Increased PARP Activity and DNA Damage in NSCLC Patients: The Influence of COPD

Tang, Jun; Curull, Víctor; Wang, Xuejie; Ampurdanés, Coral; Duran, Xavier; Pijuán, Lara; Rodríguez-Fuster, Alberto; Aguiló, Rafael; Yélamos, José; Barreiro, Esther

doi:10.3390/cancers12113333

Cited by 3 publications

(4 citation statements)

References 43 publications

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“…Results showed that patients with COPD and cancer had an increase in the DNA damage marker levels compared to those with cancer but without COPD. However, in contrast to the findings of our research, active smoking was not a criterion for inclusion of samples, allowing statistically significant differences between groups in relation to tobacco use [33].…”

Section: Plos Onecontrasting

confidence: 99%

“…Our results showed that patients with COPD and lung cancer did not have a significant increase in DNA damage than that in the patients with COPD. Although these results indicate that the previous state of COPD without the initial presence of cancer does not determine further damage to DNA to influence the development of cancer, Tang et al showed opposite results, inferring that the patients with lung cancer and COPD had increased levels of DNA damage markers than patients with lung cancer alone [ 33 ].…”

Section: Discussionmentioning

confidence: 99%

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DNA damage and antioxidant capacity in COPD patients with and without lung cancer

et al. 2022

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Background and objective Chronic obstructive pulmonary disease (COPD) is characterized by chronic inflammation of the lower airways, and COPD patients show two to five times higher risk of lung cancer than smokers with normal lung function. COPD is associated with increased oxidative stress, which may cause DNA damage and lung carcinogenesis. Our aim was to evaluate DNA damage and oxidative stress (lipid peroxidation and antioxidant status) and their relationship in patients with COPD with and without lung cancer. Methods We evaluated 18 patients with COPD, 18 with COPD with lung cancer, and 18 controls (former or current smokers). DNA damage was evaluated in peripheral blood lymphocytes using a comet assay; the concentration of malondialdehyde (MDA) and hydrophilic antioxidant performance (HAP) were measured in the plasma. Results DNA damage was higher in patients with COPD with cancer than in the controls (p = 0.003). HAP was significantly lower in patients with COPD with cancer than in those without cancer and controls. The presence of lung cancer and COPD showed a positive association with DNA strand breaks and the concentration of MDA. Conclusion COPD with lung cancer was associated with elevated DNA damage in peripheral lymphocytes, and cancer and COPD showed a positive correlation with DNA damage. The antioxidant capacity showed a negative association with the interaction COPD and cancer and presence of COPD. The mechanisms underlying the increased incidence of lung cancer in COPD are unknown; DNA damage may be involved. Further research may provide insights into their development and treatment.

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Section: Plos Onecontrasting

confidence: 99%

Section: Discussionmentioning

confidence: 99%

DNA damage and antioxidant capacity in COPD patients with and without lung cancer

et al. 2022

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“…In patients with COPD, particularly in emphysema phenotype, LC development was five times greater than in smokers with no COPD [4,5]. Recently, our group and others have demonstrated the implications of relevant biological mechanisms in the increased LC predisposition seen in patients with COPD [6][7][8][9][10][11][12][13].…”

Section: Introductionmentioning

confidence: 87%

Systemic Profiles of microRNAs, Redox Balance, and Inflammation in Lung Cancer Patients: Influence of COPD

et al. 2021

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Lung cancer (LC) risk increases in patients with chronic respiratory diseases (COPD). MicroRNAs and redox imbalance are involved in lung tumorigenesis in COPD patients. Whether systemic alterations of those events may also take place in LC patients remains unknown. Our objectives were to assess the plasma levels of microRNAs, redox balance, and cytokines in LC patients with/without COPD. MicroRNAs (RT-PCR) involved in LC, oxidized DNA, MDA-protein adducts, GSH, TEAC, VEGF, and TGF-beta (ELISA) were quantified in plasma samples from non-LC controls (n = 45), LC-only patients (n = 32), and LC-COPD patients (n = 91). In LC-COPD patients compared to controls and LC-only, MDA-protein adduct levels increased, while those of GSH decreased, and two patterns of plasma microRNA were detected. In both LC patient groups, miR-451 expression was downregulated, while those of microRNA-let7c were upregulated, and levels of TEAC and TGF-beta increased compared to the controls. Correlations were found between clinical and biological variables. A differential expression profile of microRNAs was detected in patients with LC. Moreover, in LC patients with COPD, plasma oxidative stress levels increased, whereas those of GSH declined. Systemic oxidative and antioxidant markers are differentially expressed in LC patients with respiratory diseases, thus implying its contribution to the pathogenesis of tumorigenesis in these patients.

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“…Several biological mechanisms have been shown to participate in the greater risk for LC development in COPD patients [ 5 ]. For instance, increased oxidative stress [ 6 ], inflammation including a differential inflammatory profile [ 7 ], epigenetics abnormalities [ 8 ] and the pattern of expression of stroma markers [ 9 ] have all been demonstrated to be differentially expressed in tumours of patients with mild-to-moderate COPD. In addition, overall survival was also shown to be significantly altered on the basis of the inflammatory profile in lung tumours of patients with underlying COPD compared to LC patients without COPD [ 10 ].…”

Section: Introductionmentioning

confidence: 99%

Gene expression profile of epithelial–mesenchymal transition in tumours of patients with nonsmall cell lung cancer: the influence of COPD

et al. 2022

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Epithelial-mesenchymal transition (EMT) is involved in the pathophysiology of lung cancer (LC) and chronic obstructive pulmonary disease (COPD), and the latter is an important risk factor for LC. We hypothesized that gene expression profile of EMT and signaling cascade may differ in LC patients with COPD from those with no respiratory diseases. In lung tumor specimens obtained through video-assisted thoracoscopic surgery (VATS) from LC (n=20, control group) and LC-COPD patients (n=30), gene expression (qRT-PCR) of EMT markers: SMAD3, SMAD4, ZEB2, TWIST1, SNAI1, ICAM1, VIM, CDH2, MMP1, and MMP9 were detected. In lung tumors of LC-COPD compared to LC patients, gene expression of SMAD3, SMAD4, ZEB2, and CDH2 significantly declined, while no significant differences were detected for the other analyzed markers. A significant correlation was found between packs-years (smoking burden) and SMAD3 gene expression among LC-COPD patients. LC-COPD patients exhibited mild-to-moderate airway obstruction and a significant reduction in diffusion capacity compared to LC patients. In lung tumor samples of patients with COPD, several markers of EMT expression, namely SMAD3, SMAD4, ZEB2, and CDH2 were differentially expressed suggesting that these markers are likely to play a role in the regulation of EMT in patients with this respiratory disease. Cigarette smoke did not seem to influence the expression of EMT markers in this study. These results have potential clinical implications in the management of patients with LC, particularly in those with underlying respiratory diseases.

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Increased PARP Activity and DNA Damage in NSCLC Patients: The Influence of COPD

Cited by 3 publications

References 43 publications

DNA damage and antioxidant capacity in COPD patients with and without lung cancer

DNA damage and antioxidant capacity in COPD patients with and without lung cancer

Systemic Profiles of microRNAs, Redox Balance, and Inflammation in Lung Cancer Patients: Influence of COPD

Gene expression profile of epithelial–mesenchymal transition in tumours of patients with nonsmall cell lung cancer: the influence of COPD

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