scholarly journals The Prognostic Value of LDH And ADA in Serum and Pleural Fluid of Non-Small Cell Lung Cancer

2021 ◽  
Author(s):  
Shuang Zhao ◽  
Jun Zeng ◽  
Juanli Wu
Keyword(s):  
Lung Cancer ◽  
Pleural Effusion ◽  
Small Cell Lung Cancer ◽  
Pleural Fluid ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Small Cell Lung ◽  
Diagnosis Method ◽  
Nsclc Patients ◽  
Worse Prognosis

Abstract Objective: To explore the value of dehydrogenase (LDH) and adenosine deaminase (ADA) in serum and pleural fluid in predicting the prognosis of non-small cell lung cancer.Methods: A total of 134 patients with non-small cell lung cancer (NSCLC) with pleural effusion were enrolled. LDH in Serum and LDH and ADA in pleural fluid were detected, and the cancer ratio (serum LDH/pleural fluid ADA ratio) was calculated. Patients were followed until death. To analyze the correlation between the above indicators and the clinical pathological characteristics of the patients, and the predictive value for the prognosis of the patients.Results: Among the included NSCLC patients with pleural effusion, the average age was 61.76 years old, mainly male (66.7%), the right lung was more common (47.2%), adenocarcinoma was the main (82.1%), and smoking patients accounted for 48.0%. In the diagnosis method, there were 94 cases were diagnosed by pleural fluid exfoliated cells or pleural biopsy. In terms of clinical features, serum LDH is only related to adrenal metastasis (p = 0.000), and pleural fluid LDH is related to the patient's pathological type (p = 0.001). There was no correlation between pleural fluid ADA or cancer ratio and patient gender, lesion location, pathological type, diagnosis method, smoking history, and metastatic location. In terms of prognostic value, patients with ADA < 20U/L and cancer ratio >20 have shorter overall survival and worse prognosis (​​p < 0.0001 and p = 0.0178, respectively). The multivariate Cox regression analysis suggested that the cancer ratio (HR = 1.699, 95%CI: 1.097–2.630, p = 0.017) was an independent risk factor for the poor prognosis of patients.Conclusion: The NSCLC patients with pleural fluid ADA < 20U/L and cancer ratio > 20 combined with pleural effusion had a shorter overall survival and worse prognosis.

scholarly journals Tumor Transcriptome in Patients with Lower Pectoralis Muscle Area Reveals IL-8 as a Prognostic Biomarker in Non-Small Cell Lung Cancer

2019 ◽  
Author(s):  
Sarah Santiloni Cury ◽  
Diogo de Moraes ◽  
Paula Paccielli Freire ◽  
Grasieli de Oliveira ◽  
Douglas Venâncio Pereira Marques ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
In Vitro Assays ◽  
C2c12 Myotubes ◽  
Pectoralis Muscle ◽  
Small Cell Lung ◽  
Nsclc Patients ◽  
Worse Prognosis

Cachexia is a syndrome characterized by an ongoing loss of skeletal muscle mass associated with poor patient prognosis in non-small cell lung cancer (NSCLC). However, prognostic cachexia biomarkers in NSCLC are unknown. Here, we analyzed computed tomography (CT) images and tumor transcriptome data to identify potentially secreted cachexia biomarkers (PSCB) in NSCLC patients with low-muscularity. We integrated radiomics features (pectoralis muscle, sternum, and T10 vertebra) from CT of 89 NSCLC patients, which allowed us to identify an index for screening muscularity. Next, a tumor transcriptomic-based secretome analysis from these patients (discovery set) was evaluated to identify potential cachexia biomarkers in patients with low-muscularity. The prognostic value of these biomarkers for predicting recurrence and survival outcome was confirmed using expression data from eight lung cancer datasets (validation set). Finally, C2C12 myoblasts differentiated into myotubes were used to evaluate the ability of the selected biomarker, IL-8, in inducing muscle cell atrophy. We identified 75 over-expressed transcripts in patients with low-muscularity, which included IL6, CSF3, and IL8. Also, we identified NCAM1, CNTN1, SCG2, CADM1, IL8, NPTX1, and APOD as PSCB in the tumor secretome. These PSCB were capable of distinguishing worse and better prognosis (recurrence and survival) in NSCLC patients. IL8 was confirmed as a predictor of worse prognosis in all validation sets. In vitro assays revealed that IL-8 promoted C2C12 myotube atrophy. Tumors from low-muscularity patients presented a set of upregulated genes encoding for secreted proteins, including pro-inflammatory cytokines that predict worse overall survival in NSCLC. Among these up-regulated genes, IL8 expression in NSCLC tissues was associated with worse prognosis and the recombinant IL-8 was capable of triggering atrophy in C2C12 myotubes.

Surrogates of response to treatment of non-small cell lung cancer with immunotherapy: Toxicity and leukocyte ratios—Experience of a center.

2021 ◽  
Vol 39 (15_suppl) ◽  
pp. e21052-e21052
Author(s):  
Alba Moratiel Pellitero ◽  
Ines Ruiz Moreno ◽  
Mara Cruellas ◽  
Natalia Alonso Marin ◽  
Maitane Ocáriz ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Immune System ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Neutrophil To Lymphocyte Ratio ◽  
Small Cell Lung ◽  
Lymphocyte Ratio ◽  
Nsclc Patients ◽  
Worse Prognosis

e21052 Background: Immunotherapy is proposed as a therapeutic novelty in metastatic non-small cell lung cancer (NSCLC), in many cases already in front line. It presents different adverse effects than traditional schemes, due to the stimulation of the immune system. There is a possible relationship between toxicity and response. Neutrophil-to-lymphocyte ratio (NLR) as a possible predictive factor of response. Objectives: Evaluating the response according to the toxicity degree in NSCLC patients in real clinical practice. Analyze whether pretreatment NLR high patients have a worse prognosis. Methods: Observational, retrospective, analytical, single-center study. HCULB stage IV NSCLC patients with inmunotherapy treatment during 2016-2018. Descriptive and multivariate analysis. Toxicity grade: CTCAE version 4.0. Response assessment: RECIST 2.0 and immunorelated criteria. Toxicity degree and response (global and individualized results according to treatment and histology). Neutrophil-to-lymphocyte ratio and response. Results: N = 43 patients (35 men, 8 women). Average age 64 years. Response: 3 complete response (CR) (toxicity ≥2), 13 partial response (PR) (toxicity ≥1), 13 stable disease (SD), 12 progression (P) (only 4 toxicity and ≤2), 2 not evaluated. Hypothyroidism as the most common irAE. Relationship between toxicity and response: the absence of irAEs conditions worse prognosis p < 0.05. Histology: 25 adenocarcinoma [18 with irAES (1 CR, 7 PR, 8 SD,) and 7 without (1 SD, 5 P, 1 no ev.)]; 17 squamous [13 with irAES (1 CR, 6 PR, 4 SD) and 4 without (3 P, 1 no ev.)]; 1 adenosquamous with irAES and CR. Drug: Atezolizumab N = 8 [6 with irAES (2 PR, 3 SD, 1 P) and 2 without (both P)], Nivolumab N = 16 [9 with irAES (1 CR, 3 PR, 3 SD, 2 P) and 7 without (1 SD, 4 P, 2 no ev.)], Pembrolizumab N = 19 [17 with irAEs (2 CR, 8 PR, 6 SD, 1 P) and 2 without (both P)]. Significant positive correlation between toxicity and response (p < 0.001) R = 0.067, (CI 99% 0.378-0.837), regardless of histology and drug. It is observed a better response in those patients who presented a NRL close to 3 or less at the beginning of treatment. On the contrary, it is observed that subjects with NRL greater than 4 obtained worse results when they were treated with immunotherapy. Conclusions: The appearance of irAES like a response indicator of immune system, seem to conditione better evolution. In contrast, the absence of toxicity predicts a worse prognosis. Further studies with a larger sample are needed to confirm our findings about the predictive value of NLR and optimize therapeutic regimens if necessary.

scholarly journals Caspase Recruitment Domain Containing Protein 9 Suppresses Non-Small Cell Lung Cancer Proliferation and Invasion via Inhibiting MAPK/p38 Pathway

2020 ◽  
Vol 52 (3) ◽  
pp. 867-885
Author(s):  
Linyue Pan ◽  
Yuting Tan ◽  
Bin Wang ◽  
Wenjia Qiu ◽  
Yulei Yin ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Pleural Effusion ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
B Cell Lymphoma ◽  
Small Cell ◽  
Small Cell Lung ◽  
Antitumor Effects ◽  
Nsclc Patients ◽  
P38 Pathway

PurposeCaspase recruitment domain containing protein 9 (CARD9) has been demonstrated to be a pro-tumor factor in various cancers. However, our previous study found a significant decrease of CARD9 in malignant pleural effusion compared with benign pleural effusion. So we investigated the role of CARD9 in non-small cell lung cancer (NSCLC) and its working mechanism. Materials and MethodsImmunohistochemistry, western blot, and quantitative real-time polymerase chain reaction were used to detect the expression of CARD9 in specimens of NSCLC patients. The Cancer Genome Atlas (TCGA) databasewas also used to analyze the expression of CARD9 in NSCLC and its predicting value for prognosis. Immunofluorescence was used for CARD9 cellular location. Cell growth assay, clonal formation assay, wound healing assay, matrigel invasion assay, and flow cytometry were used to test cell proliferation, migration, invasion, apoptosis, and cycle progression of NSCLC cells with CARD9 knockdown or CARD9 overexpression. Co-immunoprecipitation was used to identify the interaction between CARD9 and B-cell lymphoma 10 (BCL10). SB203580 was used to inhibit p38 activation.ResultsCARD9 was decreased in NSCLC tissues compared with normal tissues; low CARD9 expression was associated with poor survival. CARD9 was expressed both in tumor cells and macrophages. Downregulation of CARD9 in NSCLC cells enhanced the abilities of proliferation, invasion and migration via activated MAPK/p38 signaling, while overexpression of CARD9 presented antitumor effects. BCL10 was identified to interact with CARD9.ConclusionWe demonstrate that CARD9 is an independent prognostic factor in NSCLC patients and inhibits proliferation, migration, and invasion by suppressing MAPK/p38 pathway in NSCLC cells.

Up-regulated HMGB1 in the pleural effusion of non-small cell lung cancer (NSCLC) patients reduces the chemosensitivity of NSCLC cells

2018 ◽  
Vol 104 (5) ◽  
pp. 338-343 ◽  
Author(s):  
Ying Ma ◽  
Shirong Kang ◽  
Xu Wu ◽  
Bateer Han ◽  
Zhiyong Jin ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Pleural Effusion ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
A549 Cells ◽  
Small Cell ◽  
Small Cell Lung ◽  
Nsclc Patients

Background: Pleural effusion is one of the complications of human non-small cell lung cancer (NSCLC). High mobility group box-1 protein (HMGB1) correlates highly with invasion and metastasis in multiple tumors. The aim of this study was to explore the clinical value of HMGB1 in NSCLC patients, and to investigate the role of HMGB1 in the development of pleural effusion. In addition, we also investigated the regulatory role of HMGB1 in the sensitivity of NSCLC cells to cisplatin. Methods: 46 NSCLC malignant pleural effusion (MPE) and 31 benign pleural effusion samples were quantitatively analyzed with Enzyme-Linked Immunosorbent Assay (ELISA) for cytokines, such as IL-1beta, IL-6, IL-8 and HMGB1. The HMGB1 expression in NSCLC tissues was examined with RT-qPCR and western blotting methods. Then the influence by HMGB1 on the chemosensitivity of lung cancer A549 cells was examined with MTT assay and colony forming assay for the A549 cells post the treatment with cisplatin or (and) HMGB1. Results: The results demonstrated that HMGB1 was up-regulated in the pleural effusion of NSCLC patients, along with the up-regulated levels of proinflammatory cytokines such as IL-6 and IL-8. And the up-regulation of HMGB1 was confirmed at both the mRNA and protein levels in the NSCLC tissues. Recombinant HMGB1 reduced the sensitivity of A549 cells to cisplatin in vitro. Conclusions: In conclusion, HMGB1 was up-regulated in the pleural effusion and tumor tissues of NSCLC patients. HMGB1 reduced the sensitivity of NSCLC A549 cells to cisplatin in vitro.

P-787 Small cell lung cancer with pleural effusion: Prognostic aspects in pleural fluid

Lung Cancer ◽  
2005 ◽  
Vol 49 ◽  
pp. S326
Author(s):  
D. Orts Gimenez ◽  
R. Jimenez Yañez ◽  
L. Hernández Blasco ◽  
J. Sanchez-Paya ◽  
C. Fernandez Aracil ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Pleural Effusion ◽  
Small Cell Lung Cancer ◽  
Pleural Fluid ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Small Cell Lung

Plasma and Pleural Fluid Pharmacokinetics of Erlotinib and its Active Metabolite OSI-420 in Patients With Non–Small-Cell Lung Cancer With Pleural Effusion

2011 ◽  
Vol 12 (5) ◽  
pp. 307-312 ◽  
Author(s):  
Katsuhiro Masago ◽  
Yosuke Togashi ◽  
Masahide Fukudo ◽  
Tomohiro Terada ◽  
Kaoru Irisa ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Pleural Effusion ◽  
Small Cell Lung Cancer ◽  
Pleural Fluid ◽  
Cell Lung Cancer ◽  
Active Metabolite ◽  
Small Cell ◽  
Small Cell Lung

scholarly journals Tumor Transcriptome Reveals High Expression of IL-8 in Non-Small Cell Lung Cancer Patients with Low Pectoralis Muscle Area and Reduced Survival

Cancers ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 1251 ◽  
Author(s):  
Sarah Santiloni Cury ◽  
Diogo de Moraes ◽  
Paula Paccielli Freire ◽  
Grasieli de Oliveira ◽  
Douglas Venâncio Pereira Marques ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
C2c12 Myotubes ◽  
Pectoralis Muscle ◽  
Small Cell Lung ◽  
Nsclc Patients ◽  
Upregulated Genes ◽  
Worse Prognosis

Cachexia is a syndrome characterized by an ongoing loss of skeletal muscle mass associated with poor patient prognosis in non-small cell lung cancer (NSCLC). However, prognostic cachexia biomarkers in NSCLC are unknown. Here, we analyzed computed tomography (CT) images and tumor transcriptome data to identify potentially secreted cachexia biomarkers (PSCB) in NSCLC patients with low-muscularity. We integrated radiomics features (pectoralis muscle, sternum, and tenth thoracic (T10) vertebra) from CT of 89 NSCLC patients, which allowed us to identify an index for screening muscularity. Next, a tumor transcriptomic-based secretome analysis from these patients (discovery set) was evaluated to identify potential cachexia biomarkers in patients with low-muscularity. The prognostic value of these biomarkers for predicting recurrence and survival outcome was confirmed using expression data from eight lung cancer datasets (validation set). Finally, C2C12 myoblasts differentiated into myotubes were used to evaluate the ability of the selected biomarker, interleukin (IL)-8, in inducing muscle cell atrophy. We identified 75 over-expressed transcripts in patients with low-muscularity, which included IL-6, CSF3, and IL-8. Also, we identified NCAM1, CNTN1, SCG2, CADM1, IL-8, NPTX1, and APOD as PSCB in the tumor secretome. These PSCB were capable of distinguishing worse and better prognosis (recurrence and survival) in NSCLC patients. IL-8 was confirmed as a predictor of worse prognosis in all validation sets. In vitro assays revealed that IL-8 promoted C2C12 myotube atrophy. Tumors from low-muscularity patients presented a set of upregulated genes encoding for secreted proteins, including pro-inflammatory cytokines that predict worse overall survival in NSCLC. Among these upregulated genes, IL-8 expression in NSCLC tissues was associated with worse prognosis, and the recombinant IL-8 was capable of triggering atrophy in C2C12 myotubes.

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