TRAIL C1595T Variant Critically Alters the Level of sTRAIL in Terms of Histopathological Parameters in Colorectal Cancer
Author:
Funder
Bilimsel Araştirma Projeleri Birimi, Istanbul Üniversitesi
Publisher
Springer Science and Business Media LLC
Subject
Clinical Biochemistry
Link
https://link.springer.com/content/pdf/10.1007/s12291-023-01146-z.pdf
Reference26 articles.
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2. Nassiri M, Kooshyar MM, Roudbar Z, Mahdavi M, Doosti M. Genes and SNPs associated with non-hereditary and hereditary colorectal cancer. Asian Pac J Cancer Prev. 2013;14:5609–14. https://doi.org/10.7314/apjcp.2013.14.10.5609.
3. Li H, Zhu H, Xu CJ, Yuan J. Cleavage of BID by caspase 8 mediates the mitochondrial damage in the Fas pathway of apoptosis. Cell. 1998;94:491–501. https://doi.org/10.1016/s0092-8674(00)81590-1.
4. Micheau O, Thome M, Schneider P, Holler N, Tschopp J, Nicholson DW, et al. The long form of FLIP is an activator of caspase-8 at the Fas death-inducing signaling complex. J Biol Chem. 2002;277:45162–71. https://doi.org/10.1074/jbc.M206882200.
5. Maas C, Verbrugge I, de Vries E, Savich G, van de Kooij LW, Tait SW, et al. Smac/DIABLO release from mitochondria and XIAP inhibition are essential to limit clonogenicity of Type I tumor cells after TRAIL receptor stimulation. Cell Death Differ. 2010;17:1613–23. https://doi.org/10.1038/cdd.2010.39.
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