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Background Expensive cancer treatment calls for alternative ways such as drug repurposing to develop effective drugs. The aim of this study was to analyse the effect of post-diagnostic use of cholera vaccine on survival outcome in breast cancer patients. Methods Cancer diagnosis and cholera vaccination were obtained by linkage of several Swedish national registries. One vaccinated patient was matched with maximum two unvaccinated individuals based on demographic, clinical and socioeconomic factors. We performed proportional Cox regression model to analyse the differences in overall and disease-specific survivals between the matched patients. Results In total, 617 patients received cholera vaccine after breast cancer diagnosis. The median (interquartile range) time from diagnosis to vaccination was 30 (15–51) months and from vaccination to the end of follow-up it was 62 (47–85) months. Among them, 603 patients were matched with 1194 unvaccinated patients. Vaccinated patients showed favourable overall survival (hazard ratio (HR): 0.54, 95% confidence interval (CI): 0.37–0.79) and disease-specific survival (HR: 0.53, 95% CI: 0.33–0.84), compared to their unvaccinated counterpart. The results were still significant in multiple sensitivity analyses. Conclusions Post-diagnostic use of cholera vaccine is associated with a favourable survival rate in breast cancer patients; this provides evidence for repurposing it against breast cancer.

Background:Individuals with lactose intolerance are recommended to avoid milk or dairy products, which may affect the development of cancer.Methods:We identified individuals with lactose intolerance from several Swedish Registers linked to the Swedish Cancer Registry to calculate standardised incidence ratios (SIRs) for cancers in the breast, lung, and ovary.Results:A total of 22 788 individuals with lactose intolerance were identified, and their risks of lung (SIR=0.55), breast (SIR=0.79), and ovarian (SIR=0.61) cancers were significantly decreased. Cancer incidences in the siblings and parents of individuals with lactose intolerance were similar to those in the general population.Conclusions:In this large cohort study, people with lactose intolerance, characterised by low consumption of milk and other dairy products, had decreased risks of lung, breast, and ovarian cancers, but the decreased risks were not found in their family members, suggesting that the protective effects against these cancers may be related to their specific dietary pattern.British Journal of Cancer advance online publication, 14 October 2014; doi:10.1038/bjc.2014.544 www.bjcancer.com.

Background:Familial nervous system cancers are rare and limited data on familial aspects are available particularly on site-specific tumours.Methods:Data from five Nordic countries were used to analyse familial risks of nervous system tumours. Standardised incidence ratios (SIRs) were calculated for offspring of affected relatives compared with offspring of non-affected relatives.Results:The total number of patients with nervous system tumour was 63 307, of whom 32 347 belonged to the offspring generation. Of 851 familial patients (2.6%) in the offspring generation, 42 (4.7%) belonged to the families of a parent and at least two siblings affected. The SIR of brain tumours was 1.7 in offspring of affected parents; it was 2.0 in siblings and 9.4 in families with a parent and sibling affected. For spinal tumours, the SIRs were much higher for offspring of early onset tumours, 14.0 for offspring of affected parents and 22.7 for siblings. The SIRs for peripheral nerve tumours were 16.3 in offspring of affected parents, 27.7 in siblings and 943.9 in multiplex families.Conclusion:The results of this population-based study on medically diagnosed tumours show site-, proband- and age-specific risks for familial tumours, with implications for clinical genetic counselling and identification of the underlying genes.British Journal of Cancer advance online publication, 25 May 2010; doi:10.1038/sj.bjc.6605708 www.bjcancer.com. (Less)

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 (Less)

Background: This study quantified the risk of urinary bladder neoplasms in cancer patients taking into account the age at first diagnosis, the gender of the patients and the lead time between diagnoses. Methods: We used standardised incidence ratios (SIRs) to compare the incidence of bladder tumours in 967 767 cancer patients with the incidence rate in the general Swedish population. A total of 3324 male and 1560 female patients developed bladder tumours at least 1 year after first cancer diagnosis. Results: After bladder and renal pelvis cancers, the SIRs of bladder neoplasms were higher in female than in male patients. Men affected by lung, stomach and larynx tumours belonged to the population at high risk for bladder cancer. Treatment of breast, ovarian and cervical cancers seems to contribute to the subsequent development of bladder neoplasms. Long latencies (16–25 years) were observed after testicular, cervical and endometrial cancers. Detection bias had an important role after prostate cancer. Chemotherapy with cyclophosphamide and cisplatin, and also radiotherapy, seem to increase the risk of subsequent neoplasms in the bladder. Conclusions: These population-based results may help urologists to assess the risk of bladder neoplasms in cancer survivors. Our data should guide ongoing studies that investigate the effectiveness of bladder cancer screening in cancer patients.

BACKGROUND: Diagnosis with prostate cancer has been reported to increase the risk of subsequent tumours. However, specific data on individuals with a parental history are not available so far. METHODS: On the basis of the nationwide Swedish Family-Cancer Database including 18,207 primary invasive prostate cancers, standardised incidence ratios (SIRs) were used to estimate the relative risks of subsequent tumours after prostate cancer in the general population and among individuals with a parental history of cancer. RESULTS: A significantly increased SIR of colorectal cancer was found among prostate cancer patients with a parental history of colorectal cancer (2.26, 11 cases). The SIRs of parental concordant ( same site) tumours after prostate cancer were also increased for urinary bladder cancer (4.42, 4 cases) and chronic lymphoid leukaemia (38.0, 2 cases). CONCLUSION: A higher than additive and multiplicative interaction was observed between the individual history of prostate cancer and parental history of colorectal and urinary bladder cancers, although the number of cases did not permit the rejection of any interaction model. The results suggest that the occurrence of second tumours, for example bladder after prostate or prostate after bladder tumours, is mostly related to shared genetic and non-genetic risk factors rather than treatment of first cancer. British Journal of Cancer ( 2009) 101, 935-939. doi:10.1038/sj.bjc.6605263 www.bjcancer.com Published online 18 August 2009 (C) 2009 Cancer Research UK (Less)

We examined overall and specific cancer risks among Swedish subjects who had been hospitalised one or more times for psoriasis. A database was created by identifying such patients from the Swedish Hospital Discharge Register and linking them with the Cancer Registry. Follow-up of patients was carried out from the last hospitalisation through 2004. A total of 15 858 patients were hospitalised for psoriasis during 1965–2004, of whom 1408 developed cancer, giving an overall standardised incidence ratios (SIRs) of 1.33. A significant excess was noted for squamous cell skin cancer, and for cancers of the upper aerodigestive tract, oesophagus, stomach, liver, pancreas, lung, kidney and bladder as well as non-Hodgkin lymphoma. Many of these may reflect the effects of alcohol drinking and tobacco smoking. Patients with multiple hospitalisations showed high risk, particularly for oesophageal (SIR 6.97) and skin (SIR 4.76) cancers.

Asthma is an increasingly common disorder, affecting 5-10% of the population. It involves a dysregulated immune function, which may predispose to subsequent cancer. We examined cancer risk among Swedish subjects who had hospital admission once or multiple times for asthma. An asthma research database was created by identifying asthma patients from the Swedish Hospital Discharge Register and by linking them with the Cancer Registry. A total of 140 425 patients were hospitalised for asthma during 1965-2004, of whom 7421 patients developed cancer, giving an overall standardised incidence ratio (SIR) of 1.36. A significant increase was noted for most sites, with the exception of breast and ovarian cancers and non-Hodgkin's lymphoma and myeloma. Patients with multiple hospital admissions showed a high risk, particularly for stomach (SIR 1.70) and colon (SIR 1.99) cancers. A significant decrease was noted for endometrial cancer and skin melanoma. Oesophageal and lung cancers showed high risks throughout the study period, whereas stomach cancer increased towards the end of the period. The relatively stable temporal trends suggest that the asthmatic condition rather than its medication is responsible for the observed associations.

Using the Swedish Family-Cancer Database, among a total of 1 030 806 women followed from 1993 through 2004, invasive and borderline epithelial ovarian cancer was identified in 3306 and 822 women respectively, with data on family history, reproductive variables, residential region and socioeconomic status. Relative risks and population-attributable fractions (PAFs) were estimated by Poisson regression. The overall PAFs of invasive epithelial ovarian cancer for family history and for reproductive factors were 2.6 and 22.3%, respectively, for serous/seropapillary cystadenocarcinoma (3.0 and 19.1%), endometrioid carcinoma (2.6 and 26.6%), mucinous cystadenocarcinoma (0.5 and 23.9%) and clear-cell carcinoma (2.6 and 73.9%). The corresponding PAFs of borderline tumours due to family history were lower, but higher due to reproductive factors. Family history, low parity and young age at first birth were associated with elevated risks. The risks for women with a family history were among the highest, but these women accounted for the smallest proportion of the cases, giving the lowest PAFs.

Reliable data on familial risks are important for clinical counselling and cancer genetics. However, the estimates of familial risk of gastric cancer vary widely. We examined the risk of familial gastric cancer using the updated Swedish Family-Cancer Database with 5358 patients among offspring and 36,486 patients among parents. There were 133 families with one parent and one offspring diagnosed with gastric cancer, and 20 families with two affected offspring. Familial standardised incidence ratios (SIRs) were 1.63 and 2.93 when parents and siblings presented with gastric cancer, respectively. The high sibling risk was owing to cancer in the corpus (SIR 7.28). The SIR for cardia cancer was 1.54 when parents were diagnosed with any gastric cancer. Cardia cancer associated with oesophageal cancer, particularly with oesophageal adenocarcinoma. Among specific histologies, signet ring cancer showed an increase. A few associations were noted for discordant sites, including the urinary bladder and the endometrium. H. pylori infection, although not measured in the present study, is probably an important risk factor for the high sibling risk of corpus cancer. Familial clustering of cardia cancer is independent of H. pylori infection, and may have a genetic basis. The familial association of cardia cancer with oesophageal adenocarcinoma may provide aetiological clues.

BACKGROUND: The possibility of an association of Graves' disease (GD) with subsequent cancers raised by certain studies. METHODS: Using a database on 18 156 hospitalised GD patients, subsequent cancers were ascertained. RESULTS: Increased risks of thyroid and parathyroid tumours were limited to the early follow-up period, which is probably a surveillance bias. Cancer sites with observed excess included the mouth and breast, in contrast to decreased risks of colon cancer, melanoma and non-Hodgkin's lymphoma. CONCLUSION: Increased subsequent cancers in GD patients appeared to be balanced by decreased risks at other sites; chance cannot be excluded. British Journal of Cancer (2010) 102, 1397-1399. doi:10.1038/sj.bjc.6605624 www.bjcancer.com Published online 30 March 2010 (C) 2010 Cancer Research UK (Less)

The Swedish Family-Cancer Database was used to quantify the incidence of second tumours in melanoma patients with a parental history of cancer. Patients with parents affected by melanoma showed a 32.3-fold risk of second primary melanomas, which was greater than a multiplicative interaction.

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.

Using the Swedish Family-Cancer Database covering over 11.5 million individuals, estimated relative risks (RRs) for colorectal adenoma were using Poisson's regression. The RR of colorectal adenoma was found to be increased among first-degree relatives of patients with colorectal cancer (2.72; 95% confidence interval=2.46–3.00) and among the offspring and siblings of patients with endometrial and prostate cancers. We also found an increased risk of colorectal adenoma for the offspring of individuals with stomach cancer and leukaemia, and for siblings of those with pancreatic cancer and multiple myeloma. Our results suggest that colorectal adenoma may share a genetic aetiology with cancer even at extracolorectal sites. Increases of colorectal adenoma in families affected by prostate cancer and acute leukaemia cannot be attributed to known cancer syndromes, although the play of chance cannot be excluded.