Objectives: To describe the range and frequency of reportage of tobacco‐related disease on Australian television news. Methods: Content analysis of all news items mentioning smoking‐related disease broadcast on five free‐to‐air Sydney television channels 2 May 2005 to 31 December 2007. Results: Three in four tobacco‐related disease news reports focus on lung cancer. Other cancers and smoking attributable diseases attract modest coverage. Conclusion: Television news coverage may contribute to public misconceptions regarding the associated health risks of smoking, limiting understanding about the many risks involved. Tobacco control advocates should seek to increase the newsworthiness of diseases in addition to lung cancer. Implications: While the Australian public is generally aware of the connection between lung cancer and tobacco, considerable misconception exists as to the broad range of tobacco‐related mortality and disease. Given television's role as a key source of public information on health issues in Australia, such coverage can limit understanding about the many attributable risks involved. Tobacco control advocates need to find ways to improve the newsworthiness of tobacco related illness.

Background: The genetic alterations associated with survival in patients with diffuse large B cell lymphomas (DLBCL) treated with combined rituximab-CHOP (R-CHOP) chemo-immunotherapy are not well understood. Methods: 92 patients with DLBCL treated with R-CHOP who had a biopsy available at the time of diagnosis were included in the study. 31 patients were classified as treatment failures defined as progression < 6 months of completing R-CHOP and 61 patients were classified as treatment successes defined as a maintained remission >2 years after diagnosis. We used genome-wide BAC array comparative genomic hybridization (aCGH) to determine the genomic copy number imbalances. The presence of genetic gains and losses were determined using the intersection between visual annotations and a Hidden Markov model algorithm. DLBCL cell of origin (COO) subtype distinctions (GCB vs ABC) were determined using a Bayesian predictor model on gene expression derived from custom Affymetrix arrays (Dave, N Engl J Med, 2006;354:2431). A permutation test was used to identify genetic regions that were significantly different between treatment failures and treatment successes. Functional pathway analysis was performed using Ingenuity software. A novel model based clustering algorithm was applied to the normalized data to determine if any association with outcome correlated with the observed genetic alterations. Results: Lymphoma progressed in 31/92 (34%) patients < 6 months after R-CHOP (median follow-up = 4 y). All 92 patients had successful aCGH and 81 had COO available for this analysis. The International Prognostic Index (IPI) and COO were predictive of outcome (p=0.04, p=0.02, respectively). 451 regions containing 338 genes were associated with treatment failure with a p-value of <10−6. Gains in 9q33.3 were found in 13 patients (14%) and were significantly associated with treatment failure p<10−8. This region contains genes such as HSPA5, a negative regulator of apoptosis and PPP6C, a positive regulator of the cell cycle by targeting IKBe thereby removing inhibition of the NFkB pathway. Deletions in 17p12 were detected in 24 (26%) and were the most statistically significantly associated with treatment failure p<10−9. This region contains tumor necrosis factor (TNF) receptor superfamily member (TNFRSF13B or TACI) which, when deleted or mutated, has been previously shown to lead to activation of the noncanonical NFkB pathway and B cell proliferation. 21 of these 24 patients also had deletion of 17p13 at the TP53 locus (p<10−6). Neither 9p33.3 nor 17p12 deletion was associated with COO distinctions. Using Ingenuity, pathways involving apoptosis and cellular proliferation, specifically those involving P53, MYC and HSPA5 genes, were over-represented in treatment failures (p=2.04 × 10−4). Unsupervised clustering of the aCGH data demonstrated that 60% of cases could be stratified into 4 genetic sub-groups based on the presence of 1q+, 6q−, +7 and the concurrent presence of +3 and +18. Supervised analysis demonstrated that the +3/+18 group and the 6q− group were associated with ABC subtype of DLBCL whereas the +7 and 1q+ groups were associated with the GCB subtype. However, these genetic groups did not correlate with treatment outcome. Conclusions: Some genetic alterations cluster together and can distinguish COO subtypes of DLBCL. Gains on 9q33.3 and deletions of 17p12 are common alterations detected by high resolution aCGH in DLBCL. Most importantly, these alterations involve genes known to be critical in B cell proliferation and apoptosis and alterations at these sites are strongly associated with treatment failure (p values <10−8) in patients treated with R-CHOP.

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