Publication:
FHIT gene sequence variants and reduced fhit protein expression in glioblastoma multiforme

dc.contributor.authorGüler, Gülnür
dc.contributor.authorAksoy, Kaya
dc.contributor.buuauthorÇeçener, Gülşah
dc.contributor.buuauthorTunca, Berrin Türkei
dc.contributor.buuauthorEgeli, Ünal
dc.contributor.buuauthorBekar, Ahmet
dc.contributor.buuauthorTolunay, Şahsine
dc.contributor.departmentTıp Fakültesi
dc.contributor.departmentTıp Fakültesi
dc.contributor.departmentTıp Fakültesi
dc.contributor.departmentTıbbi Patoloji Ana Bilim Dalı
dc.contributor.departmentTıbbi Biyoloji Ana Bilim Dalı
dc.contributor.departmentBeyin ve Sinir Cerrahisi Ana Bilim Dalı
dc.contributor.orcid0000-0002-3820-424X
dc.contributor.orcid0000-0002-1619-6680
dc.contributor.orcid0000-0001-7904-883X
dc.contributor.researcheridAAP-9988-2020
dc.contributor.researcheridAAI-1612-2021
dc.contributor.researcheridABI-6078-2020
dc.contributor.researcheridAAH-1420-2021
dc.contributor.scopusid6508156530
dc.contributor.scopusid6602965754
dc.contributor.scopusid55665145000
dc.contributor.scopusid6603677218
dc.contributor.scopusid6602604390
dc.date.accessioned2022-09-09T12:56:18Z
dc.date.available2022-09-09T12:56:18Z
dc.date.issued2010-03
dc.description.abstractMolecular studies have an important role in the elucidation of the mechanisms involved in Glioblastoma multiforme (GBM) development. The occurrence of FHIT gene alterations, which has an important role in different cancers, has not yet been studied well in GBM. We aimed to investigate the occurrence of alterations of FHIT gene sequence and protein expression in the GBMs. Sequence alterations in exons 5-9 of the FHIT gene were screened in 63 GBMs using the single-strand conformational polymorphism method, followed by DNA sequencing. Additionally, the level of Fhit protein expression in tissues of 48 tumors was assessed by immunohistochemistry (IHC). In our investigation, FHIT gene alterations in the coding region were detected in 11 of the 63 GBM cases (17.5%). Two different sequence variants were determined: one novel missense variant (G -> C transition at codon 49) and one previously described silent alteration (C -> T transition at codon 88). Using web-based programs, such as SIFT and ESEfinder, it was determined that both alterations might have caused significant modification on protein function. In addition, we identified a previously reported an intronic polymorphism (T -> A transition at IVS8-17) in 47.5% of cases as a similar rate (45%) in the control group. Moreover, it was observed that Fhit protein expression was reduced in 87.5% of tumors. In conclusion, the reduction or loss of Fhit protein expression by genetic alterations or epigenetic mechanisms in GBM might be associated with brain tumorigenesis.
dc.identifier.citationÇeçener, G. vd. (2010). "FHIT gene sequence variants and reduced fhit protein expression in glioblastoma multiforme". Cellular and Molecular Neurobiology, 30(2), 301-307.
dc.identifier.endpage307
dc.identifier.issn0272-4340
dc.identifier.issn1573-6830
dc.identifier.issue2
dc.identifier.pubmed19760177
dc.identifier.scopus2-s2.0-77952095741
dc.identifier.startpage301
dc.identifier.urihttps://doi.org/10.1007/s10571-009-9452-9
dc.identifier.urihttps://link.springer.com/article/10.1007/s10571-009-9452-9
dc.identifier.urihttp://hdl.handle.net/11452/28616
dc.identifier.volume30
dc.identifier.wos000275704800014
dc.indexed.wosSCIE
dc.language.isoen
dc.publisherSpringer/Plenum Publishers
dc.relation.collaborationYurt içi
dc.relation.collaborationSanayi
dc.relation.journalCellular and Molecular Neurobiology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectGlioblastoma multiforme
dc.subjectFHIT gene
dc.subjectSequence alterations
dc.subjectSSCP
dc.subjectIHC
dc.subjectCommon fragile sites
dc.subjectCell lung-cancer
dc.subjectTumor-suppressor gene
dc.subjectBrain-tumors
dc.subjectBreast-cancer
dc.subjectTurkish patients
dc.subjectPredisposition
dc.subjectMutations
dc.subject3P14.2
dc.subjectCarcinoma
dc.subjectCell biology
dc.subjectNeurosciences & neurology
dc.subject.emtreeFragile histidine triad protein
dc.subject.emtreeAcid anhydride hydrolase
dc.subject.emtreeTumor protein
dc.subject.emtreeAdult
dc.subject.emtreeAged
dc.subject.emtreeAmino acid substitution
dc.subject.emtreeArticle
dc.subject.emtreeCarcinogenesis
dc.subject.emtreeControlled study
dc.subject.emtreeDNA sequence
dc.subject.emtreeFemale
dc.subject.emtreeGene mutation
dc.subject.emtreeGene sequence
dc.subject.emtreeGenetic association
dc.subject.emtreeGenetic screening
dc.subject.emtreeGenetic variability
dc.subject.emtreeGlioblastoma
dc.subject.emtreeHuman
dc.subject.emtreeHuman tissue
dc.subject.emtreeImmunohistochemistry
dc.subject.emtreeMajor clinical study
dc.subject.emtreeMale
dc.subject.emtreePriority journal
dc.subject.emtreeProtein expression
dc.subject.emtreeProtein function
dc.subject.emtreeSingle strand conformation polymorphism
dc.subject.emtreeBrain tumor
dc.subject.emtreeGenetic variability
dc.subject.emtreeGenetics
dc.subject.emtreeGlioblastoma
dc.subject.emtreeMetabolism
dc.subject.emtreeMiddle aged
dc.subject.emtreeMolecular genetics
dc.subject.emtreeNucleotide sequence
dc.subject.meshAcid anhydride hydrolases
dc.subject.meshAdult
dc.subject.meshAged
dc.subject.meshBase sequence
dc.subject.meshBrain neoplasms
dc.subject.meshFemale
dc.subject.meshGenetic variation
dc.subject.meshGlioblastoma
dc.subject.meshHumans
dc.subject.meshMale
dc.subject.meshMiddle aged
dc.subject.meshMolecular sequence data
dc.subject.meshNeoplasm proteins
dc.subject.meshPolymorphism, single-stranded conformational
dc.subject.meshSequence analysis, DNA
dc.subject.scopusFragile Histidine Triad Protein; Histidine; Triad
dc.subject.wosCell biology
dc.subject.wosNeurosciences
dc.titleFHIT gene sequence variants and reduced fhit protein expression in glioblastoma multiforme
dc.typeArticle
dc.wos.quartileQ3
dspace.entity.typePublication
local.contributor.departmentTıp Fakültesi/Tıbbi Biyoloji Ana Bilim Dalı
local.contributor.departmentTıp Fakültesi/Beyin ve Sinir Cerrahisi Ana Bilim Dalı
local.contributor.departmentTıp Fakültesi/Tıbbi Patoloji Ana Bilim Dalı
local.indexed.atScopus
local.indexed.atWOS

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