Investigation of the role of CTLA-4 +49A/G (rs231775) polymorphism in non-small cell lung cancer and T cell immunity
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Title |
Investigation of the role of CTLA-4 +49A/G (rs231775) polymorphism in non-small cell lung cancer and T cell immunity
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Creator |
Isenlik, Burcu Kaya
Yaylim, Ilhan Dulger, Onur Kiyan, Hilal Findik Celik, Faruk Kaan Hakan, Mehmet Tolgahan Kucukhuseyin, Ozlem Kaynak, Kamil Turna, Akif |
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Subject |
CTLA-4
Lung cancer NSCLC T cell immunity |
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Description |
713-721
Cytotoxic T-lymphocyte associated protein 4 (CTLA-4) was the first immune checkpoint molecule to be used as a drug target and led the way in the field of immunooncology. CTLA-4 increases the activation threshold of T-cells and reduces immune responses to weak antigens, such as self and tumour antigens. In our study, 56 patients were diagnosed with NSCLC, and a control group of 98 healthy volunteers was included. CTLA-4 +49A/G gene polymorphism and serum CTLA-4 levels were assessed. However, we found that CTLA-4 +49A/G gene polymorphism was associated with lymphovascular invasion (LVI)(P=0.049). The ratio of the heterozygous AG variant was 42.9% in patients with LVI, while it was 14.3% without LVI.This could indicate that the CTLA-4 +49A/G heterozygote AG variant increases the risk of LVI. In addition, we detected withthe CTLA-4 +49A/G heterozygote AG variant had the worst mean overall survival at 56 weeks in the NSCLC patient group(X±SE=56.00±11.52, 95%CI 33.41-78.58, P=0.048). Furthermore, the patient group had significantly higher CTLA-4 serum levels (X±SE=121.57±11.89 pg/mL) compared with the control group (X±SE=79.09±3.09 pg/mL)( P=0.02). Our study dataserve as a guide for future studies to elucidate the pathogenesis of NSCLC and evaluate the therapeutic significance of CTLA-4. |
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Date |
2024-09-09T06:42:37Z
2024-09-09T06:42:37Z 2024-09 |
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Type |
Article
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Identifier |
0975-1009 (Online); 0019-5189 (Print)
http://nopr.niscpr.res.in/handle/123456789/64497 https://doi.org/10.56042/ijeb.v62i09.5682 |
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Language |
en
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Publisher |
NIScPR-CSIR,India
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Source |
IJEB Vol.62(09) [September 2024]
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