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. 2011:5:213.
doi: 10.3332/ecancer.2011.213. Epub 2011 May 24.

Aspirin, salicylates and cancer: report of a meeting at the Royal Society of Medicine, London, 23 November 2010

No authors listed

Aspirin, salicylates and cancer: report of a meeting at the Royal Society of Medicine, London, 23 November 2010

No authors listed. Ecancermedicalscience. 2011.
No abstract available

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Figures

Figure 1
Figure 1
Any use of aspirin or NSAID in cases of colorectal cancer versus age and sex matched controls: 19 case–control studies.
Figure 2
Figure 2
Maximum use of aspirin or NSAID in cases of colorectal cancer versus age- and sex-matched controls: 19 case–control studies.
Figure 3
Figure 3
Colorectal cancer in the pooled analysis. UK-TIA cases with at least 5 years scheduled trial treatment.
Figure 4
Figure 4
Delayed effect of aspirin on risk of colorectal cancer in the UK-TIA Trial and British Doctors Aspirin Trial in compliant patients with scheduled treatment ≥5 years.
Figure 5
Figure 5
Pooled analysis of the effect of low-dose (75–300 mg) aspirin (thick line) versus control (thin line) on subsequent incidence and mortality due to colorectal cancer in TPT, SALT and UK-TIA.
Figure 6
Figure 6
Pooled analysis of the effect of low-dose (75–300 mg) aspirin (thick line) versus control (thin line) on subsequent incidence of proximal colorectal cancer in BDAT, TPT, SALT and UK-TIA.
Figure 7
Figure 7
Pooled analysis of the effect of low-dose (75–300 mg) aspirin (thick line) versus control (thin line) on subsequent incidence of distal colon and rectal cancer in BDAT, TPT, SALT and UK-TIA.
Figure 1
Figure 1
CAPP1 trial: patients randomised to aspirin tended to have smaller ‘biggest polyps’ versus placebo, with a trend to significance in those treated for at least one year.
Figure 2
Figure 2
Post trial divergence of colorectal cancer incidence in the CAPP2 trial, aspirin versus placebo (n = 46).
Figure 3
Figure 3
Lifetable analysis, time to first ‘Lynch Syndrome cancers’ (colorectal and endometrial) in the CAPP2 trial. Hazard ratio 0.62 (95% CI 0.41–0.96), P = 0.03.
Figure 1
Figure 1
Expression of COX-2 by normal gastrointestinal cells, adenoma and colon cancer (adapted from Eberhart et al [1].).
Figure 2
Figure 2
Immunostaining for COX-2 (dark brown areas) in colorectal tumours. Samples A and B are negative for COX-2; samples C and D are positive for COX-2.
Figure 3
Figure 3
Aspirin use after diagnosis and colorectal cancer-related and overall survival [3] (A) Colorectal cancer-related mortality (log rank P = 0.02). (B) Overall mortality (log rank P = 0.03).
Figure 4
Figure 4
Dose of aspirin and risk of adenoma [4].
Figure 5
Figure 5
Dose of aspirin and risk of colorectal cancer in women [6].
Figure 6
Figure 6
Dose of aspirin and risk of colorectal cancer in men.
Figure 7
Figure 7
Relative risk of major gastrointestinal bleeding and dose of aspirin in the Nurses’ Health Study and Health Professionals Follow-up Study cohorts.
Figure 1
Figure 1
United Kingdom 1950–2003: males and females colorectal cancer mortality at ages 35–69.
Figure 2
Figure 2
Study design for evaluating the efficacy of aspirin plus adjunctive therapy in adenoma prevention and targeting therapy.
Figure 1
Figure 1
NSAIDs – oesophageal cancer [6].
Figure 2
Figure 2
NSAIDs – stomach cancer [6].
Figure 3
Figure 3
NSAIDs – lung cancer [6].
Figure 4
Figure 4
NSAIDs – breast cancer [6].
Figure 5
Figure 5
NSAIDs – ovarian cancer [6].
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