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Write a 1000 word essay (Harvard style), choice of 1 out of 3 questions. These essays are based on the material covered in the lectures notes: 1. 1. DNA repair can be different roles in cancer...

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Write a 1000 word essay (Harvard style), choice of 1 out of 3 questions.

These essays are based on the material covered in the lectures notes:

1. 1. DNA repair can be different roles in cancer susceptibility and cancer treatment, and be considered a double-edged sword. Discuss this statement, using examples if at least two specific DNA repair pathways to illustrate your answer.

2. 2. Compare and contrast the actions of a tumour suppressor gene with those of an oncogene, using one example of each to illustrate your answer.

3. 3. Poor die, obesity, alcohol intake, and lack of exercise are interrelated lifestyle factors that can profoundly affect cancer risk and incidence. Discuss how at least two of these factors interact (with mechanistic detail) and increase your chances of developing cancer.

Answered Same Day Mar 16, 2020

Solution

Soumi answered on Mar 22 2020
138 Votes
COMPARE AND CONTRAST THE ACTIONS OF A TUMOUR SUPPRESSOR GENE WITH THOSE OF AN ONCOGENE, USING ONE EXAMPLE OF EACH TO ILLUSTRATE YOUR ANSWER
Table of Contents
3Introduction
3Comparing and Contrasting the Actions of the Tumour Suppressor Genes with those of the Oncogenes
5Conclusion
6References
Introduction
Cancer is an uncontrolled cell proliferation with the accumulation of genetic and epigenetic mutations in the cells. These mutated cells are in selective advantage over normal cells leading to tumour formation (tumourigenesis). Genes underlying tumourigenesis are involved in regulation of cell fate by inhibiting the growth (tumour suppressor genes) and promoting the growth (proto-oncogenes). The present essay highlights these functional differences between these two genes.
Figure 1: Oncogene and Tumour Suppressor Gene
(Source: Nag et al. 2013, p.254)
Comparing and Contrasting the Actions of the Tumour Suppressor Genes with those of the Oncogenes
The normal function of tumour suppressor genes is to hinder the cell proliferation by encoding protein necessary for inhibiting the tumour formation or in simple terms it acts as ‘
akes’ for cell cycle. On the other hand, proto-oncogenes are basally expressed in the system without any phenotypic significance. Mutations in those genes support the uncontrolled cell proliferation and become oncogene or simply an accelerator of cell cycle upon mutation.
As mentioned by Bouta et al. (2018), at least one copy of the functional gene is enough to control the tumour formation. Loss of both copies leads to inactivation of this gene thereby developing a tumour. Hence, tumour suppressor gene mutations are not progressive at the cellular level and are known as loss of function mutation. However, as argued by Topalian et al. (2016), Proto-oncogene activation surpasses the effects of inhibition of tumour suppressor genes leading to malignant transformation. Proto-oncogenes exhibit dominant mutations (or gain of function mutation) because of the increased activity of the encoded protein (expressing high levels of normal gene). Further, only one copy of the mutated gene is enough to promote cancer.
p53 is the crucial tumour suppressor gene whose homozygous loss is the reason for most of the cancers including
east, colon and lung carcinomas. Actually, more than 50% of the human tumours are due to mutation in this gene. This gene is located in 17-chromosome p 13.1. The inactivation of p53 leads to enhanced cell proliferation, tumour development and reduced apoptosis. At the cellular level, p53 regulate tumour formation by stimulating apoptosis (Nag et al. 2013). Under the conditions of stress and DNA damage, p53 can also activate p21 (Cell-dependent kinase inhibitor or CdKs) pathway to control the tumour formation. However, loss of p53 leads to the inactivation of p21 inducing multiple Cdks...
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