| 11. |
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| 12. |
- Hemminki, Kari, et al.
(författare)
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Survival in breast cancer is familial
- 2008
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Ingår i: Breast Cancer Research and Treatment. - : Springer. - 0167-6806 .- 1573-7217. ; 110:1, s. 177-182
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Tidskriftsartikel (refereegranskat)abstract
- Several earlier studies have assessed survival in breast cancer based on familial risk of this disease. The results have been conflicting and suggest that the risk and prognostic factors of cancer are largely distinct. As a novel concept, we searched for familial clustering of survival, i.e., concordance of survival among family members. We used the nation-wide Swedish Family-Cancer Database to estimate hazard ratios (HRs) for cause-specific and overall survival in invasive breast cancer. HR shows the probability of death in the study group compared the reference group. The study covered 1277 mother-daughter pairs with familial breast cancer. Their median follow-up times for survival ranged from 96 to 122 months. When the survival in daughters was analyzed according to the mothers' length of survival, there was a concordance of prognosis. The HR was 0.65 in daughters whose mothers had survived > or = 120 months compared to daughters whose mothers had survived less than 36 months (P-value for trend 0.02). When the analysis was reversed and HRs were derived for mothers, the results were essentially similar (P-value for trend 0.02). The survival did not differ between patients with familial or sporadic breast cancer. The results are consistent in showing that both good and poor survival in breast cancer aggregates in families, which is a novel population-level finding for any cancer. The consistency of the results suggests that the prognosis in breast cancer is in part heritable which is likely to be explained by yet unknown genetic mechanisms.
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| 13. |
- Hiripi, E., et al.
(författare)
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Familial association of pancreatic cancer with other malignancies in Swedish families
- 2009
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Ingår i: British Journal of Cancer. - : Springer Science and Business Media LLC. - 1532-1827 .- 0007-0920. ; 101:10, s. 1792-1797
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: The aim of this study was to characterise the familial association of pancreatic cancer with other malignancies. METHODS: Relative risks (RRs) of pancreatic cancer according to family history of cancer were calculated using the updated Swedish Family-Cancer Database, which includes over 11.5 million individuals. Estimates were based on Poisson regression. RRs of tumours for individuals with a parental history of pancreatic cancer were also estimated. RESULTS: The risk of pancreatic cancer was elevated in individuals with a parental history of cancers of the liver (RR 1.41; 95% CI 1.10-1.81), kidney (RR 1.37; 95% CI 1.06-1.76), lung (RR 1.50; 95% CI 1.27-1.79) and larynx (RR 1.98; 95% CI 1.19-3.28). Associations were also found between parental history of pancreatic cancer and cancers of the small intestine, colon, breast, lung, testis and cervix in offspring. There was an increased risk of pancreatic cancer associated with early-onset breast cancer in siblings. CONCLUSION: Pancreatic cancer aggregates in families with several types of cancer. Smoking may contribute to the familial aggregation of pancreatic and lung tumours, and the familial clustering of pancreatic and breast cancer could be partially explained by inherited mutations in the BRCA2 gene. British Journal of Cancer (2009) 101, 1792-1797. doi: 10.1038/sj.bjc.6605363 www.bjcancer.com Published online 13 October 2009 (C) 2009 Cancer Research UK
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| 14. |
- Hussain, Shehnaz K., et al.
(författare)
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The Effect of Having an Affected Parent or Sibling on Invasive and In Situ Skin Cancer Risk in Sweden
- 2009
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Ingår i: Journal of Investigative Dermatology. - : Elsevier BV. - 1523-1747 .- 0022-202X. ; 129:9, s. 2142-2147
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Tidskriftsartikel (refereegranskat)abstract
- Studies suggest that skin cancer aggregates within families; however, the risk of skin cancer associated with having an affected sibling or parent by subtype, tumor site, and age at diagnosis has not been established. The 2006 update of the Swedish Family-Cancer Database was used to calculate standardized incidence ratios (SIRs), representing the ratio of cancer risk among individuals with affected parents or siblings to the general population. Risk of invasive squamous cell skin cancer for individuals with an affected sibling or parent was increased between two-and three-fold compared with that in the general population. For in situ skin tumors, increased SIRs of 1.95-4.30 for squamous cell, Bowen's disease, and actinic keratosis were observed for individuals with affected siblings or parents, and SIRs were generally higher for tumors at sun-exposed versus covered sites. Finally, SIRs for in situ and invasive squamous cell skin cancer increased by increasing number of parental tumors (P <= 0.01). In conclusion, having an affected sibling or parent was associated with an increased risk of skin cancer of varied subtypes compared with that in the general population, and for some subtypes, these familial risks were increased for tumors at sun-exposed sites or by an increasing number of parental tumors.
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| 15. |
- Ji, Jianguang, et al.
(författare)
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Survival in bladder and renal cell cancers is familial
- 2008
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Ingår i: Journal of the American Society of Nephrology. - : American Society of Nephrology. - 1046-6673 .- 1533-3450. ; 19:5, s. 985-991
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Tidskriftsartikel (refereegranskat)abstract
- Having family members with cancer has been associated with increased risk for bladder and renal cell cancers, but its association with survival has not been examined. This study was an analysis of the nationwide Swedish Family-Cancer Database and revealed that survival for bladder and renal cell cancers was similar whether the cancer was familial or sporadic; however, when survival in offspring was analyzed according to the affected parents' length of survival, prognosis was concordant. Cox proportional hazard regression models revealed that for bladder cancer, the risk for death among offspring whose parents survived > or =5 yr was approximately one third that of offspring whose parents survived <5 yr, after adjustment for gender, age at diagnosis, time period of diagnosis, socioeconomic status, and geographic region (adjusted hazard ratio 0.34; 95% confidence interval 0.15 to 0.80, for overall mortality). A risk of similar magnitude was found for renal cell cancer (adjusted hazard ratio 0.38; 95% confidence interval 0.16 to 0.87, for overall mortality). These population-level findings suggest heritability of prognosis for bladder and renal cell cancers. Genetic factors likely contribute to the mechanism underlying this observation.
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| 16. |
- Ji, Jianguang, et al.
(författare)
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Survival in Familial Pancreatic Cancer
- 2008
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Ingår i: Pancreatology (Print). - : S. Karger. - 1424-3903 .- 1424-3911. ; 8:3, s. 252-256
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Family history has been reported to be associated with an increased risk of pancreatic cancer. However, its possible influence on pancreatic cancer survival has rarely been studied, probably because of the rareness of cases in the same family.METHODS: We used the nationwide Swedish Family-Cancer Database to examine the survival differences between familial and sporadic pancreatic cancers. Hazard ratios (HRs) for cause-specific and overall survival in pancreatic cancer were examined. HRs show the probability of death in the study group compared to the reference group.RESULTS: A total of 75 familial pancreatic cancers were noted. HRs were significantly higher among offspring with an affected parent compared to those without an affected parent; for cause-specific and overall survival, the HRs were 1.44 and 1.37, respectively. Reversing the analysis and deriving HRs for parents (offspring as probands) showed that familial pancreatic cancer had a worse prognosis than sporadic cases (HR 1.37 for cause-specific and 1.28 for overall survival). The HRs were close to unity among spouses with concordant pancreatic cancer.CONCLUSION: The data show that survival in familial pancreatic cancer is worse than that in sporadic disease, which could be explained by genetic factors, if other confounding factors can be excluded. and IAP.
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| 17. |
- Ji, Jianguang, et al.
(författare)
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Survival in non-Hodgkin's lymphoma by histology and family history.
- 2009
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Ingår i: Journal of Cancer Research and Clinical Oncology. - : Springer Science and Business Media LLC. - 1432-1335 .- 0171-5216. ; 135, s. 1711-1716
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Tidskriftsartikel (refereegranskat)abstract
- PURPOSE: Although survival has been studied for various subtypes of non-Hodgkin's lymphoma (NHL), there have been few comprehensive studies to quantify the prognosis, including all specific histologies. The effect of family history on survival in NHL has not been examined. METHODS: We used the Swedish Family-Cancer Database to estimate hazard ratios in NHL by histology and family history. RESULTS: Using diffuse centroblastic lymphoma as reference (HR 1.0), patients with Waldenström's macroglobulinemia and hairy-cell leukemia had the best survival. Survival advantage was also noted among patients with lymphoplasmacytic lymphoma and different kinds of follicular lymphomas. For T-cell lymphoma, mycosis fungoides showed a favorable prognosis. As for survival by family history, a total of 98 familial cases were noted in our Database with a similar prognosis compared to sporadic cases in both parental and offspring generations. A non-significant familial concordance of either good or poor survival was noted among family members when probands' prognosis was stratified by survival time. CONCLUSIONS: Our results provide quantitative prognosis data for patients with NHL according to specific histologies. Patients with a familial NHL had a similar prognosis compared to patients with sporadic disease. The data suggest familial concordance in either good or poor survival among family members.
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| 18. |
- Ji, Jianguang, et al.
(författare)
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Survival in ovarian cancer patients by histology and family history
- 2008
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Ingår i: Acta Oncologica. - : Informa Healthcare. - 0284-186X .- 1651-226X. ; 47:6, s. 1133-1139
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Tidskriftsartikel (refereegranskat)abstract
- INTRODUCTION: Earlier studies suggest that histology has no prognostic significance in patients with invasive ovarian tumors. Studies about the effect of family history on survival have given conflicting results, which we try to clarify in this study. As an additional question, we examined whether family members share survival experience.METHODS: We used the nation-wide Swedish Family-Cancer Database to estimate hazard ratios (HRs) for cause-specific and overall survival in ovarian cancer patients by histology and family history. HRs show the probability of death in the study group compared to the reference group.RESULTS: A total of 6,049 ovarian cancer patients with specific histologies were retrieved from our Database from years 1993 to 1999. Compared to women with epithelial ovarian cancer, women with borderline epithelial tumors had the best survival (HR 0.02 and 0.14 for cause-specific and overall survival). Good survival was also noted for patients with sex cord-stromal tumors and germ cell tumors. Among specific subtypes of epithelial ovarian cancers, good survival was noted for women with clear cell and endometrioid carcinomas and mucinous cystadenocarcinoma. The study covered 80 mother-daughter pairs with a family history. Patients with a family history had a poorer survival than sporadic cases in both maternal and offspring generations. When the survival was analyzed according to the probands' length of survival, there was a non-significant concordance of prognosis.CONCLUSION: Our data showed that histology and family history are prognostic factors for ovarian tumors. Patients with a family history had a more aggressive course than the sporadic cases.
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| 19. |
- Kotova, Natalia, 1975-, et al.
(författare)
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Urinary Thymidine Dimer as a Marker of Total BodyBurden of UV-Inflicted DNA Damage in Humans
- 2005
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Ingår i: Cancer Epidemiology, Biomarkers and Prevention. - 1055-9965 .- 1538-7755. ; 14:12, s. 2868-2872
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Tidskriftsartikel (refereegranskat)abstract
- High levels of DNA damage are induced in human skin following exposure to UV radiation. Cyclobutane thymidine dimer (T = T) is the most common of these lesions, which are enzymatically removed as oligonucleotides from DNA and further degraded before excretion in urine. Analysis of such repair products in the urine could serve as a biomarker of total body burden of UV exposure. The aim of this study was to examine the kinetics of T = T excretion following a single tanning session in a commercial solarium and to validate the method by delivering different doses. Ten individuals used the solarium for a total of 35 sessions of body tanning. Urine was collected before UV exposure and daily thereafter (up to 5 or 11 days) and T = T was analyzed using a very sensitive and quantitative P-32-postlabeling technique combined with high-performance liquid chromatography. Following exposure, T = T levels increased dramatically and reached a peak 3 days later; afterwards, the T = T levels gradually decreased. The total amount of T = T excreted differed about 5-fold among subjects given an equal dose. A 50% excretion time was calculated using the excretion data for the first 5 days and it was found to be between 55 and 76 hours for different individuals. There was a good correlation between the amount of T = T excreted during days 1 to 5 and the delivered UV dose. Reducing exposure time to 50% lowered the amount of T = T to 47%; if half of the lamps were covered, T = T decreased to 44%. Our data show that urinary T = T could be a suitable noninvasive biomarker for UV exposure; a finding which could also be applicable to studies in children.
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| 20. |
- Lei, Haixin, et al.
(författare)
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PAI-1 -675 4G/5G polymorphism as a prognostic biomarker in breast cancer
- 2008
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Ingår i: Breast Cancer Research and Treatment. - : Springer. - 0167-6806 .- 1573-7217. ; 109:1, s. 165-175
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Tidskriftsartikel (refereegranskat)abstract
- Extracellular matrix degradation, mediated by the urokinase plasminogen activation (uPA) system, is a critical step in tumor invasion and metastasis. High tumor levels of uPA and its inhibitor PAI-1 have been correlated with poor prognosis in breast cancer. We examined whether genetic variation in the genes of the uPA system affect breast cancer susceptibility and prognosis. We genotyped eight potentially functional single nucleotide polymorphisms (SNPs) in six genes of the uPA system in 959 Swedish breast cancer patients with detailed clinical data and up to 15 years of follow-up together with 952 matched controls. We used the unconditional logistic regression models to evaluate the associations between genotypes and breast cancer risk and tumor characteristics. The Kaplan-Meier method was used to estimate the survival probabilities; the log-rank test was used to test differences between subgroups. None of the SNPs conferred an increased breast cancer risk, but correlation with some traditional prognostic factors was observed for several SNPs. Most importantly, we identified the -675 4G/5G SNP in the PAI-1 gene as a promising prognostic biomarker for breast cancer. Compared to the 4G/4G and 4G/5G genotypes 5G/5G homozygosity correlated significantly with worse survival (RR 2.04, 95% CI 1.45-2.86, P<0.001), especially in patients with more aggressive tumors. 5G/5G homozygotes were also the group with worse survival among lymph node negative cases. Our finding suggests that genotyping PAI-1 -675 4G/5G may help in clinical prognosis of breast cancer.
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