Abstract

Despite the developments in the diagnostic and management strategies, a considerable number of colorectal cancer (CRC) patients present with disease recurrence after curative surgery. Moreover; there are no reliable indicators to determine the prognosis and response of CRC patients to therapy. By harnessing recent technological advances in molecular profiling techniques, it is anticipated that greater insight to the various combinations of genetic events or alternative pathways underlying carcinogenesis will be gained. By carrying out literature search, we were able to identify a comprehensive list of genes with high differential expression patterns in colorectal cancer that could serve as molecular markers to complement existing histopathological factors in diagnosis, follow up and therapeutic strategies for individualized care of patients.

Highlights

  • At the molecular level, activation of oncogenes and inactivation of tumour suppressor genes [1] are processes known to be involved in colorectal carcinogenesis

  • By carrying out literature search, we were able to identify a comprehensive list of genes with high differential expression patterns in colorectal cancer that could serve as molecular markers to complement existing histopathological factors in diagnosis, follow up and therapeutic strategies for individualized care of patients

  • Genome wide monitoring of gene expression is of great importance if we are to disclose the numerous and diverse events associated with carcinogenesis

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Summary

INTRODUCTION

Activation of oncogenes and inactivation of tumour suppressor genes [1] are processes known to be involved in colorectal carcinogenesis. Abrogation of mismatch repair systems [2] contributes to some colorectal cancers. Exactly how those genetic alterations bring about the development and progression of colorectal carcinomas remains to be resolved. A tool of genome monitoring, is an attempt to identify the different combinations of genetic events or alternative pathways that may be represented by cancers of a similar type. Examples of the type styles are provided throughout this document and are identified in italic type, within parentheses, following the example. Some components, such as multi-leveled equations, graphics, and tables are not prescribed, the various table text styles are provided. The formatter will need to create these components, incorporating the applicable criteria that follow

GENE EXPRESSION PROFILING IN CRC
Diagnostic and Prognostic Biomarkers
Therapeutic Targets and Treatment Response Prediction
MICRORNA EXPRESSION PROFILING IN CRC
Findings
Clinical Value of Mirna Expression in CRC
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