Oncogenetics of Lung Cancer Induced by Environmental Carcinogens

Abstract

The molecular landscape of non-tobacco-induced primary lung tumors displays specific oncogenetic features. The etiology of these tumors has been largely associated with exposure to well-established environmental lung carcinogens such as radon, arsenic, and asbestos. Environmental carcinogens can induce specific genetic and epigenetic alterations in lung tissue, leading to aberrant function of lung cancer oncogenes and tumor suppressor genes. These molecular events result in the disruption of key cellular mechanisms, such as protection against oxidative stress and DNA damage-repair, which promotes tumor development and progression. This chapter provides a comprehensive discussion of the specific carcinogenic mechanisms associated with exposure to radon, arsenic, and asbestos. It also summarizes the main protein-coding and non-coding genes affected by exposure to these environmental agents, and the underlying molecular mechanisms promoting their deregulation in lung cancer. Finally, the chapter examines the anticipated challenges in personalized intervention strategies in non-tobacco-induced lung cancer.

Role of microRNAs in Lung Carcinogenesis Induced by Asbestos

“…Carcinogenic environmental factors, such as air pollution and air emissions from fuel combustion as well as environmental exposure to radon, asbestos, certain metals (such as chromium, cadmium, and arsenic), and some organic chemicals, also contribute to the development of lung cancer [ 8 ]. Environmental carcinogens can cause specific genetic and epigenetic changes in lung tissue, leading to aberrant functions of lung cancer oncogenes and tumor suppressor genes [ 9 ].…”