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Cetuximab for treating Colorectal - Essay Example

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It is a human murine chimeric referred because it was produced from the mammalian cells (murine myeloma) cultures. Therefore, it is a recombinant molecule.
The drug…
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Cetuximab for treating Colorectal
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Download file to see previous pages and Wheeler (2011) “many human epithelial cancers including head and neck squamous cell carcinoma (HNSCC), non-small cell lung cancer (NSCLC), colorectal cancer (CRC), breast, pancreatic and brain cancer” (p.778) are the main sites for the expression for EGFR. The EGFR belongs to EGF receptor family, which also belongs to the family of tyrosine kinase. The receptor is ubiquitously expressed in many cells with epithelial, neuronal and mesenchymal origin (Harding and Burtness 2005). During homeostatic condition the regulation of these receptors are activated when ligand molecules like TGFα (transforming growth factor alpha), EGF and AR (amphiregulin) are available. These ligands have specificity for EGFR. Therefore, the target of the drug is usually expressed in many parts of the body with epithelial, neuronal and mesenchymal cells if there is a ligand molecule to initiate the expression process.
When the ligand binds to the EGFR receptors, activation takes effect, which is manifested by downstream activation of pathways like PLCy/PKC, RAS/RAF/MEK/ERK and P13K/AKT. In the absence of this process the net effect would lead to the activation of cells to proliferate, metastatic and survival of potential cancer cells (Oliveras-Ferraros et al 2008; Chen et al 2012).
The drug has high affinity for EGFR. Therefore, its affinity out-competes both the EGF and TGFα, whose binding would have initiated proliferation, metastatic and survival of cancerous and tumours cells. The drug binds to the extracellular domain of EGFR to cause lockage of ligand induced EGFR phosphorylation or ligand binding.
By hindering HER and EGFR members from binding to the receptor, the drug promoted degradation and internalisation of EGFR, thereby abrogating the downstream cascades of signal pathways (Brand et al 2011). Cells are arrested and prevented from existing the G1 phase of the cycle. Besides, interaction of the drug with the receptor decreases the expression of factors like ...Download file to see next pagesRead More
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