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DNA and cell biology 12/2011; 31(3):275-6; author reply 277-9. · 2.28 Impact Factor
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DNA and cell biology 11/2011; 31(2):135-8. · 2.28 Impact Factor
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DNA and cell biology 11/2011; 31(3):270-1. · 2.28 Impact Factor
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ABSTRACT: Previous studies have demonstrated that sunitinib has the anti-tumor activity in human non-small cell lung cancer (NSCLC). This study was aimed to investigate the efficacy of single use of sunitinib and that of concurrent or sequential administration of sunitinib and docetaxel in NSCLC cell lines that are resistant to EGFR TKIs.
NSCLC cell lines with EGFR T790M mutation and K-ras mutation were exposed to either sunitinib or docetaxel or both based on various sequential administrations. After exposure, the cell viability was measured by MTT assay, cell cycle distribution was analyzed by flow cytometry, and alterations in signaling pathway were determined by immunoblotting.
Sunitinib exhibited dose-dependent growth inhibition in NSCLC cell lines and arrested cell cycle at G1 phase, whereas docetaxel arrested at S phase. Although single or concurrent use of sunitinib and docetaxel has some anti-proliferative effects, the sequential administrations of both drugs remarkably enhanced anti-tumor activity. When cells were exposed to docetaxel followed by sunitinib, synergism was observed. The molecular basis of this synergism is that the signaling pathways that were initially activated by docetaxel exposure were efficiently suppressed by the subsequent exposure to sunitinib. In contrast, the reverse of this sequential administration resulted in antagonism, which may be due to differential effects on cell cycle arrest.
Sunitinib as a single agent exhibits anti-proliferative effects in vitro in NSCLC cell lines with EGFR T790M and K-ras mutations but the sequential administration of docetaxel followed by sunitinib is superior to sunitinib followed by docetaxel and concurrent administration.
Journal of Cancer Research and Clinical Oncology 09/2011; 137(9):1397-408. · 2.56 Impact Factor
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ABSTRACT: Epidemiological studies on the association between T8473C polymorphism of cyclooxygenase 2 (COX 2) and lung cancer risk have provided ambiguous data. To derive a more precise estimation of the association, we conducted a meta-analysis.
Systemic searches of the PubMed and MEDLINE databases were performed, with the last report up to May 2011. The meta-analysis was conducted with a fixed/random effect model.
A total of 7 studies including 4,373 lung cancer patients and 5,468 controls were covered. Crude odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of association. No obvious associations were found for all genetic models when all studies were pooled into the meta-analysis (for C vs. T: OR = 0.948, 95% CI = 0.709-1.268; for TC vs. TT: OR = 0.970, 95% CI = 0.823-1.143; for CC vs. TT: OR = 1.141, 95% CI = 0.666-1.956; for CC/TC vs. TT: OR = 1.102, 95% CI = 0.818-1.251; for CC vs. TT/TC: OR = 1.090, 95% CI = 0.716-1.660). In the subgroup analyses by ethnicity (Asian and Caucasian) and source of controls (population based and hospital based), also no significant associations were found for all genetic models.
Taken together, this meta-analysis suggests that the COX 2 T8473C polymorphism is not associated with lung cancer risk.
Asian Pacific journal of cancer prevention: APJCP 01/2011; 12(8):1941-5. · 0.66 Impact Factor
