The Acceptable Toxicity Level Of New Chemotherapeutic Regimen

1489 WordsSep 3, 20146 Pages
De-livering an outcome hard to digest: The acceptable toxicity level of new chemotherapeutic regimen in treating metastatic colorectal cancer may improve liver resections. Gia Toan Tang, z3463262. Keywords: Colorectal cancer, liver metastases, resectability, toxicity, tumours. Abbreviations: DLT, dose limiting toxicity; EGFR, epidermal growth factor receptor; mCRC, metastatic colorectal cancer; OS, overall survival; PFS, progressive-free survival. Folprecht’s et al.’s article published in Biomed Central identifies the dosage of a FOLFOXIRI (cetuximab, 5-FU, folinic acid, oxaliplatin and irinotecan) chemotherapeutic regimen that balances out its effective response rate and level of toxicity in patients with metastatic colorectal cancer…show more content…
There has been an increased research on methods of treating mCRC as a previous study has demonstrated that the OS of patients with mCRC improved through the combination of chemotherapeutic regimens and liver resections (Kopetz et al., 2009). This led to a clinical trial of using FOLFOXIRI as a new regimen, which demonstrated a maximal response rate in the decrease in tumour shrinkage of the liver and was more effective than the clinically standard FOLFIRI regimen. However, it was also found in the same study that high dosage of FOLFOXIRI produces severe side effects because of its toxicity (Falcone et al., 2007). Colorectal cancer is caused by mutations in various genes, such as the EGFR gene that results in overexpression of EGFR in the surface of intestinal cells. Overexpression of EGFR is associated with unregulated signalling pathway that leads to uncontrolled cell proliferation (Roberts et al., 2002). K-ras is a protein that is involved in the EGFR signalling pathway that causes a kinase cascade leading to cell proliferation and migration. Normally, cell division is stopped by hydrolyzing GTP to GDP in the binding site of K-ras to inactivate it. However, mutations in the GTP/GDP binding site of K-ras may prevent GTP from being hydrolysed, therefore K-ras is constantly active so cells will continually grow and divide (Scaltriti and Baselga, 2006). Individuals can either have the gene that codes for the wild type K-ras or the mutant K-ras. The K-ras status in
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