MYC Gene Mutations as Causative Pathways for Development and Treatment of Hematological Malignancies
Keywords:MYC gene, enhancer, Genome-wide association studies (GWAS), Cetuximab, Panitumumab, monoclonal antibody.
MYC is a proto-oncogene with deregulation of >50% of human cancers. The dysregulation of MYC cause
tumorigenesis, cell growth and proliferation, cell growth, and apoptosis. Novel therapy approaches lead
to the direct inhibition of the MYC gene by disruption of MYC/Max complex, MYC destabilization,
inhibition of MYC translation and/or transcription. Cetuximab and panitumumab act on the epidermal
growth factor receptor (EGFR). Cetuximab is an immunoglobin G1 isotype of a monoclonal antibody
that produces antibody-dependent cell-mediated. Panitumumab is an immunoglobulin G2 isotype
monoclonal antibody. This antibody acts on different site of EGFR with different degree of affinity.
Genome-wide association studies e.g., TWAS determine the aggregate genotypes. Enhancer is cellspecific
gene regulation that cluster for binding sites of a transcription factor with spatially coordinated
to control the expression of one or more specific target genes. In this review, we will summarize novel
drugs in targeting cancerous MYC in haematological malignancy.
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