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Absence of activating mutations of CXCR4 in pituitary tumours.

DC FieldValueLanguage
dc.contributor.author노태웅-
dc.contributor.author이용호-
dc.contributor.author이은직-
dc.date.accessioned2015-04-23T17:17:49Z-
dc.date.available2015-04-23T17:17:49Z-
dc.date.issued2010-
dc.identifier.issn0300-0664-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/102193-
dc.description.abstractOBJECTIVE: Mutations of the gsp oncogene are responsible for 30-40% of GH-producing pituitary adenomas and 10% of nonfunctioning pituitary adenomas (NFPAs). However, the pathogenetic mechanism of the remaining pituitary tumours still remains to be identified. Recently, the interaction between the chemokine stromal cell-derived factor 1 and its receptor CXCR4 was found to play an important role in GH production and cell proliferation in various pituitary adenoma cell lines. As CXCR4 is a Gi-coupled chemokine receptor, its constitutive activating mutations may be involved in pituitary tumour formation by cyclic adenosine monophosphate (cAMP)-independent, ERK-related pathways. PATIENTS AND METHODS: We investigated whether somatic activating-mutations of CXCR4 might be a possible tumourigenic mechanism for gsp-negative GH-secreting pituitary adenomas and NFPAs. Direct sequencing of polymerase chain reaction-amplified products for coding exons of CXCR4 were performed using genomic deoxyribonucleic acid samples from 37 GH-producing pituitary tumour tissues that were negative for the gsp mutation and 14 CXCR4 expressing NFPAs. RESULTS: Immunohistochemical analyses and double immunofluorescent staining of sectioned paraffin-embedded pituitary tissues revealed that CXCR4 is highly expressed in GH-producing pituitary adenomas and NFPAs. Direct sequencing showed that two synonymous mutations in exon 2 (87 C > T and 414 C > T) were detected in 4 out of 51 pituitary tumours. CONCLUSION: Our results indicate that an activating mutation of the CXCR4 may not be a common pathogenetic mechanism in GH-producing pituitary tumours and NFPAs.-
dc.description.statementOfResponsibilityopen-
dc.format.extent209~213-
dc.relation.isPartOfCLINICAL ENDOCRINOLOGY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHGrowth Hormone-Secreting Pituitary Adenoma/genetics-
dc.subject.MESHGrowth Hormone-Secreting Pituitary Adenoma/metabolism-
dc.subject.MESHHumans-
dc.subject.MESHImmunohistochemistry-
dc.subject.MESHMutation-
dc.subject.MESHPituitary Neoplasms/genetics*-
dc.subject.MESHPituitary Neoplasms/metabolism*-
dc.subject.MESHPolymerase Chain Reaction-
dc.subject.MESHReceptors, CXCR4/genetics*-
dc.subject.MESHReceptors, CXCR4/metabolism*-
dc.titleAbsence of activating mutations of CXCR4 in pituitary tumours.-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Internal Medicine (내과학)-
dc.contributor.googleauthorYong-ho Lee-
dc.contributor.googleauthorTae Woong Noh-
dc.contributor.googleauthorMi Kyung Lee-
dc.contributor.googleauthorJ. Larry Jameson-
dc.contributor.googleauthorEun Jig Lee-
dc.identifier.doi10.1111/j.1365-2265.2009.03629.x-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA02989-
dc.contributor.localIdA03050-
dc.contributor.localIdA01298-
dc.relation.journalcodeJ00571-
dc.identifier.eissn1365-2265-
dc.identifier.pmid19473177-
dc.identifier.urlhttp://onlinelibrary.wiley.com/doi/10.1111/j.1365-2265.2009.03629.x/abstract-
dc.contributor.alternativeNameNoh, Tae Woong-
dc.contributor.alternativeNameLee, Yong Ho-
dc.contributor.alternativeNameLee, Eun Jig-
dc.contributor.affiliatedAuthorLee, Yong Ho-
dc.contributor.affiliatedAuthorLee, Eun Jig-
dc.contributor.affiliatedAuthorNoh, Tae Woong-
dc.citation.volume72-
dc.citation.number2-
dc.citation.startPage209-
dc.citation.endPage213-
dc.identifier.bibliographicCitationCLINICAL ENDOCRINOLOGY, Vol.72(2) : 209-213, 2010-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers

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