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Cancer Genomics Research Paper

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[Report on Cancer Genomics]
By
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Cancer Genomics
Molecular Basis
Cancer is uniquely known for its genomic instability especially the stepwise build-up
of mutations within its main oncogenes. ErbB2 or HER2 which is a receptor tyrosine-kinase
belonging to the epidermal-growth-factor receptor family has caught the devotion of cancer
researchers since it is one of the oncogene which alters NIH3T3-cells (1). In breast cancer,
HER2 has been observed to be creating abnormal signalling as it phosphorylate in several
breast tumours (28). The trans-modulation takes place through EGFR signalling even without
ligands whereby ErbB2 operates as a signalling subcomponent of three other more receptors
(1). Notably, in breast cancer, ErbB2 has other key partners known as ErbB1 and ErbB3
which are kinase malfunctioning receptors and whose intoxicating mitogenic acts are
triggered in hetero-dimeric complexes (28). These heterodimers seems to dodge typical
inactivation procedures by reducing the degree of ligand detachment by subsequently
internalizing though rather sluggishly. Consequently, they evade the degradative conduit by
appearing on the surface of the cell and thereby powerfully recruiting subsistence and
mitogenic conduits like the mitogen triggered protein-kinases or in some instances
phosphatidylinositol-3-kinase (1). Therefore, the hyper-activated motioning via ErbB2
signalling system leads to dys-regulation of cell-sequence homeostatic mechanism, including
the up-regulation of vigorous cyclin-D/CDK multiplexes (28). It has been found that D-type
cyclins in conjunction with CDK inhibitor known as p21waf1 are crucial in the evasion
process from apoptosis (1).
This molecular understanding of breast cancer is a good example of an understanding
of cancer cell lines can result in the development of a therapy. The observation is that any
drug should belong to the tyrosine-kinase inhibitors class of medications as they specifically
target tyrosine kinases (1). Herceptin which is essentially an antibody that seeks out cells that
have a high amount of HER2 was developed based on the observation that monoclonal
antibodies can hinder growth of tumour in cancer development. Since ErbB2 possesses no
ligand, HER2 antibody can be able to target ErbB2 and thus suppress signals receptor
dimerization (1). Herceptin protein has been found to overexpress in breast cancers in the
range of 15 to 30 percentages and this is attributed to its gene amplification (28). Herceptin is
usually administered in IV and for that reason it is humanized so as to halt the antibody from
being identified by the immune-system (1). Notably, Herceptin only acts as a treatment not a
cure since the cancer reappears later as most of the transformations involved are protein to

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1 [Report on Cancer Genomics] By Insert Your Name Institution Name, Location Department University Presented to Instructor’s Name, Course 2 Cancer Genomics Molecular Basis Cancer is uniquely known for its genomic instability especially the stepwise build-up of mutations within its main oncogenes. ErbB2 or HER2 which is a receptor tyrosine-kinase belonging to the epidermal-growth-factor receptor family has caught the devotion of cancer researchers since it is one of the oncogene which alters NIH3T3-cells (1). In breast cancer, HER2 has been observed to be creating abnormal signalling as it phosphorylate in several breast tumours (28). The trans-modulation takes place through EGFR signalling even without ligands whereby ErbB2 operates as a signalling subcomponent of three other more receptors (1). Notably, in breast cancer, ErbB2 has other key partners known as ErbB1 and ErbB3 which are kinase malfunctioning receptors and whose intoxicating mitogenic acts are triggered in hetero-dimeric complexes (28). These heterodimers seems to dodge typical inactivation procedures by reducing the degree of ligand detachment by subsequently internalizing though rather sluggishly. Consequently, they evade the degradative conduit by appearing on the surface of the cell and thereby powerfully recruiting subsistence and mitogenic conduits like the mitogen triggered protein-kinases or in some instances phosphatidylinositol-3-kinase (1). Therefore, the hyper-activated motioning via ErbB2 s ...
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