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Comparison analysis in synchronous and metachronous metastatic colorectal cancer based on microarray expression profile.
Hepatogastroenterology ; 61(136): 2215-8, 2014.
Article en En | MEDLINE | ID: mdl-25699354
ABSTRACT
BACKGROUND/

AIMS:

Colorectal cancer (CRC) is one of the most common malignancies, and liver metastasis is one of the major causes of death of CRC. This study aimed to compare the genetic difference between metachronous lesions (MC) and synchronous lesions (SC) and explore the molecular pathology of CRC metastasis.

METHODOLOGY:

Microarray expression profile data (GSE10961) including 8 MC and 10 SC was downloaded from Gene Expression Omnibus. The differentially expressed genes (DEGs) between the two groups were identified based on T test. Furthermore, GO enrichment analysis was performed for the down-regulated DEGs using DAVID. Finally, Classify validation of known CRC genes based on previous studies between MC and SC samples was conducted.

RESULTS:

Total of 36 DEGs including 35 down-regulated DEGs and 1 up-regulated DEGs were identified. The expressional differences of the 5 informative oncogenes EGFr, PIK3R1, PTGS2 (COX-2), PTGS1 (COX1), and ALOX5AP between SC and MC were really tiny.

CONCLUSIONS:

Some DEGs, such as NFAT5, OLR1, ERAP2, HOXC6 and TWIST1 might play crucial roles in the regulation of CRC metastasis (both SC and MC) and by disrupting some pathways. However, our results indeed demand further research and experiment.
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Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Neoplasias Colorrectales / Neoplasias Primarias Secundarias / Transcriptoma / Neoplasias Hepáticas / Neoplasias Primarias Múltiples Límite: Humans Idioma: En Revista: Hepatogastroenterology Año: 2014 Tipo del documento: Article
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Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Neoplasias Colorrectales / Neoplasias Primarias Secundarias / Transcriptoma / Neoplasias Hepáticas / Neoplasias Primarias Múltiples Límite: Humans Idioma: En Revista: Hepatogastroenterology Año: 2014 Tipo del documento: Article
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