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Sestrin-2 is significantly increased in malignant pleural effusions due to lung cancer and is potentially secreted by pleural mesothelial cells

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Auteur
Tsilioni I., Filippidis A.S., Kerenidi T., Budanov A.V., Zarogiannis S.G., Gourgoulianis K.I.
Date
2016
Language
en
DOI
10.1016/j.clinbiochem.2016.02.002
Sujet
lactate dehydrogenase
sestrin 2
tumor suppressor protein
unclassified drug
biological marker
nuclear protein
SESN2 protein, human
adult
Article
biochemical analysis
cell count
cellular secretion
congestive heart failure
controlled study
disease association
enzyme linked immunosorbent assay
female
human
limit of detection
lung cancer
major clinical study
male
malignant pleura effusion
mesothelium cell
middle aged
pleura fluid
pneumonia
priority journal
sensitivity and specificity
tuberculosis
complication
epithelium
exudate
follow up
lung tumor
metabolism
pathology
Pleural Effusion, Malignant
prognosis
secretion (process)
Biomarkers
Enzyme-Linked Immunosorbent Assay
Epithelium
Exudates and Transudates
Female
Follow-Up Studies
Humans
Lung Neoplasms
Male
Middle Aged
Nuclear Proteins
Pleural Effusion, Malignant
Prognosis
Elsevier Inc.
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Résumé
Objectives: Sestrin-2 (Sesn2) belongs to a family of highly conserved antioxidant proteins that were discovered as p53-inducible proteins and inhibits cell growth and proliferation. Our aim was to assess the levels of Sesn2 in malignant pleural effusions of lung cancer patients compared to benign pleural effusions. Design and methods: We enrolled 73 patients (55/males and 18/females) diagnosed with pleural effusion (PE). PEs were grouped as 44 malignant pleural effusions (MPEs; lung cancer) and 29 benign (BPE; 7 congestive heart failure, 9 tuberculosis, 13 parapneumonic). Pleural fluid (PF) Sesn2 levels were determined by enzyme-linked immunosorbent assay (ELISA) kit. Standard biochemical PF analysis was also performed and Sesn2 levels were correlated with PF lactate dehydrogenase (LDH), protein, cell counts and age. Results: Sesn2 was detected in 24/44 patients with MPEs and in 3/29 patients with BPEs (p = 0.0001). The mean value (mean ± SEM) of Sesn2 in patients with MPEs was 0.54 ± 0.22 ng/mL while in BPEs it was 0.12 ± 0.04 ng/mL (p = 0.0004). In MPEs Sesn2 pleural fluid levels did not correlate with PF LDH and cell counts (p = 0.89 and p = 0.64 respectively). Conclusions: Our study shows that Sesn2 is significantly increased in MPEs compared to BPEs. Moreover, the lack of correlation of Sesn2 levels with PF cell counts and PF LDH suggests that it is potentially secreted by pleural mesothelial cells. © 2016 The Canadian Society of Clinical Chemists.
URI
http://hdl.handle.net/11615/79970
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