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1.
Tuberculosis and Respiratory Diseases ; : 480-489, 2005.
Artigo em Coreano | WPRIM | ID: wpr-9028

RESUMO

BACKGROUND: Dysregulation of apoptosis plays an important role in carcinogenesis, tumor progression, and resistance to chemotherapy. X-linked inhibitor of apoptosis (XIAP) is considered to be the most potent caspase inhibitor of all known IAP (inhibitor of apoptosis) family members. This study was designed to assess the pattern of expression and the prognostic value of XIAP in radically resected non-small cell lung carcinoma (NSCLC) patients. METHOD: The expression of XIAP and its relationship with clinicopathologic parameters (patient age, TNM stage, TNM-pT, TNM-pN, histologic type, VEGF expression, microvessel density, PCNA index) and overall survival were analysed with formalin-fixed, paraffin-embedded blocks from eighty cases of NSCLC. In addition, the apoptotic index (AI) was also assessed. RESULTS: In a regard to histologic type, squamous cell carcinoma (SCC) showed XIAP expression in 91.3%(42/46) and adenocarcinoma (AC) in 61.8%(21/34). The difference was significant(p=0.001). There was no correlation between XIAP expression and other parameters. In the group of AC, XIAP expression showed the signifcant correlation with older age group > or = 58 years and VEGF expression(p=0.028, p=0.014, respectively). The AI in the group with or without XIAP expression were 2.5+/-4.9% and 18.5+/-28.9%, respectively(p=0.001). Both groups just aforementioned showed no significant difference in median survival time (42.5 months, 29.8 months, respectively). CONCLUSION: This study suggests that the XIAP expression in NSCLCs could have relation to inhibition of apoptosis, and show differential expression according to histologic type. However, its prognostic role during the progression of NSCLC needs to be further defined.


Assuntos
Humanos , Adenocarcinoma , Apoptose , Carcinogênese , Carcinoma de Células Escamosas , Tratamento Farmacológico , Proteínas Inibidoras de Apoptose , Pulmão , Microvasos , Prognóstico , Antígeno Nuclear de Célula em Proliferação , Carcinoma de Pequenas Células do Pulmão , Fator A de Crescimento do Endotélio Vascular , Proteínas Inibidoras de Apoptose Ligadas ao Cromossomo X
2.
Journal of Korean Society of Endocrinology ; : 362-374, 2005.
Artigo em Coreano | WPRIM | ID: wpr-124044

RESUMO

BACKGROUND: Compared with common well-differentiated thyroid carcinomas, the genetic alterations underlying the development and progression of anaplastic thyroid carcinomas(ATC) are still uncharacterized. Comparative genomic hybridization(CGH) is a cytogenetic technique that can identify gains and losses in the DNA sequence copy number in tumors. METHODS: The authors studied the changes in the DNA copy number due to CGH in paraffin-embedded tissue blocks of 17 ATC cases, and tried to ascertain whether the genomic changes correlate with the clinicopathological parameters including patients' age, sex, primary tumor size, lymphovascular invasion, extrathyroid extension, regional node metastasis and immunohistochemical expression of cyclin D1. RESULTS: Fourteen of the 17 samples(82.4%) showed chromosomal changes, with a mean number of gains or losses per carcinoma of 3.6(range 2~6; 30 gains and 21 losses). The most frequently detected imbalance was the gain of chromosome 1q, which was seen in 35.7% of cases, particularly commonly in ATC associated with a papillary thyroid carcinoma. Other commonly occurring gains were present in 11q13 and 19(28.6%, respectively). Genomic amplification was detected in all four cases showing the 11q13 gain. Genomic losses were commonly noted in 3q, 6q, 18q andchi(21.4%, respectively). When numerical CGH alterations were compared to the clinicopathological parameters, there were no significant correlations(P>0.05). Cyclin D1 expression was noted in sixteen of the 17 cases(94.1%), but the extent of cyclin D1 expression was not correlated with the numerical CGH alterations(P>0.05). CONCLUSION: Taken together, the aberrations of 1q, 3q, 6q, 11q13 and 18q are relatively common in ATC, and may play an important role it developement. These findings should lead to the characterization of tumor suppressor genes and oncogenes that are potentially involved in the carcinogenesis of ATC. The amplification of 11q13 is characteristically found, but cyclin D1 in this region may be innocent of the aggressiveness of these carcinomas.


Assuntos
Sequência de Bases , Carcinogênese , Hibridização Genômica Comparativa , Ciclina D1 , Análise Citogenética , DNA , Genes Supressores de Tumor , Metástase Neoplásica , Oncogenes , Glândula Tireoide , Neoplasias da Glândula Tireoide
3.
Korean Journal of Pathology ; : 93-99, 2004.
Artigo em Coreano | WPRIM | ID: wpr-189666

RESUMO

BACKGROUND: CD44 is a polymorphic family of transmembrane glycoproteins generated by alternative splicing of messenger RNA and is involved in the mechanism of tumor invasion and metastasis. METHODS: The expression of selected CD44 molecules (CD44s, CD44v5, and CD44v6) was determined immunohistochemically in 84 cases of non small cell lung carcinomas (NSCLCs). The results were compared with PCNA index, microvessel density (MVD), and clinicopathological parameters including patient? survival. RESULTS: CD44s showed a positive reaction in 61.9% (52/84) of NSCLCs, CD44v5 in 73.8% (62/84), and CD44v6 in 39.3% (33/84). Squamous cell carcinomas (SCCs) displayed preferential expression of all CD44 molecules in comparison with adenocarcinomas (ACs) (p<0.001). As a whole, the expression of CD44 molecules was not correlated with clinical parameters (stage, TNM-T, and TNM-N), PCNA index, or MVD. For ACs only, however, CD44v5 expression was negatively correlated with PCNA index (p<0.05). Poor survival was correlated with CD44v5 expression in ACs and CD44v6 in SCCs (both, p<0.05). CONCLUSIONS: These findings suggest that CD44 molecule in NSCLC could be a distinctive phenotypic marker for SCC, and the possibility that CD44v5 and CD44v6 are in some way instrumental in conditioning the biologic behavior of NSCLC according to major histologic types.


Assuntos
Humanos , Adenocarcinoma , Processamento Alternativo , Antígenos CD34 , Carcinoma Pulmonar de Células não Pequenas , Carcinoma de Células Escamosas , Glicoproteínas , Microvasos , Metástase Neoplásica , Antígeno Nuclear de Célula em Proliferação , RNA Mensageiro
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