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1.
Chinese Journal of Cancer ; (12): 404-412, 2015.
Artigo em Inglês | WPRIM | ID: wpr-349580

RESUMO

<p><b>INTRODUCTION</b>The rearrangement of the anaplastic lymphoma kinase (ALK) gene accounts for approximately 1%-6% of lung adenocarcinoma cases and defines a molecular subgroup of tumors characterized by clinical sensitivity to ALK inhibitors such as crizotinib. This study aimed to identify the relationship between ALK rearrangement and the clinicopathologic characteristics of non-small cell lung cancer (NSCLC) and to analyze the therapeutic responses of crizotinib and conventional chemotherapy to ALK rearrangement in NSCLC patients.</p><p><b>METHODS</b>A total of 487 lung cancer patients who underwent testing for ALK rearrangement in our department were included in this study. ALK rearrangement was examined by using fluorescence in situ hybridization (FISH) assay.</p><p><b>RESULTS</b>Among the 487 patients, 44 (9.0%) were diagnosed with ALK rearrangement by using FISH assay. In 123 patients with adenocarcinoma who were non-smokers and of a young age (≤ 58 years old), the frequency of ALK rearrangement was 20.3% (25/123). Short overall survival (OS) was associated with non-adenocarcinoma tumor type (P = 0.006), poorly differentiated tumors (P = 0.001), advanced-stage tumors (P < 0.001), smoking history (P = 0.008), and wild-type epidermal growth factor receptor (EGFR) (P = 0.008). Moreover, patients with poorly differentiated and advanced-stage tumors had a shorter time to cancer progression compared with those with well differentiated (P = 0.023) and early-stage tumors (P = 0.001), respectively.</p><p><b>CONCLUSIONS</b>ALK-rearranged NSCLC tends to occur in younger individuals who are either non-smokers or light smokers with adenocarcinoma. Patients with ALK rearrangement might benefit from ALK inhibitor therapy.</p>


Assuntos
Humanos , Adenocarcinoma , Antineoplásicos , Povo Asiático , Carcinoma Pulmonar de Células não Pequenas , Hibridização in Situ Fluorescente , Neoplasias Pulmonares , Pirazóis , Piridinas , Receptores Proteína Tirosina Quinases , Receptores ErbB , Fatores de Risco , Fumar , Resultado do Tratamento
2.
Chinese Journal of Cancer ; (12): 620-626, 2011.
Artigo em Inglês | WPRIM | ID: wpr-294482

RESUMO

Matrix metalloproteinase 2 (MMP2) has been shown to play an important role in several steps of cancer development. The -1306C/T polymorphism of the MMP2 gene displays a strikingly lower promoter activity than the T allele, and the CC genotype in the MMP2 promoter has been reported to associate with the development of several cancers. To assess the contribution of the MMP2 -1306C/T polymorphism to the risk of nasopharyngeal carcinoma (NPC), we conducted a case-control study and analyzed MMP2 genotypes in 370 patients with NPC and 390 frequency-matched controls using real-time PCR-based TaqMan allele analysis. We found that subjects with the CC genotype had an increased risk (OR = 1.55, 95% CI = 1.05-2.27) of developing NPC compared to those with the CT or TT genotypes. Furthermore, we found that the risk of NPC was markedly increased in subjects who were smokers (OR = 15.04, 95% CI = 6.65-33.99), heavy smokers who smoked ≥ 20 pack-years (OR = 18.66, 95% CI = 7.67-45.38), or young (<60 years) at diagnosis (OR = 1.52, 95% CI = 1.01-2.29). Our results provide molecular epidemiological evidence that the MMP2 -1306C/T promoter polymorphism is associated with NPC risk, and this association is especially noteworthy in heavy smokers.


Assuntos
Adulto , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Povo Asiático , Genética , Carcinoma , Estudos de Casos e Controles , China , Epidemiologia , Predisposição Genética para Doença , Genótipo , Metaloproteinase 2 da Matriz , Genética , Neoplasias Nasofaríngeas , Epidemiologia , Genética , Patologia , Estadiamento de Neoplasias , Polimorfismo de Nucleotídeo Único , Regiões Promotoras Genéticas , Reação em Cadeia da Polimerase em Tempo Real , Fatores de Risco , Fumar
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