Your browser doesn't support javascript.
loading
Montrer: 20 | 50 | 100
Résultats 1 - 3 de 3
Filtre
Ajouter des filtres








Gamme d'année
1.
Tumor ; (12): 84-90, 2014.
Article Dans Chinois | WPRIM | ID: wpr-848829

Résumé

Objective: To evaluate the association between a single nucleotide polymorphism (SNP) of 309 T/G in the promoter of murine doubleminute 2 (MDM2) gene and the susceptibility of non-small cell lung cancer (NSCLC). Methods: A computer-based online search was performed by using Cochrane Library, PubMed, EMBase, China National Knowledge Infrasrtucture (CNKI), Wanfang database and VIP database. The case-control studies were selected according to defined inclusion and exclusion criteria. After quality evaluation and data abstraction, a meta-analysis was performed by using STATA 12.0 software. The odds ratio (OR) of the association between MDM2 SNP 309T/G and NSCLC susceptibility was calculated. Then the subgroup analysis, sensitivity analysis and publication bias test were performed. Results: A total of 8 case-control studies were eligible for this analysis, including 5 343 NSCLC patients and 6 652 healthy controls. Meta-analysis showed that MDM2 SNP 309GG could significantly increase the risk of NSCLC [TT vs GG, OR = 0.77, 95% confidence interval (CD = 0.62-0.96; GT vs GG, OR = 0.83, 95% CI = 0.75-0.92; TT+GT vs GG, OR = 0.82, 95% CI = 0.75-0.91]. In the subgroup analysis of ethnicity, MDM2 SNP 309GG could significantly increase the risk of NSCLC for Asian people [TT vs GG, OR = 0.62, 95% CI = 0.52-0.73; GT vs GG, OR = 0.78, 95% CI = 0.67-0.90; TT vs GG+GT, OR = 0.71, 95% CI = 0.59-0.86; TT+GT vs GG, OR = 0.73, 95% CI = 0.63-0.84]. In the subgroup analysis of gender, MDM2 SNP 309GG could significantly increase the risk of NSCLC for female population [TT vs GG, OR = 0.70, 95% CI = 0.54-0.91; GT vs GG, OR = 0.69, 95% CI = 0.54-0.90; TT+GT vs GG, OR = 0.70, 95% CI = 0.55-0.89]. Conclusion: MDM2 SNP 309GG may be a potential biomarker for NSCLC risk, particularly for Asian people and women. Copyright© 2014 by Tumor.

2.
Tumor ; (12): 135-140, 2014.
Article Dans Chinois | WPRIM | ID: wpr-848805

Résumé

Objective: To evaluate the association between the 894G>T polymorphism of nitric oxide synthase 3 (NOS3) gene and the susceptibility to prostate cancer. Methods: A computer-based online search was performed by using Cochrane Library, PubMed, EMBase, CNKI (China National Knowledge Infrasrtucture), Wanfang database and VIP database. The case-control studies were selected according to defined inclusion and exclusion criteria. After quality evaluation and data abstraction, a Meta-analysis was performed by using STATA 12.0 software. Odds ratio (OR) of the association between NOS3 894G>T and prostate cancer susceptibility was pooled. Then the subgroup analysis, sensitivity analysis and publication bias test were performed. Results: A total of 5 case-control studies were eligible for this analysis, including 3 078 cases and 3 677 healthy controls. Meta-analysis showed that NOS3 894G>T polymorphism didn't increase the risk of prostate cancer [TT vs GG, OR = 0.95, 95% confidence interval (CI): 0.80-1.14; TT vs GT, OR = 0.88, 95% CI: 0.73-1.05; TT+GT vs GG, OR = 1.07, 95% CI: 0.97-1.18; TT vs GG+GT, OR = 0.92, 95% CI: 0.77-1.09]. In the subgroup analysis of ethnicity, NOS3 894G>T polymorphism didn't increase the risk of prostate cancer in Europeans (TT vs GG, OR = 0.87, 95% CI: 0.73-1.04; TT vs GT, OR = 0.85, 95% CI: 0.71-1.02; TT+GT vs GG, OR = 1.00, 95% CI: 0.90-1.11; TT vs GG+GT, OR = 0.86, 95% CI: 0.72-1.02). Conclusion: NOS3 894G>T polymorphism is not associated with the prostate cancer susceptibility as well as in Europeans. Copyright © 2014 by TUMOR.

3.
Tumor ; (12): 622-627, 2012.
Article Dans Chinois | WPRIM | ID: wpr-849050

Résumé

Objective: To compare the clinical characteristics and prognosis between the misdiagnosed and mistreated patients and the correctly diagnosed and treated patients with osteosarcoma. Methods: The clinical records of patients with osteosarcoma who received misdiagnosis and unplanned therapy (n = 30) and those who received correct diagnosis and therapy (n = 60) between January 2007 and February 2010 were retrospectively reviewed. The follow-up time was 6-60 months. The factors including gender, age, tumor location, Enneking's surgical staging, Karnofsky performance status score, pathological type, surgical procedure, tumor size, tumor necrosis rate, frequency of adjuvant chemotherapy, local recurrence rate, and lung metastasis rate were compared between the two groups. The two-year survival rate was calculated by Kaplan-Meier method. Results: No significant differences between the two groups were found in terms of gender, Enneking's surgical staging, Karnofsky performance status score, tumor location, pathological type, surgical procedure, frequency of adjuvant chemotherapy, time to local recurrence and time to lung metastasis (P > 0.05). The proportions of patients aged 30 years or more (46.7% vs 11.7%, P < 0.001), having a tumor's diameter of 10 cm or more (50.0% vs 23.3%, P = 0.011), and having tumor necrosis rate lower than 90.0% (80.0% vs 60.0%, P = 0.016) were significantly higher in the misdiagnosed and mistreated group than in the correctly diagnosed and treated group. The local recurrence rate (33.3% vs 10.0%, P = 0.006) and the lung metastasis rate (63.3% vs 43.3%, P = 0.037) in the misdiagnosed and mistreated group were also significantly higher than those in the correctly diagnosed and treated group. The median survival time and the two-year survival rates of the misdiagnosed and mistreated group and the correctly diagnosed and treated group were 25.5 (95% confidence interval: 7.1-58.9) months and 38.0 (95% confidence interval: 12.2-55.0) months, and 83.3% and 63.3%, respectively (P = 0.025; P = 0.036). Conclusion: The patients with osteosarcoma aged 30 years or more were more likely misdiagnosed as having benign diseases. Misdiagnosis and unplanned therapy for osteosarcoma can result in higher local recurrence rate and lung metastasis rate as well as a poor prognosis. Copyright © 2012 by TUMOR.

SÉLECTION CITATIONS
Détails de la recherche