Preoperative Body Weight and Albumin Predict Survival in Patients With Resectable Lung Neoplasms: Role of COPD

Tang, Jun; Curull, Víctor; Ramis-Cabrer, Daniel; Duran, Xavier; Rodríguez-Fuster, Alberto; Aguiló, Rafael; Barreiro, Esther

doi:10.1016/j.arbres.2020.07.021

Cited by 5 publications

(3 citation statements)

References 36 publications

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“…Skeletal muscle wasting is associated with chronic diseases including cancer. Cancer-induced cachexia is an invalidating condition that negatively influences the patients' prognosis regardless of the status of the underlying tumor [1][2][3][4][5][6]. Muscle mass loss also takes place during periods of immobilization such as prolonged bed rest, microgravity, denervation, and critical illness [7][8][9][10][11].…”

Section: Introductionmentioning

confidence: 99%

Prolonged Immobilization Exacerbates the Loss of Muscle Mass and Function Induced by Cancer-Associated Cachexia through Enhanced Proteolysis in Mice

Mañas-García

Penedo-Vázquez

López-Postigo

et al. 2020

IJMS

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We hypothesized that in mice with lung cancer (LC)-induced cachexia, periods of immobilization of the hindlimb (7 and 15 days) may further aggravate the process of muscle mass loss and function. Mice were divided into seven groups (n = 10/group): (1) non-immobilized control mice, (2) 7-day unloaded mice (7-day I), (3) 15-day unloaded mice (15-day I), (4) 21-day LC-cachexia group (LC 21-days), (5) 30-day LC-cachexia group (LC 30-days), (6) 21-day LC-cachexia group besides 7 days of unloading (LC 21-days + 7-day I), (7) 30-day LC-cachexia group besides 15 days of unloading (LC 30-days + 15-day I). Physiological parameters, body weight, muscle and tumor weights, phenotype and morphometry, muscle damage (including troponin I), proteolytic and autophagy markers, and muscle regeneration markers were identified in gastrocnemius muscle. In LC-induced cachexia mice exposed to hindlimb unloading, gastrocnemius weight, limb strength, fast-twitch myofiber cross-sectional area, and muscle regeneration markers significantly decreased, while tumor weight and area, muscle damage (troponin), and proteolytic and autophagy markers increased. In gastrocnemius of cancer-cachectic mice exposed to unloading, severe muscle atrophy and impaired function was observed along with increased muscle proteolysis and autophagy, muscle damage, and impaired muscle regeneration.

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Section: Introductionmentioning

confidence: 99%

Prolonged Immobilization Exacerbates the Loss of Muscle Mass and Function Induced by Cancer-Associated Cachexia through Enhanced Proteolysis in Mice

Mañas-García

Penedo-Vázquez

López-Postigo

et al. 2020

IJMS

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“…Mechanisms such as inflammation, oxidative stress, epigenetics alterations, and the tumor microenvironment underlie the pathophysiology of tumor development in patients with chronic respiratory disorders including stromal structures and immune cell profiles, and have an impact on the patients' survival [10][11][12]. Indeed, chronic obstructive pulmonary disease (COPD) is a major risk factor for LC development [9,13].…”

Section: Introductionmentioning

confidence: 99%

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

Tang

Curull

Wang

et al. 2020

Cancers

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(1) Background: Lung cancer (LC) is a major leading cause of death worldwide. Poly (ADP-ribose) polymerase (PARP)-1 and PARP-2 are key players in cancer. We aimed to assess PARP-1 and PARP-2 expression and activity and DNA damage in tumors and non-tumor lungs from patients with/without chronic obstructive pulmonary disease (COPD). (2) Methods: Lung tumor and non-tumor specimens were obtained through video-assisted thoracoscopic surgery (VATS) in LC patients with/without underlying COPD (two groups of patients, n = 15/group). PARP-1 and PARP-2 expression (ELISA), PARP activity (PARP colorimetric assay kit) and DNA damage (immunohistochemistry) levels were identified in all samples. (3) Results: Both PARP-1 and PARP-2 expression levels were significantly lower in lung tumors (irrespective of COPD)compared to non-tumor specimens, while DNA damage and PARP activity levels significantly increased in lung tumors compared to non-tumor specimens only in LC-COPD patients. PARP-2 expression was positively correlated with smoking burden in LC-COPD patients. (4) Conclusions: In lung tumors of COPD patients, an overactivation of PARP enzyme was observed. A decline in PARP-1 and PARP-2 protein expression was seen in lung tumors irrespective of COPD. Other phenotypic features (airway obstruction) beyond cancer may account for the increase in PARP activity seen in the tumors of patients with underlying COPD.

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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: 88%

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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Preoperative Body Weight and Albumin Predict Survival in Patients With Resectable Lung Neoplasms: Role of COPD

Cited by 5 publications

References 36 publications

Prolonged Immobilization Exacerbates the Loss of Muscle Mass and Function Induced by Cancer-Associated Cachexia through Enhanced Proteolysis in Mice

Prolonged Immobilization Exacerbates the Loss of Muscle Mass and Function Induced by Cancer-Associated Cachexia through Enhanced Proteolysis in Mice

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

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

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