Hyposalivation is a common adverse effect of anti-neoplastic therapy of head and neck cancer, causing impaired quality of life and predisposition to oral infections. However, data on the effects of hematopoietic stem cell transplantation (HSCT) on salivary secretion are scarce. The present study determined stimulated whole-saliva flow rates in HSCT recipients in comparison with a healthy control group. Stimulated whole-saliva flow rates of 228 allogeneic HSCT recipients (134 males, 94 females; mean age, 43 yrs) were examined pre-HSCT and 6, 12, and 24 months post-HSCT. Healthy individuals (n = 144; 69 males, 75 females; mean age, 46 yrs) served as the control group. Stimulated saliva flow rates (mL/min) were measured and analyzed statistically, stratifying for hematological diagnoses and conditioning therapy. Hyposalivation (≤ 0.7 mL/min) was found in 40% (p < 0.00001), 53% (p < 0.00001), 31% (p < 0.01), and 26% (n.s.) of the recipients pre-HSCT, and 6, 12, and 24 months post-HSCT, respectively, whereas 16% of the control individuals had hyposalivation. Severe hyposalivation (≤ 0.3 mL/min) was found in 11%, 18%, 4%, and 4% of the recipients pre-HSCT, and 6, 12, and 24 months post-HSCT, respectively. Additionally, conditioning regimen and sex had an impact on saliva flow. In conclusion, hyposalivation was observed to be a common but generally reversible complication among HSCT recipients.

Background Estimates of the future burden of invasive cancer attributable to current modifiable causal exposures can guide cancer prevention. Methods We linked pooled data from seven Australian cohort studies (N = 367,058) to national cancer and death registries, and estimated exposure-cancer and exposure-death associations using adjusted proportional hazards models. We estimated exposure prevalence from contemporary national health surveys and calculated population attributable fractions (PAFs) and 95% confidence intervals, using advanced methods accounting for competing risk of death. Results Current levels of past and current smoking explain 36.1% (95%CI 33.2%-38.9%), body fatness 13.6% (10.9%-16.2%) and alcohol consumption exceeding two drinks/day 2.3% (1.0%-3.6%) of cancers causally related to these exposures, corresponding to 210,000, 81,300 and 14,800 cancers in Australia in the next 10 years, respectively. Ever smoking is the leading modifiable cause of lung (82.1%), bladder (49.8%), oesophageal (42.8%), liver (39.8%), head and neck (35.6%), and pancreatic (21.3%) cancer burden. Body fatness is the leading modifiable cause of corpus uteri (42.5%), gastric cardia (33.6%), renal cell (29.1%), thyroid (20.1%), colorectal (12.6%) and postmenopausal breast (12.6%) cancer burden. The absolute numbers of cancers in the next 10 years attributable to smoking are highest for lung cancer (114,000). The numbers of cancers attributable to body fatness and alcohol are highest for colorectal cancer (23,000 and 9,900, respectively). Conclusions More reliable advanced methods demonstrate large proportions and numbers of cancers are preventable by modifying behaviours. Key messages Ever smoking and body fatness are the leading causes of preventable future burden of causally related cancers in Australia.

Background Several lifestyle factors are associated with an increased risk of colorectal cancer (CRC). Although lifestyle factors co‐occur, in most previous studies these factors have been studied focusing upon a single risk factor or assuming independent effects between risk factors. Aim To examine the pairwise effects and interactions of smoking, alcohol consumption, physical inactivity, and body mass index (BMI) with risk of subsequent colorectal cancer (CRC). Methods and results We used METCA cohort data (pooled data from seven population‐based Finnish health behavior survey studies during years 1972–2015) consisting of 171 063 women and men. Participants' smoking, alcohol consumption, physical inactivity and BMI measures were gathered, and participants were categorized into those exposed and those not exposed. The incidence of CRC was modeled by Poisson regression with main and interaction effects of key lifestyle factors. The cohort members were followed‐up through register linkage to the Finnish Cancer Registry for first primary CRC case until the end of 2015. Follow‐up time was 1715, 690 person years. The highest pairwise CRC risk was among male smokers who had overweight (BMI ≥ 25 kg/m2) (HR 1.75, 95% CI 1.36–2.26) and women who had overweight and consumed alcohol (HR 1.45, 95% CI 1.14–1.85). Overall, among men the association of lifestyle factors and CRC risk was stronger than among women. In men, both having overweight and being a smoker combined with any other adverse lifestyle factor increased CRC risk. Among women, elevated CRC risks were observed for those who were physically inactive and who consumed alcohol or had overweight. No statistically significant interactions were detected between pairs of lifestyle factors. Conclusions This study strengthens the evidence of overweight, smoking, and alcohol consumption as CRC risk factors. Substantial protective benefits in CRC risk can be achieved by preventing smoking, maintaining BMI to <25 kg/m2 and not consuming alcohol.

There is limited evidence for any dietary factor, except alcohol, in breast cancer (BC) risk. Therefore, studies on a whole diet, using diet quality indices, can broaden our insight. We examined associations of the Nordic Diet (mNDI), Mediterranean diet (mMEDI) and Alternative Healthy Eating Index (mAHEI) with postmenopausal BC risk. Five Finnish cohorts were combined including 6374 postmenopausal women with dietary information. In all, 8–9 dietary components were aggregated in each index, higher total score indicating higher adherence to a healthy diet. Cox proportional hazards regression was used to estimate the combined hazard ratio (HR) and 95% confidence interval (CI) for BC risk. During an average 10-year follow-up period, 274 incident postmenopausal BC cases were diagnosed. In multivariable models, the HR for highest vs. lowest quintile of index was 0.67 (95 %CI 0.48–1.01) for mNDI, 0.88 (0.59–1.30) for mMEDI and 0.89 (0.60–1.32) for mAHEI. In this combined dataset, a borderline preventive finding of high adherence to mNDI on postmenopausal BC risk was found. Of the indices, mNDI was more based on the local food culture than the others. Although a healthy diet has beneficially been related to several chronic diseases, the link with the etiology of postmenopausal BC does not seem to be that obvious.