Smoking is a major risk factor for lung cancer and the mortality is very high: 87% of patients eventually die. Moreover, lung cancer is still the number one cause of cancer-related deaths worldwide, despite ever-evolving new treatment options. Although lung cancer is strongly associated with cigarette smoking, nevertheless only about 15% of smokers are diagnosed with lung cancer, and a proportion of never-smokers develops this malignancy as well. Interestingly, the proportion of never-smokers among Asian patients is higher than in Caucasians. Environmental factors other than smoking include air pollution and smog, occupational circumstances, second-hand tobacco smoke, cooking oil fumes (particularly in Asian women), smoke from domestic combustion for heating, radon in uranium miners, and some rare infections and pulmonary inflammatory diseases. Gender differences in the prevalence and histology of lung cancer were observed, which may be explained by differences in lifestyle (including smoking behavior) and occupation as well as by the presence of two X chromosomes containing the largest number of immune-related genes and micro-RNAs.
Expression of many genes is different in smoking versus never-smoking lung cancer patients. Polymorphisms of several genes have been found to be risk factors in never- or light smokers but tended to be protective in heavy smokers. There are also differences in de-novo gene mutations and their frequencies in smokers as compared to never-smokers bearing lung cancer, as well as in Caucasian versus Asian and some Latin American populations.
Genetic changes are reflected in changes in proteins expressed and presented on the surface of tumor cells. These changes may be recognized by elements of both the innate and adaptive immune system, and malignant cells may be eliminated by them. This depends on the HLA class I (HLA-I) molecule expression level and repertoire of antigenic peptides bound and presented by HLA-I molecules on the surface of tumor cells. Antigen presentation by HLA-I glycoproteins depends on genetics of the extremely polymorphic HLA-I molecules themselves, on differential expression and/or activity of antigen-processing machinery (APM) elements due to some polymorphisms of their genes, and on regulatory effects of other molecules.
Smoking is also a most common, but not the only cause of another prevalent lung disease: the chronic obstructive pulmonary disease (COPD), a complex and heterogeneous disease characterized by persistent respiratory symptoms and irreversible airflow limitation. The proportion of smokers and never-smokers among COPD patients is similar to the proportion in lung cancer patients. Other causative factors of COPD are air pollution, biomass fuel smoke, occupational exposure to organic and inorganic dust, chemicals, and smoke exposure resulting from work in agriculture, mining, or heavy industry. Also, a previous history of tuberculosis is a risk factor. COPD is not curable, and patients are mainly treated with long-acting bronchodilators and, in specific cases, with inhaled corticosteroids, but immunotherapy has not been applied yet.
Interestingly, about 25% of COPD patients suffer also from lung cancer, and 40–70% of lung cancer patients have COPD as comorbidity.
With this research topic, we aim to collect recent advances in our understanding of lung cancer and COPD etiology, pathophysiology, genetics, and therapy prospects. We will collect Original Research, Review, Mini-review, and Method articles on, but not limited to, the following topics:
• Immuno-histological types of lung cancer: differences between smokers and never-smokers
• Environmental factors of lung cancer risk in smokers and never-smokers
• Gene expression in lung cancer of smokers and never-smokers
• Associations of germ-line gene polymorphisms with lung cancer in smokers and never-smokers
• Somatic gene mutations in lung cancer in smokers and never-smokers
• Treatment options for lung cancer in smokers and never-smokers
• Comparison of immune-markers for lung cancer in smokers and never-smokers with those suffering from COPD
• Immune response parameters in lung cancer and COPD in smokers versus never-smokers
• Future treatment options for COPD: is immunotherapy possible?
Manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (clinical cohort or biological validation in vitro or in vivo) are out of scope for this section.
Smoking is a major risk factor for lung cancer and the mortality is very high: 87% of patients eventually die. Moreover, lung cancer is still the number one cause of cancer-related deaths worldwide, despite ever-evolving new treatment options. Although lung cancer is strongly associated with cigarette smoking, nevertheless only about 15% of smokers are diagnosed with lung cancer, and a proportion of never-smokers develops this malignancy as well. Interestingly, the proportion of never-smokers among Asian patients is higher than in Caucasians. Environmental factors other than smoking include air pollution and smog, occupational circumstances, second-hand tobacco smoke, cooking oil fumes (particularly in Asian women), smoke from domestic combustion for heating, radon in uranium miners, and some rare infections and pulmonary inflammatory diseases. Gender differences in the prevalence and histology of lung cancer were observed, which may be explained by differences in lifestyle (including smoking behavior) and occupation as well as by the presence of two X chromosomes containing the largest number of immune-related genes and micro-RNAs.
Expression of many genes is different in smoking versus never-smoking lung cancer patients. Polymorphisms of several genes have been found to be risk factors in never- or light smokers but tended to be protective in heavy smokers. There are also differences in de-novo gene mutations and their frequencies in smokers as compared to never-smokers bearing lung cancer, as well as in Caucasian versus Asian and some Latin American populations.
Genetic changes are reflected in changes in proteins expressed and presented on the surface of tumor cells. These changes may be recognized by elements of both the innate and adaptive immune system, and malignant cells may be eliminated by them. This depends on the HLA class I (HLA-I) molecule expression level and repertoire of antigenic peptides bound and presented by HLA-I molecules on the surface of tumor cells. Antigen presentation by HLA-I glycoproteins depends on genetics of the extremely polymorphic HLA-I molecules themselves, on differential expression and/or activity of antigen-processing machinery (APM) elements due to some polymorphisms of their genes, and on regulatory effects of other molecules.
Smoking is also a most common, but not the only cause of another prevalent lung disease: the chronic obstructive pulmonary disease (COPD), a complex and heterogeneous disease characterized by persistent respiratory symptoms and irreversible airflow limitation. The proportion of smokers and never-smokers among COPD patients is similar to the proportion in lung cancer patients. Other causative factors of COPD are air pollution, biomass fuel smoke, occupational exposure to organic and inorganic dust, chemicals, and smoke exposure resulting from work in agriculture, mining, or heavy industry. Also, a previous history of tuberculosis is a risk factor. COPD is not curable, and patients are mainly treated with long-acting bronchodilators and, in specific cases, with inhaled corticosteroids, but immunotherapy has not been applied yet.
Interestingly, about 25% of COPD patients suffer also from lung cancer, and 40–70% of lung cancer patients have COPD as comorbidity.
With this research topic, we aim to collect recent advances in our understanding of lung cancer and COPD etiology, pathophysiology, genetics, and therapy prospects. We will collect Original Research, Review, Mini-review, and Method articles on, but not limited to, the following topics:
• Immuno-histological types of lung cancer: differences between smokers and never-smokers
• Environmental factors of lung cancer risk in smokers and never-smokers
• Gene expression in lung cancer of smokers and never-smokers
• Associations of germ-line gene polymorphisms with lung cancer in smokers and never-smokers
• Somatic gene mutations in lung cancer in smokers and never-smokers
• Treatment options for lung cancer in smokers and never-smokers
• Comparison of immune-markers for lung cancer in smokers and never-smokers with those suffering from COPD
• Immune response parameters in lung cancer and COPD in smokers versus never-smokers
• Future treatment options for COPD: is immunotherapy possible?
Manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (clinical cohort or biological validation in vitro or in vivo) are out of scope for this section.
