What is the relationship between environment and cancers?
There is a significant relationship between cancer and the environment because cancer-causing substances exist in some environment. The changes in some genes can alter cellular function and the way the cell functions. There is a wide range of genetic changes that develop as a result of DNA replication in the cell division process. Never the less, environment exposure can damage the DNA (Casey et al., 2015). For example, in industrialized regions, high ambient pollution such as polycyclic aromatic hydrocarbons (PAH) from coal used in home heating and industrial areas have tended to have a significant damage on the DNA. From some experimental bioassays, it was found that the PAH tend to be both transplacental carcinogens and developmental toxicants. PAH causes cancer in both the parent and the developing infant.
Modulation of adducts levels such as glutathione S-transferees MI (GSTM1) and cytochrome P4501A1 (CYP1A1) Msp restriction fragment length polymorphism (RFLP) has also shown that these adducts are linked to the risk of lung cancer. The PAH-induced DNA damage is increased by air pollution which is more enhanced in the fetus because of the CYP1A1 Mspl polymorphism (Casey et al., 2015). Environmental factors initiate genetic mutation that after the normal pathways of cellular proliferation. These types of genetic mutation occur in Ontogenesis, Tumor suppressor genes, Apoptosis genes, and DNA repair genes which alter the normal cell division processes.
Describe the effect of tobacco, alcohol, radiation exposure, and diet and obesity on carcinogenesis.
Tobacco is itself a carcinogen, therefore, inhabiting the carcinogenetic exposure can help in preventing cancer by reducing exposure to these carcinogens. Nicotine in tobacco is not carcinogenic but smoking delivers carcinogens and toxicants into the lungs. Create smoke carcinogens include carbonations or epoxides react with DNA to form DNA addicts necessary for the carcinogenic process causing mutations.
Alcohol also has a local carcinogenetic effect. Ethanol is alcohol and ethanol is a mutagen and it has a metabolic effect. Acetaldehyde is highly carcinogenic and has the potential of cytotoxic effect in the local cells that line the mouth, pharynx, and esophagus making them more vulnerable to the genotypic activity of the DNA damaging agents. Radiation carcinogenesis through ionizing radiation causes mutation in the phenotypes leading to the loss of cell death control and apoptosis. In most cases, apoptosis less to uncontrolled cancerous growth
Radiation indices mutation by inducing mutation and deletion. When energy is absorbed from the ionizing radiation, the genetic materials in the cells are damaged and this damages the DNA leading to cell death. In most cases, chromosomes aberration and genetic mutation are caused by radiating
Obesity and carcinogenesis are also significantly correlated. For example, inflammatory changes cause macrophage polarization and alter the adipokine profile of the cells. Insulin resistances develop as a result of obesity (Bruyere, 2015). Whenever there are changes in the metabolism in the presence of free fatty acids (FFA), dancer development is I nitrated. Free fatty acids have monogenic signals that can be increased by the increase in fatty acids syntheses (FASN). In women suffering from breast cancer, and ovarian tumors, cancer is the main precursor lesion because of the increased fatty acids syntheses activity (Herceg et al., 2017). To reduce the proliferation of cancer cells, the FASN activity is inhibited which means that free fatty acid is a major energy source for the cancer cells.
References
Path physiology: The biologic basis for disease in adults and children (7th Ed.). St. Louis: Mosby. ISBN 978-0323088541
Bruyere, H. (2015). Essentials of Pathophysiology + 100 Case Studies in Pathophysiology. Lippincott Williams & Wilkins.
Casey, S., Vaccari, M., Al-Mulla, F., Al-Temaimi, R., Amedei, A., & Barcellos-Hoff, M. et al. (2015). The effect of environmental chemicals on the tumor microenvironment. Carcinogenesis, 36(Suppl 1), S160-S183. doi: 10.1093/carcin/bgv035
Herceg, Z., Ghantous, A., Wild, C., Sklias, A., Casati, L., & Duthie, S. et al. (2017). Roadmap for investigating epigenome deregulation and environmental origins of cancer. International Journal Of Cancer, 142(5), 874-882. doi: 10.1002/ijc.31014
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