Biological and Genetic Mechanisms of COPD, Its Diagnosis, Treatment, and Relationship with Lung Cancer

Abstract

Chronic obstructive pulmonary disease (COPD) is one of the most prevalent chronic adult diseases, with significant worldwide morbidity and mortality. Although long-term tobacco smoking is a critical risk factor for this global health problem, its molecular mechanisms remain unclear. Several phenomena are thought to be involved in the evolution of emphysema, including airway inflammation, proteinase/anti-proteinase imbalance, oxidative stress, and genetic/epigenetic modifications. Furthermore, COPD is one main risk for lung cancer (LC), the deadliest form of human tumor; formation and chronic inflammation accompanying COPD can be a potential driver of malignancy maturation (0.8–1.7% of COPD cases develop cancer/per year). Recently, the development of more research based on COPD and lung cancer molecular analysis has provided new light for understanding their pathogenesis, improving the diagnosis and treatments, and elucidating many connections between these diseases. Our review emphasizes the biological factors involved in COPD and lung cancer, the advances in their molecular mechanisms’ research, and the state of the art of diagnosis and treatments. This work combines many biological and genetic elements into a single whole and strongly links COPD with lung tumor features.

The Impact of Fine Particulate Matters (PM10, PM2.5) from Incense Smokes on the Various Organ Systems: A Review of an Invisible Killer

“…[ 133,134 ] COPD is a coronary lung disease normally observed in cigarette smokers. [ 135 ] This finding agrees with other studies that demonstrate a cigarette smoke has a similar health risk to incense smoke. Several studies have confirmed that households having a culture of daily incense burning have their residents at a 12% greater risk of cardiac disorders.…”

Effectiveness of Immunotherapy in Non-Small Cell Lung Cancer Patients with a Diagnosis of COPD: Is This a Hidden Prognosticator for Survival and a Risk Factor for Immune-Related Adverse Events?

“…Epigenetic modifications, such as DNA methylation/demethylation and histone acetylation, can alter the gene expression patterns in both COPD and NSCLC [97]. Aberrant epigenetic marks can affect the function of genes involved in inflammation, cell cycle regulation, and DNA repair, among others.…”

Respiratory Tract Oncobiome in Lung Carcinogenesis: Where Are We Now?

“…The harmful substances present in cigarette smoke and air pollution (mainly particulate matter-PM 2.5), apart from directly damaging cells and tissues in the respiratory system, lead to an increased production of reactive oxygen species (ROS) and cause an oxidant-antioxidant imbalance. Smoking, additionally, decreases the effectiveness of antioxidants like glutathione peroxidase (GPx), which help neutralize ROS and maintain the balance between oxidants and antioxidants [37,38]. An increasing number of free radicals can harm critical metabolic pathways within bacteria-also those naturally present in that niche-weakening their ability to survive and thrive in the lung environment.…”