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Globally, 39% of the world's adult population is overweight or obese and 23% is insufficiently active. These percentages are even larger in high-income countries with 58% overweight/obese and 33% insufficiently active. Fourteen cancer types have been declared by the World Cancer Research Fund to be causally associated with being overweight or obese: oesophageal adenocarcinoma, stomach cardia, colon, rectum, liver, gallbladder, pancreas, breast, endometrium, ovary, advanced/fatal prostate, kidney, thyroid and multiple myeloma. Colon, postmenopausal breast and endometrial cancers have also been judged causally associated with physical inactivity. We aimed to quantify the proportion of cancer cases that would be potentially avoidable in Australia if the prevalence of overweight/obesity and physical inactivity in the population could be reduced. We used the simulation modelling software PREVENT 3.01 to calculate the proportion of avoidable cancers over a 25-year period under different theoretical intervention scenarios that change the prevalence of overweight/obesity and physical inactivity in the population. Between 2013 and 2037, 10–13% of overweight/obesity-related cancers in men and 7–11% in women could be avoided if overweight and obesity were eliminated in the Australian population. If everyone in the population met the Australian physical activity guidelines for cancer prevention (i.e. engaged in at least 300 min of moderate-intensity physical activity per week), an estimated 2–3% of physical inactivity-related cancers could be prevented in men (colon cancer) and 1–2% in women (colon, breast and endometrial cancers). This would translate to the prevention of up to 190,500 overweight/obesity-related cancers and 19,200 inactivity-related cancers over 25 years.

The International Agency for Research on Cancer first concluded that alcohol causes cancer in humans in 1988. The World Cancer Research Fund has declared that alcohol causes cancer of the oral cavity, pharynx, larynx, oesophagus (squamous cell carcinoma), female breast, colon, rectum, stomach and liver. It recommended that alcohol be avoided altogether to prevent cancer. We aimed to quantify the impact of reducing alcohol consumption on future cancer incidence in Australia. We used PREVENT 3.01 simulation modelling software to estimate the proportion of cancers that could potentially be prevented over a 25-year period under two hypothetical intervention scenarios and two latency periods (20 and 30 years). Under a scenario where alcohol consumption abruptly ceases, we estimated up to 4% of alcohol-related cancers could be avoided over a 25-year period (~49,500 cancers, depending on assumed latency). If the maximum consumption of all Australian adults was ≤20 g/day (~two Australian standard drinks), up to 2% of alcohol-related cancers could be avoided (~29,600 cancers). The maximum proportions were higher for men (6% for no alcohol consumption; 5% for ≤20 g/day) than women (3%; 1%). The proportion avoidable was highest for oesophageal squamous cell carcinoma (17% no alcohol consumption; 9% ≤20 g/day), followed by cancers of the oral cavity (12%; 5%) and pharynx (11%; 5%). The cancer sites with the highest numbers of potentially avoidable cases were colon in men (11,500; 9,900) and breast in women (14,400; 4,100). Successful interventions to reduce alcohol intake could lead to significant reductions in cancer incidence.

Background: Information on stage at diagnosis for childhood blood cancers is essential for surveillance but is not available on a population basis in most countries. Our aim was to apply the internationally endorsed Toronto Paediatric Cancer Stage Guidelines to children (<15 years) with acute lymphoblastic leukemia (ALL), acute myeloid leukemia (AML), Hodgkin lymphoma (HL), or non-Hodgkin lymphoma (NHL) and to assess differences in survival by stage at diagnosis. Procedure: Stage was defined by extent of involvement of the central nervous system (CNS) for ALL and AML and using the Ann Arbor and St Jude-Murphy systems for HL and NHL, respectively. The study cohort was drawn from the population-based Australian Childhood Cancer Registry, consisting of children diagnosed with one of these four blood cancers between 2006 and 2014 with follow-up to 2015. Five-year observed survival was estimated from the Kaplan–Meier method. Results: Stage was assigned to 2201 of 2351 eligible patients (94%), ranging from 85% for AML to 95% for ALL, HL, and NHL. Survival following ALL varied from 94% (95% CI = 93%–95%) for CNS1 disease to 89% (95% CI = 79%–94%) for CNS2 (P = 0.07), whereas for AML there was essentially no difference in survival between CNS − (77%) and CNS + disease (78%; P = 0.94). Nearly all children with HL survived for five years. There was a trend (P = 0.04) toward worsening survival with higher stage for NHL. Conclusions: These results provide the first population-wide picture of the distribution and outcomes for childhood blood cancers in Australia by extent of disease at diagnosis and provide a baseline for future comparisons.

Public campaigns encouraging sun protection for skin cancer prevention began in Queensland, Australia, in the early 1980s. We examined recent trends to assess whether earlier evidence of stabilizing melanoma incidence in young people has persisted. Anonymized incidence and mortality data for in situ and invasive melanoma for the 20 years 1995–2014 were obtained from the Queensland Cancer Registry. Time trends were analyzed using JoinPoint regression. Birth cohort patterns were assessed using age–period–cohort models. Melanoma incidence in Queensland remains the highest recorded in the world (age-standardized incidence of invasive melanoma (2010–2014) = 72/100,000/annum). Over the 20-year period, incidence of in situ melanoma increased in all age groups. Incidence of both thin (≤1 mm) and thick (>1 mm) invasive melanoma was either stable or decreased in people under 60, while it increased in those aged 60 and above, particularly in men. Age–period–cohort analysis revealed decreasing age-specific incidence of invasive melanoma under 40 years of age, beginning with the birth cohort born around the mid-1960s, with steepest falls for those born around 1980 and later. Age-specific incidence was stable between 40 and 59 years of age from the 1945 birth cohort onwards. Melanoma mortality over the period was stable or decreased in all groups except in men aged 60 or over. These findings are evidence of real advances in the prevention and early detection of invasive melanoma in this very high-risk population. They make a compelling case for continued public health efforts to reduce the burden of melanoma in susceptible populations.

Background: Cancer stage at diagnosis is crucial for assessing global efforts to increase awareness of childhood cancer and improve outcomes. However, consistent information on childhood cancer stage is absent from population cancer registries worldwide. The Toronto Childhood Cancer Stage Guidelines, compiled through an international consensus process, were designed to provide a standard framework for collection of information on stage at diagnosis of childhood cancers. We aimed to assess the feasibility of implementing the Toronto Guidelines within a national population cancer registry. Methods: We did a population-based registry study using data from the Australian Childhood Cancer Registry and included data from children aged 0–14 years diagnosed between Jan 1, 2006, and Dec 31, 2010 with one of 16 childhood cancers listed in the Toronto Guidelines (acute lymphoblastic leukaemia, acute myeloid leukaemia, Hodgkin's lymphoma, non-Hodgkin lymphoma, neuroblastoma, Wilms' tumour, rhabdomyosarcoma, non-rhabdomyosarcoma soft tissue sarcoma, osteosarcoma, Ewing's sarcoma, retinoblastoma, hepatoblastoma, testicular cancer, ovarian cancer, medulloblastoma, and ependymoma). We extracted data from medical records, and assigned stage according to the Tier 1 criteria (basic) and Tier 2 criteria (more detailed, requiring data from cytology, imaging, and other diagnostic tests, where available) using computer algorithms derived from the Toronto Guidelines. Additionally, expert reviewers independently assigned Tier 2 stage to a random subsample of 160 cases (ten per malignancy type). Feasibility of the guidelines was assessed on the percentage of cases that could be staged, agreement between stage assigned by the algorithms and the expert reviewers, and the mean time (min) taken to collect the required data. Findings: We obtained data for 1412 eligible children. Stage could be assigned according to Tier 2 criteria for 1318 (93%) cases, ranging from 48 (84%) of 57 cases of non

Background: The Distress Thermometer (DT) is widely recommended for screening for distress after cancer. However, the validity of the DT in men with prostate cancer and over differing time points from diagnosis has not been well examined. Method: Receiver operating characteristics analyses were used to evaluate the diagnostic accuracy of the DT compared with three commonly used standardised scales in two prospective and one cross-sectional survey of men with prostate cancer (n = 740, 189 and 463, respectively). Comparison scales included the Impact of Event Scale – Revised (IES-R, Study 1), the Hospital Anxiety and Depression Scale (HADS, Study 2) and the Brief Symptom Inventory-18 (BSI-18, Study 3). Results: Study 1: the DT showed good accuracy against the IES-R at all time points (area under curves (AUCs) ranging from 0.84 to 0.88) and sensitivity was high (>85%). Study 2: the DT performed well against both the anxiety and depression subscales for HADS at baseline (AUC = 0.84 and 0.82, respectively), but sensitivity decreased substantially after 12 months. Study 3: validity was high for the anxiety (AUC = 0.90, sensitivity = 90%) and depression (AUC = 0.85, sensitivity = 74%) subscales of the BSI-18 but was poorer for somatization (AUC = 0.67, sensitivity = 52%). A DT cut-off between ≥3 and ≥6 maximised sensitivity and specificity across analyses. Conclusions: The DT is a valid tool to detect cancer-specific distress, anxiety and depression among prostate cancer patients, particularly close to diagnosis. A cut-off of ≥4 may be optimal soon after diagnosis, and for longer-term assessments, ≥3 was supported.

We report cancer incidence and mortality among Indigenous children in Australia and compare the results with corresponding data for non-Indigenous children. This information is important in understanding the overall burden of cancer in this population, and where disparities exist, to plan what action is required. Age-standardized rates, and indirectly standardized incidence and mortality ratios (SIRs and SMRs) were calculated for the years 1997–2008. There were 224 cancers identified among Indigenous children (99.5 per million per year) and 52 Indigenous children died from cancer during the study period (22.9 per million per year). The SIR for all cancers was 0.64 (95% CI = 0.56–0.73; P < 0.001) while the SMR was 0.81 (95% CI = 0.61–1.07). These results provide a baseline with which to monitor cancer among Indigenous children over time.