Telomere length, COPD and emphysema as risk factors for lung cancer

de-Torres, Juan P.; Sánchez-Salcedo, Pablo; Bastarrika, Gorka; Alcaide, Ana B.; Pı́o, Rubén; Pajares, María J.; Campo, Arantza; Bertó, Juan; Montuenga, Luis M.; Ocón, María del Mar; Monente, Carmen; Celli, Bartolomé R.; Zulueta, Javier

doi:10.1183/13993003.01521-2016

Cited by 15 publications

(10 citation statements)

References 15 publications

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“…Earlier reports from our laboratory and others have shown that smoking and COPD is associated with the mitochondrial damage and dysfunction, altering the process of cellular metabolism and function (Ahmad et al, 2015;Lerner et al, 2016). Similarly, telomere dysfunction was also associated with smoking and COPD (Morla et al, 2006;de-Torres et al, 2017). Mitochondrial and telomere dysfunction also play a causative role in the progression of IPF (Povedano et al, 2015;Molina-Molina and Borie, 2018;Zank et al, 2018).…”

Section: Introductionmentioning

confidence: 76%

Age-Dependent Assessment of Genes Involved in Cellular Senescence, Telomere, and Mitochondrial Pathways in Human Lung Tissue of Smokers, COPD, and IPF: Associations With SARS-CoV-2 COVID-19 ACE2-TMPRSS2-Furin-DPP4 Axis

Maremanda

Sundar

et al. 2020

Front. Pharmacol.

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Background: Aging is one of the key contributing factors for chronic obstructive pulmonary diseases (COPD) and other chronic inflammatory lung diseases. Here, we determined how aging contributes to the altered gene expression related to mitochondrial function, cellular senescence, and telomeric length processes that play an important role in the progression of COPD and idiopathic pulmonary fibrosis (IPF). Methods: Total RNA from the human lung tissues of non-smokers, smokers, and patients with COPD and IPF were processed and analyzed using a Nanostring platform based on their ages (younger: <55 years and older: >55 years). Results: Several genes were differentially expressed in younger and older smokers, and patients with COPD and IPF compared to non-smokers which were part of the mitochondrial biogenesis/

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Section: Introductionmentioning

confidence: 76%

Age-Dependent Assessment of Genes Involved in Cellular Senescence, Telomere, and Mitochondrial Pathways in Human Lung Tissue of Smokers, COPD, and IPF: Associations With SARS-CoV-2 COVID-19 ACE2-TMPRSS2-Furin-DPP4 Axis

Maremanda

Sundar

et al. 2020

Front. Pharmacol.

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“…It is well-established that lung cancer is more prevalent in (old) patients with COPD ( 59 ). Whether or not our observation of a different co-regulation of TL and mtDNA-CN in old patients with COPD relates to their higher incidence of lung cancer deserves further investigation ( 60 ).…”

Section: Discussionmentioning

confidence: 96%

Telomere Length but Not Mitochondrial DNA Copy Number Is Altered in Both Young and Old COPD

et al. 2021

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Accelerated ageing is implicated in the pathogenesis of respiratory diseases as chronic obstructive pulmonary disease (COPD), but recent evidence indicates that the COPD can have roots early in life. Here we hypothesise that the accelerated ageing markers might have a role in the pathobiology of young COPD. The objective of this study was to compare two hallmarks of ageing, telomere length (TL), and mitochondrial DNA copy number (mtDNA-CN, as a surrogate marker of mitochondrial dysfunction) in young (≤ 50 years) and old (>50 years) smokers, with and without COPD. Both, TL and mtDNA-CN were measured in whole blood DNA by quantitative PCR [qPCR] in: (1) young ever smokers with (n = 81) or without (n = 166) COPD; and (2) old ever smokers with (n = 159) or without (n = 29) COPD. A multivariable linear regression was used to assess the association of TL and mtDNA-CN with lung function. We observed that in the entire study population, TL and mtDNA-CN decreased with age, and the former but not the latter related to FEV1/FVC (%), FEV1 (% ref.), and DLCO (% ref.). The short telomeres were found both in the young and old patients with severe COPD (FEV1 <50% ref.). In addition, we found that TL and mtDNA-CN were significantly correlated, but their relationship was positive in younger while negative in the older patients with COPD, suggesting a mitochondrial dysfunction. We conclude that TL, but not mtDNA-CN, is associated with the lung function impairment. Both young and old patients with severe COPD have evidence of accelerated ageing (shorter TL) but differ in the direction of the correlation between TL and mtDNA-CN in relation to age.

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“…Some studies reported that deregulations of the LRP1B gene are associated with resistance to chemotherapy and worse survival in cancer [27,28]. Other studies discovered several mechanisms mediating lung cancer development in patients with COPD, such as telomere shortening [29,30], oxidative stress [31] and chronic inflammation [32]. Although increasing understandings of carcinogenesis and genomic pathways of COPD lung cancer have been made, there still no available targeting therapy directly to treat these devastated patients.…”

Section: Discussionmentioning

confidence: 99%

Presence of Chronic Obstructive Pulmonary Disease (COPD) Impair Survival in Lung Cancer Patients Receiving Epidermal Growth Factor Receptor-Tyrosine Kinase Inhibitor (EGFR-TKI): A Nationwide, Population-Based Cohort Study

Rau

Lee

et al. 2019

JCM

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The emergence of epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) caused a paradigm shift in the treatment of non-small cell lung cancer (NSCLC). Although several clinicopathologic factors to predict the response to and survival on EGFR-TKI were recognized, its efficacy has not been confirmed for patients with underlying pulmonary disease, such as chronic obstructive pulmonary disease (COPD). We conducted the study to evaluate the impact of COPD on survival for NSCLC patients that underwent EGFR-TKI treatment. The nationwide study obtained clinicopathologic data from the National Health Insurance Research Database in Taiwan between 1995 and 2013. Patients receiving EGRR-TKI were divided into COPD and non-COPD groups, and adjusted for age, sex, comorbidities, premium level and cancer treatments. Overall survival (OS) and progression-free survival (PFS) were calculated by Kaplan–Meier analysis. In total, 21,026 NSCLC patients were enrolled, of which 47.6% had COPD. After propensity score (PS) matching, all covariates were adjusted and balanced except for age (p < 0.001). In the survival analysis, the median OS (2.04 vs. 2.28 years, p < 0.001) and PFS (0.62 vs. 0.69 years, p < 0.001) of lung cancer with COPD were significantly worse than those without COPD. Lung cancer patients on EGFR-TKI treatment had a worse survival outcome if patients had pre-existing COPD.

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Telomere length, COPD and emphysema as risk factors for lung cancer

Abstract: Telomeres are DNA-protein structures that protect chromosome ends from degradation and shorten progressively with each cell division [1].

Cited by 15 publications

References 15 publications

Age-Dependent Assessment of Genes Involved in Cellular Senescence, Telomere, and Mitochondrial Pathways in Human Lung Tissue of Smokers, COPD, and IPF: Associations With SARS-CoV-2 COVID-19 ACE2-TMPRSS2-Furin-DPP4 Axis

Age-Dependent Assessment of Genes Involved in Cellular Senescence, Telomere, and Mitochondrial Pathways in Human Lung Tissue of Smokers, COPD, and IPF: Associations With SARS-CoV-2 COVID-19 ACE2-TMPRSS2-Furin-DPP4 Axis

Telomere Length but Not Mitochondrial DNA Copy Number Is Altered in Both Young and Old COPD

Presence of Chronic Obstructive Pulmonary Disease (COPD) Impair Survival in Lung Cancer Patients Receiving Epidermal Growth Factor Receptor-Tyrosine Kinase Inhibitor (EGFR-TKI): A Nationwide, Population-Based Cohort Study

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