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Prognostic role of macrophage migration inhibitory factor in patients with clear cell renal cell carcinoma

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dc.contributor.authorAn, Hyo Jung-
dc.contributor.authorKoh, Hyun Min-
dc.contributor.authorLee, Jong Sil-
dc.contributor.authorSong, Dae Hyun-
dc.date.accessioned2022-12-26T12:04:25Z-
dc.date.available2022-12-26T12:04:25Z-
dc.date.issued2020-12-11-
dc.identifier.issn0025-7974-
dc.identifier.issn1536-5964-
dc.identifier.urihttps://scholarworks.gnu.ac.kr/handle/sw.gnu/5790-
dc.description.abstractMacrophage migration inhibitory factor (MIF) is a cytokine that mediates the interaction between malignant cells and the innate immune system. Recently, MIF has received attention for its role in tumorigenesis. We evaluated the prognostic role of MIF in clear cell renal cell carcinoma (CCRCC). A total of 152 patients, who underwent nephrectomy for CCRCC were enrolled in this study. Immunohistochemical staining of tissue microarray blocks containing 298 cores-2 cores per CCRCC patient was performed. The relationship between MIF expression and clinicopathological factors was evaluated. Total RNA and protein were extracted from 7 RCC (renal cell carcinoma) cell lines. MIF was knocked down in Caki-2 cells, and a wound healing assay was performed to evaluate migratory activity. Among the 298 cores, 180 (60.4%) were positive for MIF. Multivariate analysis, showed that, CCRCC patients with negative MIF expression exhibited poor disease-free survival (hazard ratio: 2.087, 95% confidence interval: 0.821-5.307, P value: .023) and poor disease-specific survival (hazard ratio: 2.101, 95% confidence interval: 1.009-4.374, P value: .047). The wound healing assay revealed that cell confluence was lower in MIF-deficient Caki-2 cells than in control cells. Negative MIF expression might be an independent prognostic marker for patients with CCRCC.-
dc.language영어-
dc.language.isoENG-
dc.publisherLippincott Williams & Wilkins Ltd.-
dc.titlePrognostic role of macrophage migration inhibitory factor in patients with clear cell renal cell carcinoma-
dc.typeArticle-
dc.publisher.location미국-
dc.identifier.doi10.1097/MD.0000000000023277-
dc.identifier.scopusid2-s2.0-85098607263-
dc.identifier.wosid000612838800033-
dc.identifier.bibliographicCitationMedicine, v.99, no.50, pp E23277-
dc.citation.titleMedicine-
dc.citation.volume99-
dc.citation.number50-
dc.citation.startPageE23277-
dc.type.docTypeArticle-
dc.description.isOpenAccessY-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaGeneral & Internal Medicine-
dc.relation.journalWebOfScienceCategoryMedicine, General & Internal-
dc.subject.keywordPlusFACTOR MIF-
dc.subject.keywordPlusPROSTATIC ADENOCARCINOMA-
dc.subject.keywordPlusEXPRESSION-
dc.subject.keywordPlusGROWTH-
dc.subject.keywordPlusANGIOGENESIS-
dc.subject.keywordPlusMECHANISM-
dc.subject.keywordPlusVITRO-
dc.subject.keywordAuthorclear cell-
dc.subject.keywordAuthormacrophage migration inhibitory factor-
dc.subject.keywordAuthorrenal cell carcinoma-
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