Tissue microarrays in Chinese human rectal cancer: study of expressions of the tumor-associated genes.
Hepatogastroenterology
; 58(112): 1937-42, 2011.
Article
em En
| MEDLINE
| ID: mdl-22024062
ABSTRACT
BACKGROUNDS/AIMS:
The cellular basis for rectal cancer development is still unclear. The aim of this study was to evaluate the relationship between the expression of p53, cyclinD1, bcl-2, ß-catenin, c-myc, cyclooxygenase-2 (COX-2) and nm23-H1 and the clinicopathological characteristics of rectal cancer.METHODOLOGY:
Expressions of p53, cyclinD1, bcl-2, ß-catenin, c-myc, COX-2 and nm23-H1 proteins were detected by immunohistochemical staining to two tissue microarrays containing tissues accumulated from 54 human rectal cancers and 40 para-cancer mucosa.RESULTS:
Significant differences were demonstrated between the rectal cancers and their benign para-cancer counterparts according to the expressions of p53, cyclinD1, bcl-2, ß-catenin, c-myc, COX-2 and nm23-H1 (p<0.05). Additionally, positive correlations of ß-catenin with cyclinD1 and c-myc (r=0.412, p=0.002; r=0.447, p=0.000) and of p53 with bcl-2 (r=0.332, p=0.001) were found. Cancer tissues with overexpression of ß-catenin or bcl-2 were less likely to differentiate to advanced grade. Expression of cyclinD1 had a correlation with clinical stages (p=0.039). In addition, a negative correlation was found between nm23-H1 expression and the histological grades, distance metastasis and Duke's stages.CONCLUSIONS:
Aberrant expression of p53, cyclinD1, bcl-2, ß-catenin, c-myc, COX-2 and nm23-H1 might attribute to the carcinogenesis of human rectal cancer. Furthermore, cyclinD1 and nm23-H1 might be involved in rectal cancer progression. This study recommends the application of tissue microarrays in rectal cancer research for its reliable quick throughput.
Texto completo:
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Base de dados:
MEDLINE
Assunto principal:
Neoplasias Retais
/
Análise Serial de Tecidos
Tipo de estudo:
Risk_factors_studies
Limite:
Adult
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Aged
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Aged80
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Female
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Humans
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Male
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Middle aged
Idioma:
En
Ano de publicação:
2011
Tipo de documento:
Article