• Asian Pacific Journal of Cancer Prevention
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• v.16 no.10
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• pp.4347-4351
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• 2015

Background: Previous studies showed that genetic polymorphisms of glutathione S-transferase P1 (GSTP1) were involved in glutathione metabolism and genetic polymorphisms of ribonucleotide reductase (RRM1) were correlated with DNA synthesis. Here we explored the effects of these polymorphisms on the chemosensitivity and clinical outcome in Chinese non-small cell lung cancer (NSCLC) patients treated with gemcitabine-cisplatin regimens. Materials and Methods: DNA sequencing was used to evaluate genetic polymorphisms of GSTP1 Ile105Val and RRM1 C37A-T524C in 47 NSCLC patients treated with gemcitabine-cisplatin regimens. Clinical response was evaluated according to RECIST criteria after 2 cycles of chemotherapy and toxicity was assessed by 1979 WHO criteria (acute and subacute toxicity graduation criteria in chemotherapeutic agents). Results: There was no statistical significance between sensitive and non-sensitive groups regarding the genotype frequency distribution of GSTP1 Ile105Val polymorphism (p>0.05). But for RRM1 C37A-T524C genotype, sensitive group had higher proportion of high effective genotype than non-sensitive group (p=0.009). And according to the joint detection of GSTP1 Ile105Val and RRM1 C37A-T524C polymorphisms, the proportion of type A (A/A + high effective genotype) was significantly higher in sensitive group than in non-sensitive group (p=0.009). Toxicity showed no correlation with the genotypes between two groups (p>0.05). Conclusions: Compared with single detection of genetic polymorphisms of GSTP1 Ile105Val or RRM1 C37A-T524C, joint detection of both may be more helpful for patients with NSCLC to receive gemcitabine-cisplatin regimens as the first-line chemotherapy. Especially, genetic polymorphism of RRM1 is more likely to be used as an important biomarker to predict the response and toxicity of gemcitabine-cisplatin combination chemotherapy in NSCLC.

• Tuberculosis and Respiratory Diseases
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• v.78 no.4
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• pp.315-320
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• 2015

Background: The efficacy of epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) therapy can be measured based on the rate of treatment response, based on the Response Evaluation Criteria in Solid Tumors (RECIST) criteria or progression-free survival (PFS). However, there are some patients harboring sensitive EGFR mutations who responded poorly to EGFR-TKI therapy. In addition, there is variability in the PFS after EGFR-TKI treatment. Methods: We performed a retrospective analysis of the medical records of 85 patients with non-small cell lung cancer, who had achieved a stable disease or better response at the first evaluation of treatment response, after receiving a 2-month course of gefitinib. We calculated the tumor shrinkage rate (TSR) by measuring the longest and perpendicular diameter of the main mass on computed tomography before, and 2 months after, gefitinib therapy. Results: There was a significant positive correlation between the TSR and PFS (R=0.373, p=0.010). In addition, a simple linear regression analysis showed that the TSR might be an indicator for the PFS ($B{\pm}standard$ error, $244.54{\pm}66.79$; p=0.001). On univariate analysis, the sex, histologic type, smoking history and the number of prior chemotherapy regimens, were significant prognostic factors. On multivariate regression analysis, both the TSR (${\beta}$=0.257, p=0.029) and adenocarcinoma (${\beta}$=0.323, p=0.005) were independent prognostic factors for PFS. Conclusion: Our results showed that the TSR might be an early prognostic indicator for PFS in patients receiving EGFRTKI therapy.

• Korean Journal of Radiology
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• v.19 no.6
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• pp.1066-1076
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• 2018

Objective: The reliability of size measurements of liver metastases from neuroendocrine tumors (NETs) on contrast-enhanced computed tomography (CT) phases made by different readers may be hampered due to transient, variable rim enhancement in arterial phase (AP) or portal venous phase (PVP) images. We aimed to assess the reliability of tumor size measurements in pre- and post-contrast scans. Materials and Methods: The study coordinator selected target lesions according to Response Evaluation Criteria in Solid Tumors 1.1 guidelines in 44 consecutive patients with pathologically confirmed NET liver metastases. Two blinded readers measured the longest diameters of target lesions on pre-contrast, AP, and PVP images twice with a 4-week interval. Inter- and intra-observer agreements were evaluated using Bland-Altman plots and 95% limit of agreement (LOA) calculations. Results: Of the 79 target lesions (approximate mean size of 3 cm), 45 showed rim enhancement. Inter-observer agreement assessed based on LOA was highest in pre-contrast CT images (-6.1-5.7 mm), followed by PVP (-7.9-7.1 mm) and AP (-8.5-7.4 mm) images. Intra-observer agreement showed the same trend: -2.8-2.9 mm and -2.9-2.9 mm for readers 1 and 2, respectively, on pre-contrast CT, -2.8-2.9 mm and -3.0-3.2 mm, respectively, on PVP, and -3.2-4.2 mm and -3.4-3.2 mm, respectively, on AP images. Mean tumor diameters differed significantly among the phases in the following increasing order: pre-contrast CT, PVP, and AP images. Conclusion: There was better inter- and intra-observer agreement in size measurements of NET liver metastases on pre-contrast scans than on AP and PVP scans. Pre-contrast CT may be the optimal for measuring NET liver metastases if its accuracy is proven.