic cancer in men. Tobacco smoke constituents other than nicotine or its metabolites may account for the relationship between smoking and pancreatic cancer. What's new? While smoking is a well-established risk factor for pancreatic cancer, the effect of smokeless tobacco is less well understood. Smokeless tobacco like snus yields lower exposure to tobacco carcinogens compared with smoking, because it does not undergo combustion, but delivers an equivalent dose of nicotine. Using pooled individual data from the Swedish Collaboration on Health Effects of Snus Use, here the authors show that Swedish snus use does not appear to be implicated in the development of pancreatic cancer in men. Tobacco smoke constituents other than nicotine or its metabolites may account for the relationship between smoking and pancreatic cancer.
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