Aberrant activation-induced cytidine deaminase gene expression links BCR/ABL1-negative classical myeloproliferative neoplasms

Basit Öğe Kaydı
dc.authoridVeysel Sabri Hançer / 0000-0003-2994-1077en_US
dc.authorscopusidVeysel Sabri Hançer / 6506533543
dc.authorwosidVeysel Sabri Hançer / X-8971-2018en_US
dc.contributor.authorDermenci, Hasan
dc.contributor.authorDağlar Aday, Aynur
dc.contributor.authorAkadam Teker, Ayşegül Başak
dc.contributor.authorHançer, Veysel
dc.contributor.authorGelmez, Metin Yusuf
dc.contributor.authorNalçacı, Meliha
dc.contributor.authorYavuz, Akif Selim
dc.date.accessioned2022-07-18T11:33:29Z
dc.date.available2022-07-18T11:33:29Z
dc.date.issued2022en_US
dc.departmentİstinye Üniversitesi, Tıp Fakültesi, Temel Tıp Bilimleri Bölümüen_US
dc.description.abstractAim: Activation-induced cytidine deaminase (AID) has been associated with tumor initiation and development because of its ability to generate DNA damage and somatic mutations that cause genomic instability. This study aimed to investigate the relationship between AID expression levels and the risk of developing BCR/ABL1-negative myeloproliferative neoplasms (MPNs) by comparing the AID expression levels of the patients and controls. Methods: This case-control study was conducted on 117 cases (64 essential thrombocythemia, 23 primary myelofibrosis, and 30 polycythemia vera) with MPNs and 69 healthy controls. The JAK2 V617F somatic mutation analysis was performed using a real-time polymerase chain reaction (RT-PCR). The relative expression levels of AID in the patient and the control groups were analyzed using quantitative RT-PCR and the 2-??CT method. Results: AID expression levels were significantly higher in the patient group compared to the control group (p<0.001). AID expression levels were higher in patients with the JAK2 V617F mutation compared to patients without the mutation, but the difference was not statistically significant. Conclusion: The results of our study suggest that although overexpression of AID does not seem to support the JAK2 driver gene, it may contribute to the development of MPNs through other mechanisms.en_US
dc.identifier.citationDERMENCİ H,ADAY A. D,TEKER A. B. A,HANÇER V,GELMEZ M. Y,NALÇACI M,YAVUZ A. S (2022). Aberrant Activation-Induced Cytidine Deaminase Gene Expression Links BCR/ABL1-Negative Classical Myeloproliferative Neoplasms. Haseki Tıp Bülteni, 60(3), 228 - 233. Doi: 10.4274/haseki.galenos.2022.8133en_US
dc.identifier.doi10.4274/haseki.galenos.2022.8133en_US
dc.identifier.endpage233en_US
dc.identifier.issn1302-0072en_US
dc.identifier.issue3en_US
dc.identifier.scopus2-s2.0-85133963081en_US
dc.identifier.scopusqualityQ4en_US
dc.identifier.startpage228en_US
dc.identifier.trdizinid530948en_US
dc.identifier.urihttp://doi.org/10.4274/haseki.galenos.2022.8133
dc.identifier.urihttps://hdl.handle.net/20.500.12713/3008
dc.identifier.volume60en_US
dc.identifier.wosWOS:000823150600006en_US
dc.identifier.wosqualityN/Aen_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakTR-Dizinen_US
dc.institutionauthorHançer, Veysel Sabri
dc.language.isoenen_US
dc.publisherTR- Dizinen_US
dc.relation.ispartofHaseki Tıp Bültenien_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectCytidine Deaminaseen_US
dc.subjectMutationsen_US
dc.subjectGenomic Instabilityen_US
dc.titleAberrant activation-induced cytidine deaminase gene expression links BCR/ABL1-negative classical myeloproliferative neoplasmsen_US
dc.typeArticleen_US

Dosyalar

Orijinal paket
Listeleniyor 1 - 1 / 1
Küçük Resim
İsim:
c2b0f586-0833-44fe-9958-769f98b7b929.pdf
Boyut:
195.12 KB
Biçim:
Adobe Portable Document Format
Açıklama:
Tam Metin / Full Text
İndir
Lisans paketi
Listeleniyor 1 - 1 / 1
Küçük Resim Yok
İsim:
license.txt
Boyut:
1.44 KB
Biçim:
Item-specific license agreed upon to submission
Açıklama:
İndir

Koleksiyon

TR-Dizin İndeksli Yayınlar Koleksiyonu
Scopus İndeksli Yayınlar Koleksiyonu
Temel Tıp Bilimleri Bölümü Makale Koleksiyonu
WoS İndeksli Yayınlar Koleksiyonu