Department of Epidemiology, Harvard School of Public Health, 677 Huntington Ave, Boston, MA, 02115, USA, swtoh@hsph.harvard.edu.

OBJECTIVE: To evaluate the effect of antidepressant use on lung cancer risk. METHODS: We conducted a case-control study nested in a cohort of patients 40-84 year-old in 1995-2004, without a prior diagnosis of cancer using The Health Improvement Network (THIN) database in the UK. Cases comprised 4,336 patients with a first diagnosis of primary lung cancer. A sample of 10,000 controls was frequency-matched to the cases for age, sex, and the calendar year of diagnosis. The index date for exposure definition was one year before the diagnosis for cases and one year before a random date for controls. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using conditional logistic regression models adjusted for potential confounders. RESULTS: Selective serotonin reuptake inhibitor (SSRI) use during the year preceding the index date with treatment duration of at least one year had an OR of 0.59 (95% CI 0.41, 0.86). The corresponding OR was 1.23 (95% CI 0.96, 1.58) for tricyclic antidepressants (TCAs). CONCLUSIONS: SSRI use did not increase the lung cancer risk and might be associated with a reduced risk. However, residual confounding might explain the apparent protective effect found for SSRI use, as well as the marginally elevated risk observed among TCA users.

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Cytosolic serine hydroxymethyltransferase (cSHMT) is key to intersection of folate-metabolic pathway, participating in the pyrimidine synthesis for DNA repair. Based on the hypothesis that variants of the cSHMT C1420T together with methionine synthase (MS A2756G) and 5,10-methylenetetrahydrofolate reductase (MTHFR C677T and A1298C) are associated with breast cancer, we performed a multigenic case-control study of the effects to breast cancer risk of four polymorphisms of folate-metabloizing genes against duration of estrogen exposure. Support of our hypothesis came from the following observations: (i) Allelic frequency of cSHMT C1420T was higher in the controls than in the cases, manifesting a 0.56-fold risk reduction in breast cancer (95%CI = 0.39-0.80); and this association was more significant in those women are susceptible to time of estrogen exposure. (ii) A joint effect of the cSHMT and MS polymorphisms significantly reduced susceptibility to breast cancer (aOR = 0.55; 95%CI = 0.34-0.88). (iii) There was a trend toward a reduced risk of breast cancer in women carrying a greater number of putative low-risk genotypes (P ( trend )= 0.048). (iv) This synergistic effects on risk reduction was significantly interacted with length of estrogen exposure, exhibiting a longer time of estrogen exposure (>/=30 years), menarche-to-FFTP interval (>11 years), age at the first full-term pregnancy (</=25 years), and body mass index (</=24). In conclusion, our study provides support to account for the preferential role of cSHMT polymorphism to lower risk of female breast cancer, and such reduced risk would be more significant in carriers with the polymorphisms of MS and MTHFR genes.

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New Cancer Research
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Hepatocellular carcinoma (HCC), the most common liver cancer, occurs mainly in men. Similar gender disparity is seen in mice given a chemical carcinogen, diethylnitrosamine (DEN). DEN administration caused greater increases in serum interleukin-6 (IL-6) concentration in males than it did in females. Furthermore, ablation of IL-6 abolished the gender differences in hepatocarcinogenesis in mice. DEN exposure promoted production of IL-6 in Kupffer cells (KCs) in a manner dependent on the Toll-like receptor adaptor protein MyD88, ablation of which also protected male mice from DEN-induced hepatocarcinogenesis. Estrogen inhibited secretion of IL-6 from KCs exposed to necrotic hepatocytes and reduced circulating concentrations of IL-6 in DEN-treated male mice. We propose that estrogen-mediated inhibition of IL-6 production by KCs reduces liver cancer risk in females, and these findings may be used to prevent HCC in males.

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