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The Molecular Mechanism of RAS Wild-type mCRC Resistance to Anti-EGFR-antibody

Colorectal Cancer Clinical Trial

Official title:
The Molecular Mechanism of RAS Wild-type Metastatic Colorectal Cancer (mCRC) Resistance to Anti Epidermal Growth Factor Receptor (EGFR) Antibody

Clinical Trial Summary

Establishing the genetic map of primary and secondary resistance of Chinese wild RAS colorectal cancer received anti-EGFR treatment through tissues and peripheral blood NGS testing. Combination genetic data with clinical characteristics, prognosis and treatment data to explore the molecular mechanism of resistance of anti-EGFR-antibody.

Clinical Trial Description

Cetuximab is a chimeric (mouse/human) monoclonal antibody, an epidermal growth factor receptor (EGFR) inhibitor. Many large clinical trials demonstrated that for RAS wild-type metastatic colorectal cancer (mCRC), especially left-sided RAS wild-type mCRC, cetuximab can prolong OS. But some of patients have primary resistance to cetuximab and for all patients received cetuximab will develop secondary resistance. Cell-free or circulating tumour DNA (ctDNA) including primary site and metastatic site genetic information, which can avoid tumor heterogeneity. The results of paired test detection of tissue and ctDNA showed there is 93% consistency in RAS testing. Therefore, dynamic monitoring ctDNA during anti-EGFR targeted treatment of RAS wild-type mCRC patients can implement prognosis of efficacy and response evaluation in real-time. Besides, it can monitor the variation features of resistance gene and find resistance gene in real-time. According the situation of gene change to find potential drug resistance mechanism and formulate individualization treatment plan. ;

Study Design

Related Conditions & MeSH terms

Clinical Trial Details
NCT number NCT04466267
Study type Observational
Source Sun Yat-sen University
Contact
Status Completed
Phase
Start date March 1, 2017
Completion date July 4, 2020
View Details
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