Journal of Parasitic Diseases: Diagnosis and Therapy

All submissions of the EM system will be redirected to Online Manuscript Submission System. Authors are requested to submit articles directly to Online Manuscript Submission System of respective journal.
Reach Us +447723862070

Mini Review - Journal of Parasitic Diseases: Diagnosis and Therapy (2022) Volume 7, Issue 6

The prevalence of oesophageal cancer associated with parasitosis.

Farin Zhang *

Department of Environmental and Occupational Health, School of Public Health and Health Services, The George Washington University, Washington, DC 20052, United States

*Corresponding Author:
Farin Zhang
Department of Environmental and Occupational Health
School of Public Health and Health Services, The George Washington University
Washington, DC 20052, United States
E-mail: [email protected]

Received: 20-Oct-2022, Manuscript No. AAPDDT-22-81705; Editor assigned: 20-Oct-2022, PreQC No. AAPDDT-22-81705(PQ); Reviewed:05-Nov-2022, QC No. AAPDDT-22-81705; Revised:09-Nov-2022, Manuscript No. AAPDDT-22-81705 (R); Published: 16-Nov-2022, DOI: 10.35841/2591-7846-7.6.127

Citation: The prevalence of oesophageal cancer associated with parasitosis. J Parasit Dis Diagn Ther 2022; 7(6):127

Abstract

Due to its incredibly aggressive nature and low survival rate, oesophageal cancer is one of the least understood and deadly tumours in the world. In terms of overall cancer mortality, it comes in sixth. An increased risk of oesophageal squamous cell carcinoma has been linked in retrospective investigations of EsC to smoking, hot tea drinking, red meat consumption, poor oral health, limited intake of fresh fruit and vegetables, and low socioeconomic position. In clinical practise, dysplasia continues to be the only criteria relevant for identifying patients at elevated risk for the development of oesophageal adenocarcinoma, despite the fact that Barrett's oesophagus is clearly recognised as a risk factor for EsC. In this study, we looked into the epidemiologic trends and root causes of EsC. We produced the most recent stage distribution and 5-year relative survival by stage at diagnosis for 1998-2009 using population-based cancer data from the Surveillance, Epidemiology and End Results Program of the United States. The fact that oesophageal cancer, specifically adenocarcinoma, is one of the relatively few cancers that is causing an increase in the mortality rate of men in the United States deserves special attention. It is hoped that additional research into the EsC's mechanism of development would reduce its prevalence and enhance outcomes

Keywords

Risk factor, Barrett’s oesophagus, Cyclin D1 G870A, Oesophageal neoplasm, Susceptibility, Polymorphism.

Introduction

Squamous cell carcinoma and adenocarcinoma are two types of oesophageal cancer that are regarded as severe malignancies due to their poor prognosis and typically deadly outcome. Over 450000 people worldwide suffer from oesophageal cancer, and the prevalence is rising quickly. EsC is currently the eighth most frequent cancer occurrence in the globe due to its incredibly aggressive character and low survival rate. The epidemiologic trend of EsC is unique compared to that of all other malignancies. Both by time period and birth cohort, the incidence of oesophageal adenocarcinoma has dramatically grown during the past few decades. It requires etiological research to understand why this deadly cancer is spreading so quickly [1].

Anatomy of oesophageal cancer

SCCs, which develop from the stratified squamous epithelial lining of the organ, and adenocarcinomas, which affect the columnar glandular cells that replace the squamous epithelium, are the two main types of oesophageal cancer that commonly arise. Small cell carcinomas and sarcomas typically account for 1%–2% of all oesophageal cancer cases. Rarely, the oesophagus may also develop various carcinomas, melanomas, leiomyosarcomas, carcinoids, and lymphomas. The most common histologic subtype of oesophageal cancer is SCC. Squamous cell carcinoma of the oesophagus is more common as people age and reaches its peak frequency in the seventh decade of life. Black people are three times more likely than white people to get squamous cell oesophageal cancer, whereas white men are more likely to develop adenocarcinomas[2,3].

Risk factors

Squamous cell carcinoma, which develop from the stratified squamous epithelial lining of the organ, and adenocarcinomas, which affect the columnar glandular cells that replace the squamous epithelium, are the two main types of oesophageal cancer that commonly arise. Small cell carcinomas and sarcomas typically account for 1%–2% of all oesophageal cancer cases. Rarely, the oesophagus may also develop various carcinomas, melanomas, leiomyosarcomas, carcinoids, and lymphomas. The most common histologic subtype of oesophageal cancer is SCC. Squamous cell carcinoma of the oesophagus is more common as people age and reaches its peak frequency in the seventh decade of life. Black people are three times more likely than white people to get squamous cell oesophageal cancer, whereas white men are more likely to develop adenocarcinomas[4].

Smoking increases risk of SCC and adenocarcinoma of the oesophageal

Moderate to heavy smokers face an increased risk of both SCC and adenocarcinoma of the oesophagus. Research suggests that when a smoker ingests tobacco condensates, it causes tobacco carcinogens, particularly nitrosamines, to come in contact with the oesophageal mucosa. There is a direct correlation between the number of cigarettes a smoker smokes per day; the length of time the smoker spends smoking, and the risk of oesophageal cancer.

Genetic changes: Smaller sample size studies on polymorphism for oesophageal cancer have also been conducted. Multiple malignancies have been linked to the cytoclin D1 G870A polymorphism. Investigations into the relationship between the CCND1 G870A polymorphism and the risk of oesophageal cancer, however, have produced inconsistent results. Overall results point to a potential link between CCND1 G870A mutations and a higher risk of developing oesophageal cancer. According to the initial research, which was published in 2005, CCND1 G870A was a risk factor for oesophageal cancer. According to research by Liu's team, CCND1 G870A was not linked to an increased risk of developing oesophageal cancer. Liu's team attributed the mismatch to the fact that all earlier investigations relied on scant samples [5].

Preventive factors

The keys to prevention of oesophageal cancer vary by cell type. For SCC, reduction or elimination of tobacco and alcohol consumption provide the best means to reduce the incidence of this cancer. However, no one particular risk factor is responsible for the rising incidence of oesophageal adenocarcinoma. Several preventive strategies are under investigation using such agents as nonsteroidal anti-inflammatory drugs, selenium, alpha-difluoromethylornithine, and retinoids. Vegetable intake, and fruit intake is considered to be a preventive role. Carotene, vitamin C, and vitamin E are protective, most likely in combination with each other and other micronutrients. The role of vitamin A is not clear because of conflicting findings in the studies reviewed. When intake of raw vegetables and cooked vegetables was analyzed separately, raw vegetables were found to be more protective. Because fruits are relatively expensive in most places, increased consumption may reflect higher socioeconomic status.

Conclusion

The precise causes of EsC have not been identified. Despite uncertainties in our understanding of the causes of mechanistic pathways of oesophageal cancer, there is sufficient evidence to take effective steps to prevent the majority of SCC in western countries, while more information is needed to curb the epidemic increase in adenocarcinoma.

References

  1. 1.Mao WM, Zheng WH, Ling ZQ .Epidemiologic risk factors for esophageal cancer development Pac J Cancer Prev. 2011;12:2461–2466
  2. Indexed at, Google Scholar

  3. 2.Blot WJ, McLaughlin JK. The changing epidemiology of esophageal cancer. Semi Oncol. 1999;26:2-8.
  4. Google Scholar

  5. 3.Blot WJ, Devesa SS, Fraumeni JFhttps://jamanetwork.com/journals/jama/article-abstract/408439 target="_blank"> Continuing climb in rates of esophageal adenocarcinoma: an update. . J Am Med Assoc. 1993;270:1320..
  6. Indexed at, Google Scholar

  7. 4.Kwatra KS, Prabhakar BR, Jain S, et al. Sarcomatoid carcinoma (carcinosarcoma) of the esophagus with extensive areas of osseous differentiation: a case report. Ind J Pathol Microbiol. 2003;46:49-51.
  8. Indexed at, Google Scholar

  9. 5.Cook MB. Non-acid reflux: the missing link between gastric atrophy and esophageal squamous cell carcinoma?. Am J Gastroenterol. 2011;106:1930–1932.
  10. Indexed at, Google Scholar, Cross Ref

Get the App

Vizag Tech Summit