No abstract

BACKGROUND: Sleep disorders have emerged as potential cancer risk factors. OBJECTIVE: This review discusses the relationships between sleep, obesity, and breathing disorders with concomitant risks of developing cancer. RESULTS: Sleep disorders result in abnormal expression of clock genes, decreased immunity, and melatonin release disruption. Therefore, these disorders may contribute to cancer development. Moreover, in sleep breathing disorder, which is frequently experienced by obese persons, the sufferer experiences intermittent hypoxia that may stimulate cancer cell proliferation. DISCUSSION: During short- or long- duration sleep, sleep-wake rhythm disruption may occur. Insomnia and obstructive sleep apnea increase cancer risks. In short sleepers, an increased risk of stomach cancer, esophageal squamous cell cancer, and breast cancer was observed. Among long sleepers (>9 hours), the risk of some hematologic malignancies is elevated. CONCLUSION: Several factors including insomnia, circadian disruption, obesity, and intermittent hypoxia in obstructive sleep apnea are contributing risk factors for increased risk of several types of cancers. However, further studies are needed to determine the more significant of these risk factors and their interactions.

Background/Aim: Although genetic factors are presumed to account only for a part of the inter-individual variation in lung cancer susceptibility, the results are conflicting and there are no data available regarding the Polish population. We, therefore, performed a case-control study to investigate the association of seven selected single nucleotide polymorphisms (SNPs), in genes coding for excision repair cross-complimentary group 1 (ERCC1: rs11615, rs3212986, rs2298881), nuclear factor ĸB (NFKB2: rs7897947, rs12769316), bone morphogenetic protein 4 (BMP4: rs1957860), complement receptor 1 (CR1: rs7525160) and del/ins polymorphism in the family hypoxia inducible factor 2 gene (EGLN2: rs10680577), with non-small cell lung cancer (NSCLC) risk. Materials and Methods: Real-time PCR with melting curve analysis was used for genotyping of NSCLC patients and healthy individuals of Polish origin. Results: The ERCC1 rs11615 T allele and rs3212986 GG homozygosity were found to be associated with a higher risk of developing NSCLC. In addition, NFKB2 rs12769316 GG homozygosity was more frequently detected among male patients than controls, while no significant differences were found between the five polymorphisms. Conclusion: ERCC1 polymorphisms may affect NSCLC risk in the Polish population, while the NFKB2 variant may be a possible marker of the disease in males.

Introduction: Lung cancer belongs to the most common carcinoma worldwide and is the leading cause of cancer-related death. Bone morphogenetic protein-4 (BMP-4) is extracellular signaling molecule involved in many important processes, including cell proliferation and mobility, apoptosis and angiogenesis. Thrombospondin-1 (TSP-1) belongs to the extracellular matrix proteins. It participates in the cell-to-cell and cell-to-matrix interactions and thus plays important role in tumor microenvironment for cancer development and metastasis formation. Aim: To investigate serum levels of TSP-1 and BMP-4 together with BMP-4 polymorphism in lung cancer patients. Material and Methods: A total of 111 patients (76 men) with newly diagnosed lung cancer, including 102 patients with non-small cell lung cancer and 9 patients with small-cell lung cancer. Advanced stage of lung cancer was diagnosed in 99 (89%) of patients: stage IV—in 48, stage IIIB—in 33, stage IIIA—in 18 patients; there were six patients with stage II and six patients with stage I. The control group consisted of 61 healthy persons. In all the subjects, serum levels of BMP-4 and TSP-1 were measured by ELISA. With a Real-Time PCR system genotyping of BMP-4 was performed. Results: BMP-4 and TSP-1 serum levels were significantly lower in the patients with lung cancer than in the controls (TSP-1:10,109.2 ± 9581 ng/mL vs. 11,415.09 ± 9781 ng/mL, p < 0.05; BMP-4: 138.35 ± 62.59 pg/mL vs. 226.68 ± 135.86 pg/mL p < 0.001). In lung cancer patients TSP-1 levels were lower in advanced stages (9282.07 ± 4900.78 ng/mL in the stages III-IV vs. 16,933.60 ± 6299.02 ng/mL in the stages I-II, p < 0.05) and in the patients with than without lymph nodes involvement (10,000.13 ± 9021.41 ng/mL vs. 18,497.75 ± 12,548.25 ng/mL, p = 0.01). There was no correlation between TSP-1 and BMP-4 serum levels. BMP-4 gene polymorphism did not influence the results of the study. Conclusion: Decreased levels of TSP-1 and BMP-4 may serve as potential indices of lung cancer, with additional importance of low TSP-1 level as a marker of advanced stage of the disease.

Background: Obstructive sleep apnea (OSA) and chronic obstructive pulmonary disease (COPD) may lead to chronic alveolar hypoventilation. The coexistence of OSA and COPD has been termed the ‘overlap syndrome’. The aim of the study was to determine the relationship between the severity of COPD and the occurrence of chronic alveolar hypoventilation in patients with OSA and to evaluate the impact of chronic alveolar hypoventilation in patients with the overlap syndrome on the severity of breathing disorders during sleep. Material and methods: The study included 64 obese patients (BMI 40.0 ± 6.5 kg/m2) with OSA (AHI > 15; mean AHI 52 ± 22) coexisting with COPD. We analysed the results of polysomnography, spirometry and arterial blood gas analysis. Results: Chronic alveolar hypoventilation was present in 67% of the patients, including 60.5%, 85% and 100% of patients with moderate, severe and very severe COPD by spirometry, respectively. Patients with chronic alveolar hypoventilation had lower values of FVC (2.7 ± 0.8 l vs. 3.6 ± 0.9 l; p < 0.001), FEV1 (1.7 ± 0.6 l vs. 2.2 ± 0.5 l; p < 0.001) and mean SaO2 at the end of obstructive sleep apneas and hypopneas (75% ± 10% vs. 84% ± 5%; p < 0.001). Conclusions: Chronic alveolar hypoventilation is observed in the majority of obese patients with moderate to severe OSA and coexisting COPD, including moderate COPD. The occurrence of chronic alveolar hypoventilation in obese patients with OSA coexisting with COPD is associated with a marked arterial hypoxia during obstructive sleep apneic and hypopneic episodes.