Please use this identifier to cite or link to this item: http://hdl.handle.net/11452/28616
Title: FHIT gene sequence variants and reduced fhit protein expression in glioblastoma multiforme
Authors: Güler, Gülnür
Aksoy, Kaya
Uludağ Üniversitesi/Tıp Fakültesi/Tıbbi Biyoloji Anabilim Dalı.
Uludağ Üniversitesi/Tıp Fakültesi/Beyin ve Sinir Cerrahisi Anabilim Dalı.
Uludağ Üniversitesi/Tıp Fakültesi/Tıbbi Patoloji Anabilim Dalı.
0000-0002-3820-424X
0000-0002-1619-6680
0000-0001-7904-883X
Çeçener, Gülşah
Tunca, Berrin Türkei
Egeli, Ünal
Bekar, Ahmet
Tolunay, Şahsine
AAP-9988-2020
AAI-1612-2021
ABI-6078-2020
AAH-1420-2021
6508156530
6602965754
55665145000
6603677218
6602604390
Keywords: Glioblastoma multiforme
FHIT gene
Sequence alterations
SSCP
IHC
Common fragile sites
Cell lung-cancer
Tumor-suppressor gene
Brain-tumors
Breast-cancer
Turkish patients
Predisposition
Mutations
3P14.2
Carcinoma
Cell biology
Neurosciences & neurology
Issue Date: Mar-2010
Publisher: Springer/Plenum Publishers
Citation: Çeçener, G. vd. (2010). "FHIT gene sequence variants and reduced fhit protein expression in glioblastoma multiforme". Cellular and Molecular Neurobiology, 30(2), 301-307.
Abstract: Molecular 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.
URI: https://doi.org/10.1007/s10571-009-9452-9
https://link.springer.com/article/10.1007/s10571-009-9452-9
http://hdl.handle.net/11452/28616
ISSN: 0272-4340
1573-6830
Appears in Collections:Scopus
Web of Science

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