Cancers in Australia in 2010 attributable to the consumption of alcohol

Objective: To estimate the proportion and numbers of cancers occurring in Australia in 2010 that are attributable to alcohol consumption. Methods: We estimated the population attributable fraction (PAF) of cancers causally associated with alcohol consumption using standard formulae incorporating prevalence of alcohol consumption and relative risks associated with consumption and cancer. We also estimated the proportion change in cancer incidence (potential impact fraction [PIF]) that might have occurred under the hypothetical scenario that an intervention reduced alcohol consumption, so that no‐one drank >2 drinks/day. Results: An estimated 3,208 cancers (2.8% of all cancers) occurring in Australian adults in 2010 could be attributed to alcohol consumption. The greatest numbers were for cancers of the colon (868) and female breast cancer (830). The highest PAFs were for squamous cell carcinomas of the oral cavity/pharynx (31%) and oesophagus (25%). The incidence of alcohol‐associated cancer types could have been reduced by 1,442 cases (4.3%) – from 33,537 to 32,083 – if no Australian adult consumed >2 drinks/day. Conclusions: More than 3,000 cancers were attributable to alcohol consumption and thus were potentially preventable. Implications: Strategies that limit alcohol consumption to guideline levels could prevent a large number of cancers in Australian adults.     

Cancers in Australia in 2010 attributable to insufficient physical activity

Objectives: To estimate the proportion and numbers of cancers occurring in Australia in 2010 attributable to insufficient levels of physical activity. Methods: We estimated the population attributable fraction (PAF) of cancers causally associated with insufficient physical activity (colon, post‐menopausal breast and endometrium) using standard formulae incorporating prevalence of insufficient physical activity (<60 minutes at least 5 days/week), relative risks associated with physical activity and cancer incidence. We also estimated the proportion change in cancer incidence (potential impact fraction [PIF]) that may have occurred assuming that everyone with insufficient activity levels increased their exercise by 30 minutes/week. Results: An estimated 1,814 cases of colon, post‐menopausal breast and endometrial cancer were attributable to insufficient levels of physical activity: 707 (6.5%) colon; 971 (7.8%) post‐menopausal breast; and 136 (6.0%) endometrial cancers. If those exercising below the recommended level had increased their activity level by 30 minutes/week, we estimate 314 fewer cancers (17% of those attributable to insufficient physical activity) would have occurred in 2010. Conclusions: More than 1,500 cancers were attributable to insufficient levels of physical activity in the Australian population. Implications: Increasing the proportion of Australians who exercise could reduce the incidence of several common cancers.     

Cancers in Australia in 2010 attributable to and prevented by the use of menopausal hormone therapy

Objectives: To estimate the proportion and number of cancers occurring in Australia in 2010 attributable to menopausal hormone therapy (MHT) use. Methods: We estimated the population attributable fraction for cancers causally associated with MHT (breast, endometrium, ovary), and the proportion of colorectal cancers prevented by MHT. We used standard formulae incorporating Australian prevalence data, relative risks of cancer associated with MHT and cancer incidence. We also estimated potential change in cancer incidence under two hypothetical scenarios whereby 25% fewer Australian women used MHT, or women exclusively used oestrogen‐only MHT. Results: An estimated 539 cancers in Australia in 2010 were attributable to MHT: 453 breast, 67 endometrial and 19 ovarian cancers equating to 3.4%, 3.1% and 1.6% of each cancer type, respectively. In contrast, MHT may have prevented 52 colorectal cancers. If 25% fewer women used MHT, then 141 cancers may have been avoided. If women exclusively used oestrogen‐only MHT then 240 cancers may have been avoided. Conclusions: MHT use caused more than 500 cancers in Australian women in 2010 and prevented ～50 colorectal cancers. Implications: MHT use continues to cause an excess of cancers. The risks, benefits, regimen and treatment duration should be carefully considered for each woman before MHT is commenced.     

Cancers in Australia in 2010 attributable to inadequate consumption of fruit,non‐starchy vegetables and dietary fibre

Objectives: To estimate the number and proportion of cancers occurring in Australia in 2010 attributable to consumption deficits in fruit, non‐starchy vegetables and dietary fibre. Methods: We estimated the population attributable fraction (PAF) for cancers causally associated with inadequate intake of fruit and non‐starchy vegetables (oral cavity, pharynx, oesophageal squamous cell carcinoma, stomach, larynx); inadequate intake of fruit (lung); and insufficient intake of fibre (colorectum). We used standard formulae incorporating prevalence of exposure (1995 National Nutrition Survey) and relative risks from independent studies. Results: Overall, 1,555 (1.4% of all) and 311 (0.3% of all) cancers were attributable to inadequate intakes of fruit and non‐starchy vegetables, respectively. A further 2,609 colorectal cancers (18% of colorectal) were attributable to insufficient fibre intake. If Australians increased their fibre intake by eating the recommended daily intakes of fruit and vegetables, an estimated 1,293 (8.8%) colorectal cancers could be prevented. Conclusions: One in six colorectal cancer cases was attributable to inadequate intake of dietary fibre and about 1,800 cancers at other sites were attributable to insufficient fruit and non‐starchy vegetable consumption. Implications: Increasing the proportion of Australians who consume the recommended intake of fruit, vegetables and fibre could prevent up to 4% of all cancers.     

Cancers in Australia in 2010 attributable to total breastfeeding durations of 12 months or less by parous women

Objectives: To estimate the proportion and number of cancers occurring in Australia in 2010 attributable to parous women having breastfed for total durations of ≤12 months. Methods: We estimated the population attributable fraction (PAF) of breast cancers (the only cancer site with convincing evidence of causal association) associated with women breastfeeding for ≤12 months in total, using standard formulae incorporating breastfeeding prevalence data, relative risks associated with breastfeeding and cancer incidence. We also estimated the proportion change in disease incidence (potential impact fraction [PIF]) that might have occurred under two hypothetical scenarios of women breastfeeding for longer durations. Results: An estimated 235 (1.7%) breast cancer cases that occurred in Australian in 2010 could be attributed to women breastfeeding for total durations of ≤12 months. Assuming a hypothetical increase in breastfeeding, we estimated that the number of breast cancers prevented would range from 36 to 51 (prevented fraction = 0.3% to 0.4%). Conclusions: More than 200 breast cancers were attributable to women breastfeeding for total durations of ≤12 months. Implications: Policies to increase breastfeeding duration may help prevent breast cancers in the future.     

Cancers in Australia in 2010 attributable to overweight and obesity

Objectives: To estimate the proportion and number of cancers occurring in Australia in 2010 attributable to overweight/obesity. Methods: We estimated the population attributable fraction (PAF) and number of cancers causally associated with overweight/obesity. We used standard formulae incorporating Australian prevalence data for body mass index (BMI), relative risks associated with BMI and cancer. We also estimated the proportion change in cancer incidence (potential impact fraction [PIF]) that may have occurred assuming that the prevalence of overweight/obesity had remained at 1990 levels. Results: An estimated 3,917 cancer cases (3.4% of all cancers) diagnosed in 2010 were attributable to overweight/obesity, including 1,101 colon cancers, 971 female post‐menopausal breast cancers and 595 endometrial cancers (PAFs of 10%, 8% and 26%, respectively). Highest PAFs were observed for oesophageal adenocarcinoma (31%), endometrial cancer (26%) and kidney cancer (19%). If the prevalence of overweight/obesity in Australia had remained at levels prevailing in 1990, we estimate there would have been 820 fewer cancers diagnosed in 2010 (PIF 2%). Conclusions: Overweight/obesity causes a substantial number of cancers in Australia. Implications: Public health strategies to reduce the prevalence of overweight and obesity will reduce the incidence of cancer, particularly of the colon, breast and endometrium.     

Cancers in Australia in 2010 attributable to modifiable factors: introduction and overview

Objective: To describe the approach underpinning a national project to estimate the numbers and proportions of cancers occurring in Australia in 2010 that are attributable to modifiable causal factors. Methods: We estimated the population attributable fraction (PAF) (or prevented fraction) of cancers associated with exposure to causal (or preventive) factors using standard formulae. Where possible, we also estimated the potential impact on cancer incidence resulting from changes in prevalence of exposure. Analyses were restricted to factors declared causal by international agencies: tobacco smoke; alcohol; solar radiation; infectious agents; obesity; insufficient physical activity; insufficient intakes of fruits, vegetables and fibre; red and processed meat; menopausal hormone therapy (MHT); oral contraceptive pill (OCP); and insufficient breast feeding. Separately, we estimated numbers of cancers prevented by: aspirin; sunscreen; MHT; and OCP use. We discuss assumptions pertaining to latent periods between exposure and cancer onset, choices of prevalence data and risk estimates, and approaches to sensitivity analyses. Results: Numbers and population attributable fractions of cancer are presented in accompanying papers. Conclusions: This is the first systematic assessment of population attributable fractions of cancer in Australia.     

Processed Meat and Colorectal Cancer Risk: A Pooled Analysis of Three Italian Case-Control Studies

To add evidence to the limited data available from southern Europe, we assessed the association between processed meat consumption and colorectal cancer risk. We analyzed data from three case-control studies conducted between 1985 and 2010 in various Italian areas, including a total of 3745 incident cases and 6804 hospital-based controls. We calculated odds ratios (ORs) and 95% confidence intervals (CIs) by unconditional multiple logistic regression models. The median consumption of processed meat was around 20 g/day both in cases and controls. The OR of colorectal cancer was 1.02 (95% CI 0.99–1.04) for an increase of 10 g/day of processed meat. The association was statistically significant for colon cancer (OR 1.03, 95% CI 1.00–1.06), particularly for proximal colon cancer (OR 1.09, 95% CI 1.04–1.14), while there was no relation with rectal cancer (OR 0.99, 95% CI 0.95–1.03). The OR of proximal colon cancer was 1.38 (95% CI 1.08–1.75) for the highest sex-specific tertile of consumption (>25 g/day for men, >21.5 for women) compared with the lowest (<15 g/day), whereas no significant ORs were found for other anatomical subsites. Our findings indicate that there is no association with colorectal cancer overall, in the presence, however, of a positive association with proximal colon cancer.     

Red meat intake may increase the risk of colon cancer in Japanese, a population with relatively low red meat consumption

Asian populations have changed from traditional to Westernized diets, with increased red meat intake. They are suggested to be particularly susceptible to the adverse effects of red meat on the development of colorectal cancers, however, few prospective studies of this putative link have been conducted. We examined associations between the consumption of red and processed meat and the risk of subsite-specific colorectal cancer by gender in a large Japanese cohort. During 1995-1998, a validated food frequency questionnaire was administered to 80,658 men and women aged 45-74 years. During 758,116 person-years of follow-up until the end of 2006, 1,145 cases of colorectal cancer were identified. Higher consumption of red meat was significantly associated with a higher risk of colon cancer among women [multivariate hazard ratios (95%CIs) for the highest versus lowest quintiles (HR): 1.48 (1.01, 2.17; trend p=0.03)], as was higher consumption of total meat among men [HR=1.44 (1.06, 1.98; trend p=0.07)]. By site, these positive associations were found for the risk of proximal colon cancer among women and for distal colon cancer among men. No association was found between the consumption of processed meat and risk of either colon or rectal cancer. In conclusion, red meat intake may modestly increase the risk of colon cancer in middle-aged Japanese, although the highest quintile of red meat consumption could be considered moderate by Western standards.     

Cancers prevented in Australia in 2010 through the consumption of aspirin

Objectives: To estimate the proportion and number of cancers in Australia in 2010 that may have been prevented from occurring due to daily use of aspirin in the population. Methods: We calculated the Prevented Fraction (PF) of colorectal and oesophageal cancers using standard formulae. The PF is the proportion of the hypothetical total load of cancer in the population that was prevented by exposure to aspirin. The formula incorporates estimates of the prevalence of aspirin use in Australian adult populations, the relative risks associated with aspirin use and cancer incidence. Results: An estimated 335 colorectal cancers, 22 oesophageal adenocarcinomas and 29 oesophageal squamous cell carcinomas (SCC) were potentially prevented due to daily aspirin use. These figures equate to 2.2%, 3.1% and 5.4% of all colorectal cancers, oesophageal adenocarcinomas and oesophageal SCCs, respectively, that would otherwise have occurred but were potentially avoided due to the daily use of aspirin pertaining in the Australian population. Conclusions: At current levels of consumption, a small but measurable reduction in cancer incidence can be attributed to daily aspirin use. Implications: Assuming the benefits outweigh the harms of known gastrointestinal toxicity and other hazards, aspirin use may be considered for some people to prevent the development of particular gastrointestinal cancers.     

Cancers in Australia in 2010 attributable to and prevented by the use of combined oral contraceptives

Objectives: To estimate the proportion and number of cancers occurring in Australia in 2010 attributable to combined oral contraceptive pill (OCP) use. Methods: We estimated the population attributable fraction (PAF) for cancers causally associated with combined OCP use (breast, cervix), and the proportion of endometrial and ovarian cancers prevented (prevented fraction [PF]). We used standard formulae incorporating prevalence of combined OCP use in the Australian population, relative risks of cancer associated with this exposure and cancer incidence. Results: An estimated 105 breast and 52 cervical cancers (0.7% and 6.4% of each cancer, respectively) in Australia in 2010 were attributable to current use of combined OCP. Past combined OCP use was estimated to have prevented 1,032 endometrial and 308 ovarian cancers in 2010, reducing the number of cancers that would otherwise have occurred by 31% and 19%, respectively. Conclusions: A small proportion of breast and cervical cancers is attributable to combined OCP use; OCP use is likely to have prevented larger numbers of endometrial and ovarian cancers. Implications: Women seeking contraceptive advice should be told of potential adverse effects, but should also be told that – along with reproductive health benefits – combined OCP use can reduce long‐term risks of ovarian and endometrial cancers.     

Cancers in Australia in 2010 attributable to tobacco smoke

Objectives: To estimate the population attributable fraction (PAF) and numbers of cancers occurring in Australia in 2010 attributable to tobacco smoking, both personal and by a partner. Methods: We used a modified Peto‐Lopez approach to calculate the difference between the number of lung cancer cases observed and the number expected assuming the entire population developed lung cancer at the same rate as never smokers. For cancers other than lung, we applied the standard PAF formula using relative risks from a large cohort and derived notional smoking prevalence. To estimate the PAF for partners' smoking, we used the standard formula incorporating the proportion of non‐smoking Australians living with an ever‐smoking partner and relative risks associated with partner smoking. Results: An estimated 15,525 (13%) cancers in Australia in 2010 were attributable to tobacco smoke, including 8,324 (81%) lung, 1,973 (59%) oral cavity and pharynx, 855 (60%) oesophagus and 951 (6%) colorectal cancers. Of these, 136 lung cancers in non‐smokers were attributable to partner tobacco smoke. Conclusions: More than one in eight cancers in Australia is attributable to tobacco smoking and would be avoided if nobody smoked. Implications: Strategies to reduce the prevalence of smoking remain a high priority for cancer control.     

Health and environmental implications of the CSIRO Total Wellbeing Diet

The Commonwealth Scientific and Industrial Research Organisation Total Wellbeing diet allows high intakes of meat and fish with emphasis on red meat. A person following this diet could be eating 200 g of red meat per day or more. The evidence for the link between red and processed meat and colorectal cancer has been strengthened by recent studies. The production of red meat consumes large amounts of water, and generates high levels of greenhouse gas emissions. The Australian Guide to Healthy Eating recommends three to four serves (each 65–100 g) of red meat per week. Compared with the lower end of this range (three servings (70 g) of red meat per week), consumption of 200 g red meat per day would use an extra 15 000 L of water in a week, and generate an extra 4.3 tonnes of greenhouse gas in a year. Thus, there are compelling health and environmental reasons for avoiding this diet in its usual form.     

Cancers in Australia in 2010 attributable to infectious agents

Objectives: To estimate the proportion and numbers of cancers in Australia in 2010 attributable to infectious agents. Methods: The population attributable fraction (PAF) and number of cancers caused by hepatitis B and C viruses (HBV, HCV), Helicobacter pylori and human immunodeficiency virus (HIV) were calculated using standard formulae incorporating prevalence of infection in the Australian population, the relative risks associated with that infection and cancer incidence. For cancers with very strong associations to the infectious agent (Epstein‐Barr virus [EBV], human papillomavirus [HPV] and HIV/Kaposi's sarcoma herpes virus [KSHV]), calculations were based on viral prevalence in the tumour. Results: An estimated 3,421 cancers (2.9% of all cancers) in Australia in 2010 were attributable to infections. Infectious agents causing the largest numbers of cancers were HPV (n=1,706), H. pylori (n=793) and HBV/HCV (n=518). Cancer sites with the greatest number of cancers caused by infections were cervix (n=818), stomach (n=694) and liver (n=483). Cancers with highest proportions attributable to infectious agents were Kaposi's sarcoma (100%), cervix (100%), nasopharynx (87%), anus (84%) and vagina (70%). Conclusions: Infectious agents cause more than 3,000 cancers annually in Australia. Implications: Opportunities for cancer prevention through infection control are considerable, even in a ‘first world’ nation like Australia.     

Review of the association between meat consumption and risk of colorectal cancer

The incidence of colorectal cancer (CRC) is rapidly increasing in developing countries, especially among populations that are adopting Western-style diets. Several, but not all, epidemiological and experimental studies suggest that a high intake of meat, especially red and processed meat, is associated with increased CRC risk. Potential reasons for the association between high red and processed meat intake and CRC risk include the content of the meat (e.g. protein, heme) and compounds generated by the cooking process (e.g. N-nitroso compounds, heterocyclic amines). These factors can affect the large intestine mucosa with genotoxicity and metabolic disturbances. Increased bacterial fermentation (putrefaction) of undigested protein and production of bacterial metabolites derived from amino acids may affect colon epithelial homeostasis and renewal. This correlates with the fact that most colonic cancers are detected in the distal colon and rectum where protein fermentation actively occurs. However, there are still large controversies on the relationship between red meat consumption and CRC risk. Therefore, the purpose of this review is to enhance the current understanding on the association between high red and processed meat intakes with CRC risk. A principal focus of this review will be to discuss the meat-related components, such as proteins in the meat, heme, N-nitroso compounds, and heterocyclic amines, and the effects they have upon the large intestine mucosa and the intestinal gut microbiota.     

Cancers in Australia in 2010 attributable to modifiable factors: summary and conclusions

Objective: To estimate the numbers and proportions of cancers occurring in Australia in 2010 attributable to modifiable causal factors. Methods: We estimated the population attributable fraction (PAF) of cancers associated with exposure to 13 causal factors using standard formulae incorporating exposure prevalence and relative risk data. We also calculated the potential impact of changing exposure to some factors. Results: A total of 32% of all cancers diagnosed in Australia in 2010 (excluding keratinocyte cancers) were attributable to the 13 factors assessed (men 33%; women 31%). Leading factors were tobacco smoke (PAF all cancers: 13.4%), solar radiation (6.2%), inadequate diet (6.1%) and overweight/obesity (3.4%). Factors conferring highest PAFs differed by sex: highest PAFs for men were tobacco smoke (15.8%), solar radiation (7.1%) and alcohol (3.0%); while highest PAFs for women were tobacco smoke (10.1%), solar radiation (5.0%) and overweight/obesity (4.5%). Sites with the highest counts of potentially preventable cancers were lung (8,569), colorectal (7,404), melanoma of the skin (7,220) and breast (3,233). Conclusions: At least one in three cancers in Australia is attributable to exposure to known modifiable factors. Implications: Up to 37,000 cancers could be prevented in Australia each year if the population avoided exposure to 13 common factors known or strongly suspected to cause cancer.     

Associations of red and processed meat intake with major molecular pathological features of colorectal cancer

Red and processed meat is an established risk factor for colorectal cancer (CRC). However, exact mechanisms to explain the associations remain unclear. Few studies have investigated the association with CRC by molecular tumor features, which could provide relevant information on associated molecular pathways. In this population-based case–control study from Germany (DACHS), 2449 cases and 2479 controls provided information on risk factors of CRC and completed a food frequency questionnaire. Multivariable logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CI) for the associations between meat intake and risk of CRC by molecular pathologic features and specific subtypes. Red and processed meat intake was associated with increased risk of colorectal (>1 time/day vs ≤1 time/week OR 1.66, 95% CI 1.34–2.07), colon and rectal cancer. Among the single molecular tumor features investigated, the results were similar for associations of red and processed meat with CRC risk by microsatellite instability, CpG island methylator phenotype, BRAF, oestrogen receptor-β and p53 status. Red and processed meat intake was associated less strongly with risk of KRAS-mutated CRC (OR >1 time/day vs ≤1 time/week: 1.49, 95% CI 1.09–2.03) than with risk of KRAS-wildtype CRC (OR 1.82, 95% CI 1.42–2.34; p _{heterogeneity} 0.04). These results support an association between red and processed meat and CRC risk similar for subsites of CRC and most of the investigated major molecular pathological features. Potential differences were observed in more specific subtype analyses. Further large studies are needed to confirm these results and to help further elucidate potential underlying mechanisms.     

Foodstuffs and colorectal cancer risk: a review

BACKGROUND AND AIMS: To assess the relationships between food intake and colorectal cancer risk. METHODS: Systematic review of available prospective studies on dietary intake and colorectal cancer. RESULTS: Twelve out of 15 studies found no significant relationship between vegetable intake and colorectal cancer risk; also, 11 out of 14 studies found no relationship with fruit consumption. Conversely, the combined consumption of vegetables and fruit reduced colorectal cancer risk in three out of six studies, although the relationship was somewhat inconsistent between genders and anatomical localizations. Most studies found no relationship between cancer risk and red meat (15 in 20) or processed meat (seven out of 11) consumption; still, most of the reported relative risks were above unity, suggesting that high consumption of red or processed meat might increase colorectal cancer risk. The consumption of white meat, fish/seafood, dairy products, coffee or tea was mostly unrelated to colorectal cancer risk, although the consumption of smoked or salted fish actually increased risk. CONCLUSIONS: The relationships between dietary intake and colorectal cancer risk might be less important than previously reported. The combined consumption of vegetables and fruit might be protective, whereas excessive consumption of meat or smoked/salted/processed food appears to be deleterious.     

Cancer incidence and survival for indigenous Australians in the Northern Territory

OBJECTIVE: To compare cancer incidence and survival for the Northern Territory (NT) Indigenous population with that of other Australians, and to assess NT Indigenous incidence time trends. METHODS: Cancer registry data were used to calculate cancer incidence rate ratios (NT Indigenous to total Australian), the average annual change in NT Indigenous cancer incidence and the relative risk of cancer death after diagnosis of cancer (NT Indigenous to combined Western Australian and Tasmanian cases) for 1991-2001. RESULTS: For NT Indigenous people, incidence rates were high for cancers of the liver, gallbladder, cervix, vulva and thyroid and, in younger people only, for cancers of the oropharynx, oesophagus, pancreas and lung, but low for cancers of the colon and rectum, breast, ovary, prostate, bladder, kidney, melanoma and lymphoma. Incidence rate ratios ranged from 0.1 for melanoma to 7.4 for liver cancer. Incidence increased for breast and pancreatic cancers. Survival was low for almost all specific cancers examined, and for all cancers combined (relative risk of death 1.9, 95% CI 1.7-2.1). CONCLUSIONS: Compared with other Australians, NT Indigenous people have higher, and increasing, incidence for some cancers (particularly smoking-related cancers) and lower survival for most. Implications: Cancer has a greater impact on NT Indigenous people than other Australians. Well-established cancer risk factors should be more effectively tackled in Indigenous people and known effective screening programs more effectively implemented. Research is urgently required into the reasons why survival from cancer in NT Indigenous people is so much lower than in other Australians.     

Estimating cancer incidence in Indigenous Australians

Objective: To assess data quality of cancer registrations for Indigenous Australians and produce reliable national Indigenous cancer incidence statistics. Methods: Completeness of Indigenous identification was assessed for the eight Australian cancer registries using an innovative indirect assessment method based on registry‐specific registration rates for smoking‐related cancers. National age‐standardised incidence rates and rate ratios (Indigenous:non‐Indigenous) were calculated for all cancers combined and 26 individual cancer sites. Multivariate regression analysis was used to investigate trends in Indigenous cancer incidence by time or remoteness of residence, and whether the incidence rate ratio (Indigenous:non‐Indigenous) was different in younger than older age‐groups. Results: Four registries covering 84% of the Indigenous population had sufficiently complete Indigenous identification to be included in analysis. Compared to other Australians, Indigenous Australians had much higher incidence of lung and other smoking‐related cancers, cervix, uterus and liver cancer, but much lower incidence of breast, prostate, testis, colorectal and brain cancer, melanoma of skin, lymphoma and leukaemia. Incidence was higher in remote areas for some cancers (including several smoking‐related cancers) but lower for others. The incidence rate ratios (IRRs) for smoking‐related cancers were higher in younger than older people. Conclusions: Indigenous Australians have a different pattern of incidence of specific cancers than other Australians and large geographical variations for several cancers. Implications: All cancer registries need to further improve Indigenous identification, but national Indigenous cancer incidence statistics can, and should, be regularly reported. Tobacco control is a critical cancer‐control issue for Indigenous Australians.