Essay Sample: Oncogenes Affected in Colon Cancer and FDA-approved Drugs for Use

Oncogenes affected in colon cancer and FDA-approved drugs for use

'TP53, KRAS, PIK3CA, and BRAF are the four most commonly mutated genes in patients affected with colon cancer' [1]. In this regard, Dr. Pelech 30.45 noted that the mutation frequency of the biomarkers has a significant influence on the Colon Cancer development. The oncogenes are in the order of decreasing frequency as per the rate of mutation. 'TP53 has the highest mutation at the rate of 43.89 % with 5750 mutations found' [2]. Three oncogenes TP53, PIK3CA, and BRAF, belong to protein serine/threonine kinase. 'In particular, the drug recommended for BRAF include vemurafenib and dabrafenib' [3]. On the other hand, TP53 and PIK3CA would benefit from the use of palbociclib and sorafenib. Lastly, according to Porru et al. KRAS belongs to the tyrosine protein substrate [4]. However, there are no drugs discovered to down-regulate or inactivate the mutation of KRAS a primary oncogene in colon cancer. However, Dr. Pelech purports that more than 50% of newly formed medication will be released within the decade [4]. Therefore, oncogenes such as KRAS will receive valuable treatment soon.

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Cancer-inducing amino acid mutations

The common types of mutation in p53 and BRAF include the missense, somatic and germline. The identification of the three types of mutation ushered in a new era of colon cancer treatment based on these discoveries. An assessment of KRAS mutation is a predictive biomarker since it plays a crucial role in determining treatment for colon cancer. As a result, Neumann et al. identified glycine to aspartate on cordon 12, glycine to valine on cordon 12 and glycine to aspartate on cordon 13 as the most frequent KRAS mutation [5]. Conversely, the mutations in PIK3CA to be analyzed include missense, somatic, and mutations that result in the alterations of the amino acid glutamic which are replaced by amino acid glycine. 'An assessment of these mutations will help in the identification of the cancer stages crucial in determining the type of treatment to be administered' [6].

References

Ahmed D, Eide P, Eilertsen I, Danielsen S, Eknaes M, Hektoen M, Lind G, Lothe R. Epigenetic and genetic features of 24 colon cancer cell lines. Oncogenesis. 2013 Sept; 2: 60-71.

Human Cancer Protein KnowledgeBase [Internet] 2017 Aug 1 [updated 2017 Aug1; cited 2018 Nov 2]. Available from http://www.onconet.ca/Report/index?query=Cancer+Gene+Mutation&searchTerm=TP53

Bhullar K, Lagaron N, McGowan E, Parmar I, Jha A, Hubbard B, Rupasinghe V. Kinase-targeted cancer therapies: Progress, challenges and future directions. Molecular Cancer. 2018 Feb; 17(1): 48.

Porru M, Pompili L, Caruso C, Biroccio A, Leonetti C. Targeting KRAS in metastatic colorectal cancer: current strategies and emerging opportunities. Journal of Experimental & Clinical Cancer Research. 2018 Mar; 31(1): 57.

Pelech S. Molecular basis of cancer. Canada: University of British Columbia; 2018.

Neumann J, Zeindi-Eberhart E, Kirchner T, Jung A. Frequency and type of KRAS mutations in routine diagnostic analysis of metastatic colorectal cancer. Pathology Research Practice. 2009 Aug; 205(12): 858-62.

The American Society. Treatment of colon cancer, by stage [Internet] 2018 Feb 21 [updated 2018 Oct 19; Cited 2018 Nov 2]. Available from https://www.cancer.org/cancer/colon-rectal-cancer/treating/by-stage-colon.htmlb