Objective To evaluate whether an early change in 18F-fluorodeoxyglucose (18F-FDG) uptake can predict tumor response to epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) and prognosis in patients with non-small cell lung cancer (NSCLC). Methods From August 2009 to April 2015, 22 patients with NSCLC who were eligible to EGFR-TKI treatment were enrolled. PET-CT scan was performed before (baseline) and 1 month after EGFR-TKI administration. Up to 5 hottest single tumor lesions (no more than 2 per organ) were considered to be target lesions. Maximum standardized uptake values (SUVmax) were measured, and post-treatment percentage changes in SUVmax (ΔSUV%) were calculated. PET responses were classified using PET response criteria in solid tumors (PERCIST). Then conventional CT scan was performed every 2 months for follow-up. Kappa statistic was used to compare agreement between the RERCIST recommendations-based therapeutic response evaluation and those based on RECIST1.1 criteria. Fisher exact test was used to compare the probability of disease progression in the early metabolic response and non-response groups. Predictive accuracy of ΔSUV% with respect to response or non-progression at CT scan was evaluated by ROC analysis. Progression-free survival (PFS) was determined by Kaplan-Meier survival analysis, and between-group comparison was performed by log-rank test. Results After 1 month of EGFR-TKI treatment, 12 patients (55%) showed partial metabolic response (PMR), 6 (27%) had stable metabolic disease (SMD), and 4 (18%) had progressive metabolic disease (PMD). There was a moderate agreement(Kappa=0.506,P<0.05) between PET response at 1 month based on PERCIST recommendations and CT response at 3 months according to RECIST 1.1. Non-progression was significantly more frequent in patients with an early PMR (χ2=11.941, P=0.005). Progression had been confirmed later during therapy in all patients with PMD . By using ROC analysis, the area under the curve for prediction of response was 0.906 (95% CI, 0.766—1.000; P=0.002), corresponding to a sensitivity of 88.9% and specificity of 84.6% at a cut-off of 40.36% in ΔSUV%. Using a cut-off value of 25.84% in ΔSUV%, highΔSUV% group (ΔSUV% ≥ 25.84%) had significantly longer PFS than low ΔSUV% group (ΔSUV%<25.84%). Conclusion Early assessment of PET-CT at 1 month of EGFR-TKI treatment could be useful to predict tumor response and clinical outcome in patients with NSCLC.

Objective: To explore the molecular characteristics of follicular variant papillary thyroid carcinoma (FVPTC), follicular thyroid adenoma (FTA) and follicular thyroid carcinoma (FTC), and investigate their role in tumorigenesis, differential diagnosis and prognosis evaluation in patients with follicular thyroid neoplasm. Methods: We retrospectively analyzed 50 surgical resection samples of follicular thyroid neoplasm. DNA was obtained from formalin-fixed, paraffin-embedded tissue, and subjected to next-generation sequencing (NGS) to analyze 50 hotspots for mutation in genes. Results: 47 samples passed quality control, including 29 FVPTCs, 8 FTAs and 10 FTCs. 75.9% of FVPTCs harbored mutated genes: BRAF V600E (31.0%, 9/29) was the most frequent, followed by TP53 (27.6%, 8/29), and N/KRAS (20.7%, 6/29). In contrast, 37.5% (3/8) FTAs carried NRAS Q61R mutation with 12.5% (1/8) FTA carrying mutated BRAF G466E. 20% (2/10) FTCs harbored NRAS Q61R mutation, and 20% (2/10) FTCs with TP53 mutations. BRAF V600E gene mutation only appeared in FVPTC, and was associated with age of onset and lymph node metastasis. There was no significant correlation between N/KRAS mutations and clinical pathologic features. Patients with lymph node metastasis group seems to have more TP53 mutation. Conclusions BRAF V600E gene mutation can be used to identity FVPTC from FTA/FTC. N/KRAS mutations cannot be used as the exclusive indicator of benign and malignant in thyroid follicular tumor. TP53 mutations play an important role in the process of follicular thyroid neoplasm, indicating more aggressive behavior and poor prognosis.

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Objective To explore the molecular characteristics of follicular variant papillary thyroid carcinoma (FVPTC), follicular thyroid adenoma ( FTA) and follicular thyroid carcinoma ( FTC), and investigate their role in tumorigenesis, differential diagnosis and prognosis evaluation in patients with follicular thyroid neoplasm. Methods We retrospectively analyzed 50 surgical resection samples of follicular thyroid neoplasm. DNA was obtained from formalin?fixed, paraffin?embedded tissue, and subjected to next?generation sequencing ( NGS) to analyze 50 hotspots for mutation in genes. Results 47 samples passed quality control, including 29 FVPTCs, 8 FTAs and 10 FTCs. 75.9% of FVPTCs harbored mutated genes:BRAF V600E (31.0%, 9／29) was the most frequent, followed by TP53 (27.6%, 8／29), and N／KRAS (20.7%, 6／29). In contrast, 37.5%(3／8) FTAs carried NRAS Q61R mutation with 12.5%(1／8) FTA carrying mutated BRAF G466E. 20%(2／10) FTCs harbored NRAS Q61R mutation, and 20%( 2／10) FTCs with TP53 mutations. BRAF V600E gene mutation only appeared in FVPTC, and was associated with age of onset and lymph node metastasis. There was no significant correlation between N／KRAS mutations and clinical pathologic features. Patients with lymph node metastasis group seems to have more TP53 mutation. Conclusions BRAF V600E gene mutation can be used to identity FVPTC from FTA／FTC. N／KRAS mutations cannot be used as the exclusive indicator of benign and malignant in thyroid follicular tumor. TP53 mutations play an important role in the process of follicular thyroid neoplasm, indicating more aggressive behavior and poor prognosis.

Objective To determine the role of Bmi-1 in the submandibular gland (SMG) of mice.Methods SMG of 4-week wild-type(WT) and Bmi-1 null(Bmi-1-/-) mice was analyzed on the weight,salivary flow rate,hematoxylin-eosin staining morphological differences and the changes in proliferation and aging by histology,immunohistochemistry and Western blotting.Results Compared with WT mice,the average static salivary flow rate [WT:(0.21 ±0.02) μg/min,Bmi-1-/-:(0.10 ±0.02) μg/min] (P =0.001) and the submandibular gland weight [WT:(1.89 ± 0.15) μg],Bmi-1-/-:[(1.34 ± 0.07) μg] (P =0.003) of the male Bmi-1-/-mice were significantly decreased,the number of gland duct increased,and the granular convoluted duct showed reduced diameter and branches.More senescence-associated β-galactosidase positive cells existed in SMG of Bmi-1-/-mice (WT:0.00,Bmi-1-/-:0.18 ± 0.02),and Ki-67 immunopositive cells decreased in SMG of Bmi-1-/-mice(WT:0.40 ～ 0.47,Bmi-1-/-:0.18 ～ 0.20) (P =0.000).The expression of p16 (WT:1.00 ± 0.12,Bmi-1-/-:0.00 ±0.00) (P =0.003) and p19(WT:0.97 ±0.09,Bmi-1-/-:5.09 ±0.21) (P =0.004) were up-regulated dramatically in SMG of the Bmi-1-/-mice.Conclusions Bmi-1 gene deficiency causes abnormal function of SMG by inducing senescence phenotype of SMG.

Objective To explore the molecular characteristics of follicular variant papillary thyroid carcinoma (FVPTC), follicular thyroid adenoma ( FTA) and follicular thyroid carcinoma ( FTC), and investigate their role in tumorigenesis, differential diagnosis and prognosis evaluation in patients with follicular thyroid neoplasm. Methods We retrospectively analyzed 50 surgical resection samples of follicular thyroid neoplasm. DNA was obtained from formalin?fixed, paraffin?embedded tissue, and subjected to next?generation sequencing ( NGS) to analyze 50 hotspots for mutation in genes. Results 47 samples passed quality control, including 29 FVPTCs, 8 FTAs and 10 FTCs. 75.9% of FVPTCs harbored mutated genes:BRAF V600E (31.0%, 9／29) was the most frequent, followed by TP53 (27.6%, 8／29), and N／KRAS (20.7%, 6／29). In contrast, 37.5%(3／8) FTAs carried NRAS Q61R mutation with 12.5%(1／8) FTA carrying mutated BRAF G466E. 20%(2／10) FTCs harbored NRAS Q61R mutation, and 20%( 2／10) FTCs with TP53 mutations. BRAF V600E gene mutation only appeared in FVPTC, and was associated with age of onset and lymph node metastasis. There was no significant correlation between N／KRAS mutations and clinical pathologic features. Patients with lymph node metastasis group seems to have more TP53 mutation. Conclusions BRAF V600E gene mutation can be used to identity FVPTC from FTA／FTC. N／KRAS mutations cannot be used as the exclusive indicator of benign and malignant in thyroid follicular tumor. TP53 mutations play an important role in the process of follicular thyroid neoplasm, indicating more aggressive behavior and poor prognosis.

Objective:To observe the effect of polyphyllin Ⅰ on the expressions of forkhead box Q1（FOXQ1）and epithelial-mesenchymal transition (EMT)-related factors, in order to explore the possible mechanism of polyphyllin Ⅰ in inhibiting the metastasis of colon cancer. Method:After the treatment with 1.25，2.50 μmol·L^-1 polyphyllin Ⅰ on HCT116 cells, Western blot and Real-time PCR were used to detect the expressions of FOXQ1，E-cadherin，Vimentin protein and mRNA. Result:Compared with the blank group, relative expressions of FOXQ1 protein and mRNA in low-concentration polyphyllin Ⅰ group were decreased, while relative expression of E-cadherin mRNA was increased, the differences were not statistically significant, and relative expressions of Vimentin protein and mRNA in low-concentration polyphyllin Ⅰ group were decreased (P<0.05)， and relative expression of E-cadherin protein in low-concentration polyphyllin Ⅰ group was increased (P<0.01). Compared with the blank group, relative expressions of FOXQ1, Vimentin protein and mRNA in high-concentration polyphyllin Ⅰ group were decreased，while relative expressions of E-cadherin protein and mRNA were increased (P<0.05, P<0.01). Compared with low-concentration polyphyllin Ⅰ group, relative expressions of Vimentin protein and mRNA in high-concentration polyphyllin Ⅰ group were decreased, but the difference was not statistically significant, relative expressions of E-cadherin protein and mRNA in high-concentration polyphyllin Ⅰ group were increased, whereas relative expressions of FOXQ1 protein and mRNA were decreased (P<0.05, P<0.01). Conclusion:Mechanism of polyphyllin Ⅰ inhibiting the metastasis of colon cancer may be related to the decrease of FOXQ1 and Vimentin expressions, and the up-regulation of E-cadherin.