Gastric cancer is a leading cause of cancer deaths, but analysis of its molecular and clinical characteristics has been complicated by histological and aetiological heterogeneity. Here we describe a comprehensive molecular evaluation of 295 primary gastric adenocarcinomas as part of The Cancer Genome Atlas (TCGA) project. We propose a molecular classification dividing gastric cancer into four subtypes: tumours positive for Epstein–Barr virus, which display recurrent PIK3CA mutations, extreme DNA hypermethylation, and amplification of JAK2, CD274 (also known as PD-L1) and PDCD1LG2 (also knownasPD-L2); microsatellite unstable tumours, which show elevated mutation rates, including mutations of genes encoding targetable oncogenic signalling proteins; genomically stable tumours, which are enriched for the diffuse histological variant and mutations of RHOA or fusions involving RHO-family GTPase-activating proteins; and tumours with chromosomal instability, which show marked aneuploidy and focal amplification of receptor tyrosine kinases. Identification of these subtypes provides a roadmap for patient stratification and trials of targeted therapies.

Objectives: To measure the incidence of treated non‐melanoma skin cancer (NMSC) in Australia in 2002 and investigate trends since 1985 by histological type, sex, age group, latitude and skin type. Design: Face‐to‐face survey between 1 January and 31 December 2002 using stratified sampling of households to identify people treated for skin cancer in the previous 12 months. Self‐reported diagnoses were confirmed with treatment providers. Data from similar surveys conducted in 1985, 1990 and 1995 were used to assess trends. Setting: Whole of Australia (population 19.6 million). Participants: Of 57 215 people interviewed, 4098 said they had been treated for skin cancer in the past year and 3198 gave permission for their diagnoses to be confirmed with their doctor. Results: 817 people were confirmed as having at least one skin cancer treated in the past year. The age‐standardised rate per 100 000 population for NMSC was 1170, for basal cell carcinoma (BCC) 884, and for squamous cell carcinoma (SCC) 387. The estimated number of NMSC cases in Australia for 2002 was 374 000. Cumulative risks to age 70 years of having at least one NMSC were 70% for men and 58% for women. Rates of BCC and SCC have increased since 1985, and the increases greatest for people aged 60 years and older; rates for those younger than 60 years have stabilised. Conclusions: The incidence of treated NMSC in Australia in 2002 was more than five times the incidence of all other cancers combined. Although the overall NMSC rates have risen since 1985, the stabilisation of rates for people younger than 60 years who were exposed to skin cancer prevention programs in their youth highlights the importance of maintaining and strengthening these programs.

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In a primary care setting the combination of dermoscopy and short-term SDDI reduces the excision or referral of benign pigmented lesions by more than half while nearly doubling the sensitivity for the diagnosis of melanoma.

Melanoma mortality in Australia peaked in about 1985 and has now plateaued. On the basis of trends in cohorts it can be expected to fall in coming years.