OBJECTIVESWe conducted an epidemiological study of the relationship between lung cancer incidence and smoking, with special reference to the benefits of smoking cessation for reducing lung cancer incidence, to promote a local smoking control program.

METHODSThe study was a retrospective cohort study. The population studied was 16,383 male examinees of lung cancer health examinations in 1995 in Tottori Prefecture, Japan. Smoking status from the questionnaire during the health examination was used as the exposure variable. Endpoint (lung cancer incidence) was obtained from the Tottori population-based cancer registry. A multivariable analysis using the Cox proportional hazard model was adapted for statistical analysis. The average follow-up period was 4.3 years.

RESULTSThe hazard ratio of current smokers for the incidence of lung cancer was 4.9, whereas that of ex-smokers was 2.2. The dose-response relationship between lung cancer incidence and lifetime cigarette consumption (pack year) was determined. The ratio increased among younger subjects (under 65 years old). The hazard ratio of ex-smokers decreased with years just after quitting smoking, and reached the level of never smokers after 10-19 years from smoking cessation.

CONCLUSIONSWe reconfirmed that the magnitude of risk estimates of smoking for lung cancer incidence was similar to those of previous studies, and smoking cessation was effective for reducing lung cancer risk.

We had previously reported a close association between pathological response and the maximum tumor standardized uptake value (SUVmax) measured by 18F-fluorodeoxyglucose positron emission tomography prior to chemotherapy in estrogen receptor (ER)-positive breast cancer. We hypothesized that glucose hypermetabolism by luminal B tumors may result in chemotherapy responsiveness. Using a single-gene expression assay, TargetPrint(R) (Agendia) and a 70-gene expression classifier, MammaPrint(R) (Agendia), we divided 20 patients with ER-positive primary breast cancer into luminal A and luminal B subtypes and compared the tumor SUVmax value between the two groups. A significantly higher SUVmax was measured for luminal B tumors (n=10; mean+/-SD, 7.6+/-5.6) than for luminal A tumors (n=10; mean+/-SD, 2.6+/-1.2; p=0.01). Glucose hypermetabolism could help predict intrinsic subtyping and chemotherapy responsiveness as a supplement to ER, progesterone receptor, HER2, and Ki-67 histochemical scores.
Breast ; Breast Neoplasms ; Estrogens ; Glucose ; Humans ; Phenobarbital ; Positron-Emission Tomography ; Receptors, Progesterone

Canine mammary gland tumors (CMGTs), which are the most common neoplasms in sexually intact female dogs, have been suggested as a model for studying human breast cancer because of several similarities, including relative age of onset, risk factors, incidence, histological and molecular features, biological behavior, metastatic pattern, and responses to therapy. In the present study, we established a new cell line, the SNP cell line, from a CMGT. A tumor formed in each NOD.CB17-Prkdc (scid)/J mouse at the site of subcutaneous SNP cell injection. SNP cells are characterized by proliferation in a tubulopapillary pattern and are vimentin positive. Moreover, we examined miRNA expression in the cultured cells and found that the expression values of miRNA-143 and miRNA-138a showed the greatest increase and decrease, respectively, of all miRNAs observed, indicating that these miRNAs might play a significant role in the malignancy of SNP cells. Overall, the results of this study indicate that SNP cells might serve as a model for future genetic analysis and clinical treatments of human breast tumors.
Age of Onset ; Animals ; Breast Neoplasms ; Cell Line ; Cell Line, Tumor* ; Cells, Cultured ; Dogs ; Female ; Humans ; Incidence ; Mammary Glands, Human* ; Mice ; MicroRNAs* ; Risk Factors ; Vimentin