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Inflammatory Response Genes in Genesis of Bowel Cancer Essay

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Introduction

The high prevalence of colon cancer raises concern across the world over treatment and management approaches. Cancer is one of the most prevalent chronic diseases in the world and a leading cause of death and morbidity (Mattiuzzi and Lippi, 2019). Developing countries bear 80% of the cancer burden in the world, with high mortality resulting from the high prevalence (Wambalaba et al. 2019). Colon cancer is related to unmodifiable risk factors like age and gene inheritance and modifiable risk factors like lifestyle and environmental factors (Lewandowska et al., 2022). The mutation of genes leads to cancer, which has opened research into the role of inflammatory response genes in cancer development and the possible treatment interventions to help control and treat cancer (Schmitt and Greten, 2021). The multihit cancer hypothesis posits that the suppression of tumor genes requires the inactivation of both alleles. Knudson’s hypothesis is based on the need to provide a unifying approach to understanding cancers that occur in patients with the “susceptibility gene” (Chernoff, 2021). The theory suggests that inactivating cancer-causing genes is possible when both alleles are activated, which raises inquisitions over the role of inflammatory response genes in the genesis of bowel cancer and their role in the development of effective interventions.

Overview

Cancer is highly prevalent globally, with developed nations having the highest prevalence. The CDC noted that America alone recorded approximately 1.7 million new cases in 2019 alone (2022). Nearly 600,000 people died in the country due to the disease (CDC 2022). Colon cancer is the most prevalent form of bowel cancer, with a 6.1% prevalence in the general assessment of cancer frequency (Sawicki et al., 2021). It is also the second leading cause of mortality in all forms of cancer (Sawicki et al., 2021). Colon cancer is responsible for nearly 1.4 million new cancer cases worldwide (Lewandowska et al., 2022). The high prevalence of colon cancer and its impacts demand the adoption of effective medical interventions.

Etiology

Colon cancer is caused by gene mutations that happen due to genetic inheritance, lifestyle, or environmental factors. Gene mutations lead to cell inflammation that presents a health risk when uncontrolled (Chen et al., 2017). There is more than one cause of colorectal cancer since it can develop due to lifestyle choices that an individual makes, age, or genetic factors. This makes colon cancer a multifactorial disease process (Thanikachalam and Khan, 2019). Genetic factors and age make up for a smaller percentage of the etiology, while environmental exposures like diet and healthy choices that one makes are significant factors in the development of the condition.

Pathogenesis

Colorectal cancer (CRC) occurs because of the progressive accumulation of genetic modifications that cause changes in the normal colonic mucosa to adenocarcinoma. Approximately 75% of colon cancer cases are sporadic and occur in people who lack genetic predisposition. The progression of the disease depends on its symptoms (Germini et al., 2019). The common symptoms related to the condition include fatigue and unexplained weight loss, perforations or intestinal obstruction, abdominal discomfort and perforations, rectal bleeding, and a persistent change in bowel sounds. Any of these symptoms is an indicator of the development of cancer. Therefore, patients are highly advised to visit the hospital for diagnosis and possible treatment if the condition is realized. The early diagnosis of colorectal cancer allows for its treatment, which reduces the need for extensive care and costs that come with the advanced spread of the disease. Three primary pathways emerge in colon cancer genesis. The CIN pathway represents approximately 70% of sporadic CRC (Germini et al., 2019). The cancers exhibit chromosomal abnormalities and chromosomal rearrangements. The MSI pathway is due to DNA MMR genes. CIMP is the third pathway, and it is characterized by CpG island methylation. Each pathway facilitates the development of CRC.

Chromonosomal instability CIN
Figure 1

Treatment

There are various treatments for colorectal cancer based on its development. Surgery is the most recommended curative option at the early stages of cancer. However, the later stages entail palliative care for the patient (Mojtahedi et al., 2021). Palliative care entails relieving the symptoms of the patient to make the condition of the patient conducive. The use of chemotherapy and other interventions has been developed over the years as researchers look for more effective ways of treating CRC (Zhang et al., 2017). The current approach entails physicians considering the extent of the tumor and the medication preferences of the patient in the determination of the type of care the patient will receive. Research is responsible for exploring and using inflammatory response genes to manage colon cancer.

Role of Inflammatory Response Genes

Inflammation is an essential trait in tumors since it determines the growth of cells during cancer development. The two forms of tumor-related inflammation are systemic and local inflammation. Each form of inflammation promotes tumor growth and progression through subversion of the anti-tumor immune response. They also affect the sensitivity of tumor cells and trigger immune gene mutations leading to tumors. The role of inflammation in tumor development is vital in understanding and treating cancer. Research shows that infiltration of chronic inflammatory cells and systemic cell inflammatory response assessment can help determine colon cancer prognosis in patients. The establishment of the role of inflammation in tumor growth in the genesis of colorectal cancer has resulted in promising treatment options for the disease.

A study by Liang et al. (2021) indicates the potential for inflammatory response genes in the prognosis of colon cancer. The researchers sought to identify and validate a novel inflammatory response-related gene to determine the course of treatment for colon cancer. The researchers explored a new treatment course based on inflammatory response-related genes for colon cancer patients. The study outcomes revealed that colon cancer patients at different risk levels had varying immune cell infiltration and tumor microenvironment. The prognostic genes had different protein levels among colon cancer patients. The prognostic genes could regulate the malignant phenotype of colon cancer. The researchers concluded that inflammation-related gene signatures might be used to predict the prognosis of cancer patients. Determining the role of inflammatory response genes can help determine the required modifications in the immune microenvironment for CRC patients to enhance management and treatment.

Inflammatory response genes can help to improve the immune microenvironment of cancer patients. The microenvironment of a tumor is crucial to the development of tumors (Wang et al., 2022). The environment is responsible for the aggregation and activation of immune signaling, leading to tumor cell proliferation through the secretion of pro-inflammatory chemokines and cytokines (Ferrari et al. 2019). The correlation between the immune microenvironment and inflammatory response shows the role that the microenvironment can play in the management and treatment of colon cancer. Wang et al. (2022) note that the inflammatory response directly affects the prognosis and immune infiltration. Expressing inflammatory response genes is essential in repairing genes when addressing CRC (Germini et al., 2019). Studies have shown that inflammation alters cell proliferation and immunity, disrupting the ability to control cell growth capacity and leading to cancer cell growth. They also indicate that managing the inflammatory environment can help manage cancerous cell growth.

Research on the inflammatory response can help to advance immunotherapy development for colon cancer patients. Existing literature shows the role of inflammatory response in cancer cell growth (Jiang et al., 2018). With the right environment, colon cancer cells can grow significantly, leading to the need for treatment and control. Research on the use of inflammatory response to treat and manage colon cancer is ongoing. However, the number of studies that have been done on the topic is scarce. There is a need for further research on the role of inflammation response genes in managing colon cancer and other cancer forms. The environment has been proven responsible for determining tumor growth, encouraging research into controlling the environment to prevent cancer development.

Conclusion

Colon cancer is one of the most prevalent forms of cancer in the world. Both controllable and uncontrollable factors cause colorectal cancer. A gene mutation at the core of the issue leads to tumor growth. The research shows that inflammation response genes and the environment in which tumors grow are crucial determinants in the genesis of colon cancer. As colon cancer control and treatment advancements advance, researchers should look into better ways of preventing tumor development. Based on the outcomes of this paper, ongoing research has proven that colon cancer can be treated and managed using inflammatory response genes. Further exploration of inflammatory response genes can help improve treatment options for colorectal cancer and possibly lead to a lower incidence of the disease. Current research experiences shortfalls from the small number of studies that are being done on the treatment approach and the prolonged period that it takes to research and implement interventions.

Reference List

CDC. (2022). . Centers for Disease Control and Prevention. Web.

Chen, L., Deng, H., Cui, H., Fang, J., Zuo, Z., Deng, J., Li, Y., Wang, X., and Zhao, L. (2017) ‘’, Oncotarget, 9(6), pp. 7204–7218. Web.

Chernoff, J. (2021) ‘,’ Molecular biology of the cell, 32(22). Web.

Ferrari, S. M., Fallahi, P., Galdiero, M. R., Ruffilli, I., Elia, G., Ragusa, F., Paparo, S. R., Patrizio, A., Mazzi, V., Varricchi, G., Marone, G., and Antonelli, A. (2019) ‘’, International Journal of Molecular Sciences, 20(18), p. 4413. Web.

Germini, D. E., Franco, M. I., Fonseca, F. L., de Sousa Gehrke, F., da Costa Aguiar Alves Reis, B., Cardili, L., Oshima, C. T., Theodoro, T. R., and Waisberg, J. (2019) ‘’, Tumor Biology, 41(4), p. 101042831984304. Web.

Jiang, H., Dong, L., Gong, F., Gu, Y., Zhang, H., Fan, D., and Sun, Z. (2018) ‘’, International Journal of Molecular Medicine. Web.

Lewandowska, A., Rudzki, G., Lewandowski, T., Stryjkowska-Góra, A., and Rudzki, S. (2022) ‘,’ Cancer Control, 29, p. 107327482110566. Web.

Liang, Y., Wu, X., Su, Q., Liu, Y., and Xiao, H. (2021) ‘’, Journal of Inflammation Research, 14, pp. 3809–3821. Web.

Mattiuzzi, C., and Lippi, G. (2019) ‘,’ Journal of Epidemiology and Global Health, 9(4), pp. 217–222. Web.

Mojtahedi, Z., Koo, J. S., Yoo, J., Kim, P., Kang, H. T., Hwang, J., Joo, M. K., and Shen, J. J. (2021) ‘,’ Cancer management and research, 13, pp. 7569–7577. Web.

Sawicki, T., Ruszkowska, M., Danielewicz, A., Niedźwiedzka, E., Arłukowicz, T., and Przybyłowicz, K. E. (2021) ‘,’ Cancers, 13(9), p. 2025. Web.

Thanikachalam, K., and Khan, G. (2019) ‘Colorectal cancer and nutrition,’ Nutrients, 11(1), 164.

Schmitt, M., and Greten, F. R. (2021) ‘’, Nature Reviews Immunology, 21(10), pp. 653–667. Web.

Wambalaba, F. W., Son, B., Wambalaba, A. E., Nyong’o, D., and Nyong’o, A. (2019) ‘,’ Cancer Control: Journal of the Moffitt Cancer Center, 26(1), p. 1073274819886930. Web.

Wang, Y., Zhang, L., Shi, G., Liu, M., Zhao, W., Zhang, Y., Wang, Y., and Zhang, N. (2021) ‘,’ Frontiers in genetics, 13, p. 886949. Web.

Zhang, Y., Chen, Z., and Li, J. (2017). . Medicine, 96(40). Web.

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