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Association of serum follistatin levels with histological types and progression of tumor in human lung cancer.

ABSTRACT: Background:Follistatin (FST), an activin-binding protein, inhibits activin action by interfering with activin binding to its receptor. The prognostic value of FST has been studied in various cancers. However, these studies rarely focus on lung cancer. In our study, we investigated the relationship between serum FST levels and lung cancer with histologic types, TNM staging, and recurrence. Methods:A total of 150 serum samples were collected, including 91 from patients with SCLC or NSCLC, 22 from patients with benign lung diseases, and 37 from healthy subjects. Enzyme-linked immunosorbent assay was used to determine serum FST levels in healthy subjects, patients with benign lung diseases and patients with lung cancers. Results:Serum FST levels in patients with LADC, SCC, LASC, LCLC, and SCLC were much higher than those in healthy subjects and in patients with lung benign disease. A ROC curve was constructed for differentiating the lung cancer from the healthy subjects and benign lung diseases. The results indicated that the area under the ROC curve (AUC) was 0.971 and 0.728 respectively. According to TNM staging, serum FST level increased significantly in patients with stage III and IV of LADC. Moreover, serum FST expression were increased in LADC patients with different TNM category. Furthermore, we found that a higher expression of serum FST was correlated with recurrence in LADC patients. Conclusions:The serum FST levels gradually increased with the rise of TNM staging and category in lung cancer patients. These data suggest that serum FST levels not only can be used in auxiliary diagnosis for lung cancer but also might be associated with the disease progression and metastasis of lung cancers.

SUBMITTER: Zhang P

PROVIDER: S-EPMC6195981 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature

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Association of serum follistatin levels with histological types and progression of tumor in human lung cancer.

Zhang Pengyu P Ruan Yingxin Y Xiao Jun J Chen Fangfang F Zhang Xuejun X

Cancer cell international 20181020

<h4>Background</h4>Follistatin (FST), an activin-binding protein, inhibits activin action by interfering with activin binding to its receptor. The prognostic value of FST has been studied in various cancers. However, these studies rarely focus on lung cancer. In our study, we investigated the relationship between serum FST levels and lung cancer with histologic types, TNM staging, and recurrence.<h4>Methods</h4>A total of 150 serum samples were collected, including 91 from patients with SCLC or ...[more]

PMID: 30377409

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Project description:The tumor microenvironment (TME), including immune cells, cancer-associated fibroblasts, endothelial cells, adjacent normal cells, and others, plays a crucial role in influencing tumor behavior and progression. Here, we characterized the TME in 83 primary renal tumors and matched metastatic or recurrence tissue samples (n = 15) from papillary renal cell carcinoma (pRCC) types 1 (n = 20) and 2 (n = 49), collecting duct carcinomas (CDC; n = 14), and high-grade urothelial carcinomas (HGUC; n = 5). We investigated 10 different markers of immune infiltration, vasculature, cell proliferation, and epithelial-to-mesenchymal transition by using machine learning image analysis in conjunction with immunohistochemistry. Marker expression was compared by Mann-Whitney and Kruskal-Wallis tests and correlations across markers using Spearman's rank correlation coefficient. Multivariable Poisson regression analysis was used to compare marker expression between histological types, while accounting for variation in tissue size. Several immune markers showed different rates of expression across histological types of renal carcinoma. Using pRCC1 as reference, the incidence rate ratio (IRR) of CD3+ T cells (IRR [95% confidence interval, CI] = 2.48 [1.53-4.01]) and CD20+ B cells (IRR [95% CI] = 4.38 [1.22-5.58]) was statistically significantly higher in CDC. In contrast, CD68+ macrophages predominated in pRCC1 (IRR [95% CI] = 2.35 [1.42-3.9]). Spatial analysis revealed CD3+ T-cell and CD20+ B-cell expressions in CDC to be higher at the proximal (p < 0.0001) and distal (p < 0.0001) tumor periphery than within the central tumor core. In contrast, expression of CD68+ macrophages in pRCC2 was higher in the tumor center compared to the proximal (p = 0.0451) tumor periphery and pRCC1 showed a distance-dependent reduction, from the central tumor, in CD68+ macrophages with the lowest expression of CD68 marker at the distal tumor periphery (p = 0.004). This study provides novel insights into the TME of rare kidney cancer types, which are often understudied. Our findings of differences in marker expression and localization by histological subtype could have implications for tumor progression and response to immunotherapies or other targeted therapies.

Project description:ImportanceConventional methods to diagnose and monitor chronic kidney disease (CKD) in children, such as creatinine level and cystatin C-derived estimated glomerular filtration rate (eGFR) and assessment of proteinuria in spot or timed urine samples, are of limited value in identifying patients at risk of progressive kidney function loss. Serum soluble urokinase receptor (suPAR) levels strongly predict incident CKD stage 3 in adults.ObjectiveTo determine whether elevated suPAR levels are associated with renal disease progression in children with CKD.Design, setting, and participantsPost hoc analysis of 2 prospectively followed up pediatric CKD cohorts, ie, the ESCAPE Trial (1999-2007) and the 4C Study (2010-2016), with serum suPAR level measured at enrollment and longitudinal eGFR measured prospectively. In the 2 trials, a total of 898 children were observed at 30 (ESCAPE Trial; n = 256) and 55 (4C Study; n = 642) tertiary care hospitals in 13 European countries. Renal diagnoses included congenital anomalies of the kidneys and urinary tract (n = 637 [70.9%]), tubulointerstitial nephropathies (n = 92 [10.2%]), glomerulopathies (n = 69 [7.7%]), postischemic CKD (n = 42 [4.7%]), and other CKD (n = 58 [6.5%]). Total follow-up duration was up to 7.9 years, and median follow-up was 3.1 years. Analyses were conducted from October 2016 to December 2016.ExposuresSerum suPAR level was measured at enrollment, and eGFR was measured every 2 months in the ESCAPE Trial and every 6 months in the 4C Study. The primary end point of CKD progression was a composite of 50% eGFR loss, eGFR less than 10 mL/min/1.73 m2, or initiation of renal replacement therapy.Main outcomes and measuresThe primary end point in this study was renal survival, defined as a composite of 50% loss of GFR that persisted for at least 1 month, the start of renal replacement therapy, or an eGFR less than 10 mL/min/1.73 m2.ResultsOf the 898 included children, 560 (62.4%) were male, and the mean (SD) patient age at enrollment was 11.9 (3.5) years. The mean (SD) eGFR was 34 (16) mL/min/1.73 m2. The 5-year end point-free renal survival was 64.5% (95% CI, 57.4-71.7) in children with suPAR levels in the lowest quartile compared with 35.9% (95% CI, 28.7-43.0) in those in the highest quartile (P < .001). By multivariable analysis, the risk of attaining the end point was higher in children with glomerulopathies and increased with age, blood pressure, proteinuria, and lower eGFR at baseline. In patients with baseline eGFR greater than 40 mL/min/1.73 m2, higher log-transformed suPAR levels were associated with a higher risk of CKD progression after adjustment for traditional risk factors (hazard ratio, 5.12; 95% CI, 1.56-16.7; P = .007).Conclusions and relevancePatients with high suPAR levels were more likely to have progression of their kidney disease. Further studies should determine whether suPAR levels can identify children at risk for future CKD.

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Association of serum follistatin levels with histological types and progression of tumor in human lung cancer.

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Association of serum follistatin levels with histological types and progression of tumor in human lung cancer.

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