Lung cancer is recognized as a leading cause of cancer-related death worldwide and its frequency is still increasing. The prognosis in lung cancer is poor and limited by the difficulties of diagnosis at early stage of disease, when it is amenable to surgery treatment. Therefore, the advance in identification of lung cancer genetic and epigenetic markers with diagnostic and/or prognostic values becomes an important tool for future molecular oncology and personalized therapy. As in case of other tumors, aberrant epigenetic landscape has been documented also in lung cancer, both at early and late stage of carcinogenesis. Hypermethylation of specific genes, mainly tumor suppressor genes, as well as hypomethylation of oncogenes and retrotransposons, associated with histopathological subtypes of lung cancer, has been found. Epigenetic aberrations of histone proteins and, especially, the lower global levels of histone modifications have been associated with poorer clinical outcome in lung cancer. The recently discovered role of epigenetic modifications of microRNA expression in tumors has been also proven in lung carcinogenesis. The identified epigenetic events in lung cancer contribute to its specific epigenotype and correlated phenotypic features. So far, some of them have been suggested to be cancer biomarkers for early detection, disease monitoring, prognosis, and risk assessment. As epigenetic aberrations are reversible, their correction has emerged as a promising therapeutic target.

Comorbidity is the occurrence of concomitant disease in addition to an index disease of interest or the simultaneous occurrence of multiple diseases in an individual. Lung cancer is associated with age and smoking, and both age and smoking are strongly associated with comorbidity. Lung cancer is the most common malignancy in the world. Comorbidity, such as diseases of cardiovascular, pulmonary and other systems may influence prognosis in lung cancer as well as complicate its treatment. In this paper we tried to conclude the significance of the individual comorbidities in lung cancer and their impact on particular treatment method.

Tumours are characterised by an ability to avoid immune destruction and the presence of cancer-associated inflammation. Better understanding of the link between lung cancer and such inflammation is vital for early detection and personalized treatment. Thus, we examined the mRNA expression of interleukins IL-1β, IL-6, IL-17 and miR-9, miR-122 as potential useful biomarkers of NSCLC. Tumour tissues, non-cancerous tissue and blood samples were collected from 39 patients with primary NSCLC undergoing surgical treatment. The selected RNA was isolated from tissue samples and selected miRNAs from peripheral blood exosomes. This RNA was transcribed to cDNA and quantified using RT-qPCR. Significantly higher expression of the selected interleukins was observed in non-cancerous than tumour tissue, and IL-6 was significantly higher in the tumour tissue of patients with a history of ≤ 40 pack-years (PYs) (2.197, IQR: 0.821–4.415) than in those with > 40 PYs (0.461, IQR: 0.372–0.741; p = 0.037). It is clear that inflammatory processes play a role in NSCLC, as indicated by the upregulation of IL-1β and IL-6 in tumour and adjacent tissue, and that smoking has a strong influence on inflammation in tumourigenesis, demonstrated by the upregulation of IL-6 in tumour samples among patients with ≤ 40 PYs compared to > 40 PYs.

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A prenatal sex steroid environment of high prenatal testosterone and low prenatal oestrogen inhibits lung development and may predispose individuals to be vulnerable to lung disease in later life. Therefore, the aim of this report was to investigate whether there is an association between right and left 2D:4D (biomarker of prenatal sex steroids exposure) and primary lung cancer in women and men. Also, we considered the relationship between right-left 2D:4D (Δ2D:4D, a negative correlate of high prenatal testosterone and low prenatal oestrogen) and the age of lung cancer diagnosis. The study included 109 patients (61 men) with lung cancer and 197 controls (78 men). In the study we found that: (i) women with lung cancer have lower 2D:4D compared to controls (the effect was independent of smoking), (ii) among women with cancer, age at diagnosis was positively related to 2D:4D, i.e. women with masculinized 2D:4D present earlier with the cancer than women with feminized 2D:4D, (iii) among men with lung cancer, those with the most aggressive form (small-cell lung cancer) had masculinized (low) Δ2D:4D compared to those with the less aggressive form (non-small cell lung cancer). The data suggests that masculinized right 2D:4D and Δ2D:4D are associated with a predisposition to lung cancer and/or the more aggressive forms of lung cancer. Among both women and men, lung cancer is the leading cause of cancer death and in most nations, it is the most frequent neoplasm among men 1,2. The incidence of lung cancer is both age-and sex-dependent. With regard to age, rates are low in people younger than 40 years but with increases up to the age of 75-80 years. However, with regard to sex, lung cancer rates have tended to show a decline in men but an increase among women. An important causal factor in these patterns is smoking practices 3-5. The comparisons between those that smoke and never-smokers regularly show 20 to 50-fold increases in risk for the former. Moreover, duration of smoking is a strong correlate of lung cancer risk 6 and sex dependent changes in mortality reflects changes in rates of smoking among age-cohorts of women and men 7,8. However, there are risk factors other than smoking and these include various single nucleotide polymorphisms, family history, diet, alcohol, chronic lung diseases, occupational factors, air pollution and hormonal factors 9-13. With regard to hormonal factors, postnatal effects of endogenous sex steroids may have an influence on lung cancer risk. Receptors for oestrogen and progesterone are expressed in lung cells, of both normal and lung cancer lines. Oestradiol causes proliferation of lung cancer cells as do combinations of oestrogen and progesterone. The latter combination facilitates secretion of vascular endothelial growth factors and increases numbers of progenitor tumour cells 14,15. Local production of oestrogens in the lung, either by lung cells or by infiltrating macrophages and other inflammatory cells, may be a significant source of oestrogen that could drive the tumour process, i...