Purpose Occupational exposure to pesticides is thought to be associated with lung cancer, but studies have yielded conflicting results. We performed a propensity score (PS) based analyses to evaluate the relationship between occupational exposure to pesticides and lung cancer risk in the Korea National Cancer Center community-based cohort study (KNCCCS).
Materials and Methods During the follow-up period, 123 incidental lung cancer cases were identified, of the 7,471 subjects in the final statistical analysis. Information about occupational exposure to pesticides and other factors was collected at enrollment (2003-2010). Cox proportional hazards regression analyses were conducted. Four PS-based approaches (i.e., matching, stratification, inverse probability-of-treatment weighting, and the use of the PS as a covariate) were adopted, and the results were compared. PS was obtained from the logistic regression model. Absolute standardized differences according to occupational exposure to pesticides were provided to evaluate the balance in baseline characteristics.
Results In the Cox proportional hazards regression model, the hazard ratio (HR) for lung cancer according to occupational exposure to pesticides was 1.82 (95% confidence interval [CI], 1.11 to 2.98). With all the propensity score matching (PSM) methods, the HRs for lung cancer based on exposure to pesticides ranged from 1.65 (95% CI, 1.04 to 2.64) (continuous term with PSM) to 2.84 (95% CI, 1.81 to 4.46) (stratification by 5 strata of the PS). The results varied slightly based on the method used, but the direction and statistical significance remained the same.
Conclusion Our results strengthen the evidence for an association between occupational exposure to pesticides and the risk of lung cancer.
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Purpose
Caveolin-1 (CAV-1) expression is more associated with basal-like cancers than estrogen receptor- or ErbB-2–expressing breast cancers. However, the biological relevance of different levels of CAV-1 expression according to subtype in the epithelial compartment of breast cancer remains unclear.
Materials and Methods
We investigated whether CAV-1 functions as a tumor suppressor and/or modulator of the cytotoxic activity of docetaxel (DTX) in subtypes of breast cancer using in vitro and xenograft models.
Results
The levels of CAV-1 expression were closely associated with DTX sensitivity in triple-negative breast cancer cells. In addition, CAV-1 significantly inhibited cell proliferation and modulated DTX-induced apoptosis through cell cycle arrest in the G2/M phase. The mechanisms underlying DTX-induced apoptosis differed in breast cancers according to the levels of CAV- 1 expression. DTX robustly enhanced Bcl-2 inactivation by CAV-1 in MDA-MB-231 cells, while p53-mediated cell cycle arrest by DTX was more pronounced in CAV-1–low but p53-functional MCF-7 cells. In parallel with the data from breast cancer cell lines, CAV-1–transfected MCF-7 cells showed higher efficacy of DTX treatment in a xenograft model.
Conclusion
We clearly demonstrated cooperative effects between CAV-1 and DTX in mediating apoptosis, suggesting that the levels of CAV-1 expression might be an important indicator for DTX use in breast cancer.
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PURPOSE TGF-beta-1 is actually a major growth inhibitor for most cell types. We assumed that the loss of TGF-beta-1 would be occurred during carcinogenesis of the lung. Also, the mutation and expression of p53 have been known to be major moleclar change of non-small cell carcinoma of the lung. So, the relationship between the mutation of p53 and the expression of TGF-beta-1 in the non-small cell carcinomas were evaluated. MATERIALS AND METHODS In 43 non-small cell carcinoma and normal tissue of the lung, their TGF-beta-1 mRNA were measured by RT-PCR and p53 was studied by SSCP and Western blotting assay. RESULTS p53 mutation rate in non-small cell carcinomas of the lung (48.4%) was much more frequent than the normal control group (14.3%). The expression rate of TGF-beta-1 in lung carcinomas, especially squamous cell carcinoma (71.4%), was much higher than the normal control group (42.9%). p53 mutation and TGF-beta-1 mRNA in the lung carcinomas were not strongly correlated. CONCLUSION It suggests that high expression rate of TGF-beta-1 and p53 mutation are associated with carcinogenesis of non-small cell carcinoma of the lung. High expression rate of TGF-beta-1 in the lung carcinomas can be partly explained by the fact that TGF-beta-1 have capacity to control the production of many components of the extracellular matrix and enhance angiogenesis in favor of tumor growth despite of their inhibitory effects of cell growth. However, additional research is required to determine the exact role of TGF-beta-1 in carcinogenesis of the lung.
PURPOSE In squamous cell carcinomas of the lung, the angiogenesis and the expression rates of metalloproteinase were measured to examine whether they can be useful as prognostic markers and therapeutic potentials. MATERIALS AND METHODS The angiogenesis and the expression rates of metalloproteinase were analyzed by counting the number of microvessels and immunohistochemically positive cells of MMP-1 and MMP-2 in 54 squamous cell carcinoma, respectively. RESULTS Lymph node meatastasis group showed higher angiogenesis than non-metastasis one (p=0.008). Angiogenesis were elevated with increasing clinical stage. However, MMP-1 and MMP-2 expression rate as the presence or absence of lymph node metastasis and the clinical stages were statistically insignificant, respectively. Angiogenesis failed to demonstrate any significant correlation with the expression rates of MMPs. CONCLUSION Our results suggests that angiogenesis level may provide informaton relevant to prognosis as well as treatment decisions.