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      Correlation between resistin gene polymorphism and clinical aspects of lung cancer

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          Abstract

          Lung cancer is one of the most common cancers and is associated with a poor survival rate in the Chinese Han population. Analysis of genetic variants could lead to improvements in prognosis following lung cancer treatment. Resistin (RETN) is an important mediator of metabolic diseases and tumor progression. In this study, we explored the effects of RETN single nucleotide polymorphisms (SNPs) on the susceptibility and clinicopathological characteristics of patients with lung cancer. Four RETN SNPs (rs7408174, rs1862513, rs3745367, and rs3219175) were analyzed using TaqMan SNP genotyping in 371 patients with lung cancer and 451 cancer-free controls. The results showed that the RETN SNP rs3219175 with AG or at least 1 A allele was associated with a higher risk of lung cancer than wild-type (GG) carriers. Moreover, the RETN SNP rs3219175 with AG or AG + AA alleles was associated with a higher risk of distant metastasis than that in patients carrying GG alleles. We also used genotype-tissue expression datasets to compare the correlation of the RETN SNP rs3219175 in lung tissue and whole blood. In conclusion, our study demonstrated, for the first time, that RETN polymorphisms were correlated with lung cancer progression in the Chinese Han population.

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          A family of tissue-specific resistin-like molecules.

          Sahar S Bhat, Stephen G Wu, M. Wright … (2001)
          We have identified a family of resistin-like molecules (RELMs) in rodents and humans. Resistin is a hormone produced by fat cells. RELMalpha is a secreted protein that has a restricted tissue distribution with highest levels in adipose tissue. Another family member, RELMbeta, is a secreted protein expressed only in the gastrointestinal tract, particularly the colon, in both mouse and human. RELMbeta gene expression is highest in proliferative epithelial cells and is markedly increased in tumors, suggesting a role in intestinal proliferation. Resistin and the RELMs share a cysteine composition and other signature features. Thus, the RELMs together with resistin comprise a class of tissue-specific signaling molecules.
          Article 0 comments Cited 121 times – based on 0 reviews     Review now
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            Randomized phase II trial of gemcitabine-cisplatin with or without trastuzumab in HER2-positive non-small-cell lung cancer.

            James Barton, Carl G. Groth, A Ardizzoni … (2003)
            Trastuzumab provides significant clinical benefits in HER2-positive metastatic breast cancer patients when administered in combination with chemotherapy. Chemotherapy has also been shown to be beneficial in some patients with advanced non-small-cell lung cancer (NSCLC). The present randomized phase II trial examined the effect of adding trastuzumab to a standard chemotherapeutic combination (gemcitabine-cisplatin) in patients with HER2-positive NSCLC. Patients with untreated stage IIIB/IV HER2-positive NSCLC received up to six 21-day cycles of gemcitabine 1250 mg/m(2) (days 1 and 8) and cisplatin 75 mg/m(2) (day 1). Patients in the trastuzumab arm received trastuzumab 4 mg/kg intravenously (i.v.) followed by 2 mg/kg/week i.v. until progression. Of 619 patients screened, 103 were eligible. Fifty-one patients were treated with trastuzumab plus gemcitabine-cisplatin and 50 with gemcitabine-cisplatin alone. Efficacy was similar in the trastuzumab and control arms: response rate 36% versus 41%; median time to progression 6.3 versus 7.2 months; and median progression-free survival (PFS) 6.1 versus 7 months. Response rate (83%) and median PFS (8.5 months) appeared relatively good in the six trastuzumab-treated patients with HER2 3+ or fluorescence in situ hybridization (FISH)-positive NSCLC. Addition of trastuzumab to gemcitabine-cisplatin was well tolerated, side-effects were as expected, and trastuzumab did not exacerbate the known toxicity of gemcitabine and cisplatin. Symptomatic cardiotoxicity was observed in one trastuzumab-treated patient. Serum trastuzumab concentrations in the presence of gemcitabine-cisplatin were comparable to those of trastuzumab alone. Trastuzumab plus gemcitabine-cisplatin is well tolerated. Clinical benefit was not observed. Although HER2 3+/FISH-positive patients may benefit from trastuzumab, the subgroup is too small to provide definitive information. No significant effect of gemcitabine-cisplatin on trastuzumab pharmacokinetics was observed.
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              Expression profile analysis of microRNAs and downregulated miR-486-5p and miR-30a-5p in non-small cell lung cancer.

              Jianjie Zhu, Yuanyuan Zeng, Chun Ping Xu … (2015)
              Lung cancer is the leading cause of cancer-related mortality worldwide and although there have been improvements in treatment there is a low survival rate. The aim of the present study was to investigate the effect of microRNA (miRNA) on cell pathways. A miRNA microarray was used to profile miRNAs of lung cancer tissues. It was identified that 33 miRNAs with >2.0-fold change and FDR <0.05 were differentially expressed between the adjacent non-cancerous lung tissues and non-small cell lung cancers NSCLCs (P<0.005). The data were optimized in combination with physical interaction analysis to obtain crucial miRNAs. The results showed that differentially expressed miRNAs were associated with biological processes such as cell migration, protein phosphorylation and neuron differentiation, and signaling pathways such as MAPK, TGF-β and PI3K/Akt signaling pathways. Validation of significant miRNAs in independent 40 paired NSCLC tissues demonstrated that the expression level of miR-486-5p and miR-30a-5p was significantly downregulated in another 40 paired lung cancer tissues. Taken together, the results provided strong evidence of the possible involvement of miRNAs in the development and progression of NSCLC. Thus, the results are of importance for clinical investigators and for those who design miRNA‑based novel cancer therapeutics.
              Article 0 comments Cited 38 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Medicine (Baltimore)
                Journal ID (iso-abbrev): Medicine (Baltimore)
                Journal ID (publisher-id): MEDI
                Title: Medicine
                Publisher: Wolters Kluwer Health
                ISSN (Print): 0025-7974
                ISSN (Electronic): 1536-5964
                Publication date Collection: December 2017
                Publication date (Electronic): 29 December 2017
                Volume: 96
                Issue: 52
                Electronic Location Identifier: e9485
                Affiliations
                [a ]Department of Thoracic Surgery, Affiliated Dongyang Hospital of Wenzhou Medical University, Dongyang, Zhejiang, China
                [b ]Graduate Institute of Basic Medical Science, China Medical University
                [c ]Department of Biotechnology, College of Health Science, Asia University, Taichung, Taiwan
                [d ]Department of Biomedical Sciences Laboratory
                [e ]Department of Pathology, Affiliated Dongyang Hospital of Wenzhou Medical University, Dongyang, Zhejiang, China
                [f ]Department of Medical Research, Chung Shan Medical University Hospital
                [g ]Institute of Medicine, Chung Shan Medical University, Taichung, Taiwan.
                Author notes
                [∗ ]Correspondence: Chen-Ming Su, Department of Biomedical Sciences Laboratory, Affiliated Dongyang Hospital of Wenzhou Medical University, No. 60 Wuning West Rd., Dongyang, Zhejiang 322100, China (e-mail: ericsucm@ 123456163.com ); Shun-Fa Yang, Department of Medical Research, Chung Shan Medical University Hospital, Taichung, Taiwan (e-mail: ysf@ 123456csmu.edu.tw ).
                Article
                Publisher ID: MD-D-17-03223 Accession ID: 09485
                DOI: 10.1097/MD.0000000000009485
                PMC ID: 6392976
                PubMed ID: 29384942
                SO-VID: 3a2c40a5-838c-4309-9b3f-9d690e9ff59f
                Copyright © Copyright © 2017 the Author(s). Published by Wolters Kluwer Health, Inc.
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal. http://creativecommons.org/licenses/by-nc-nd/4.0

                History
                Date received : 24 May 2017
                Date revision received : 29 November 2017
                Date accepted : 7 December 2017
                Categories
                Subject: 3500
                Subject: Research Article
                Subject: Observational Study
                Custom metadata
                OPEN-ACCESS TRUE

                Keywords: lung cancer,polymorphism,resistin
                Data availability:
                Keywords: lung cancer, polymorphism, resistin

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