Interferon signaling and treatment outcome in chronic hepatitis C
By M. Sarasin-Filipowicz, E. Oakeley, F. Duong, V. Christen, L. Terracciano, W. Filipowicz, M. Heim. Proceedings of the National Academy of Sciences of the United States of America, 2008
718 citations recorded by the source corpus.
Subfields: Hepatology, Immunology, Rheumatology
View Paper: https://www.semanticscholar.org/paper/e5f9b4d96be00e607a8315850b5a90ed4727cee8
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In Hepatology
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Citations in the corpus
- Interferon-stimulated genes and their antiviral effector functions (2011, neutral): “In those who successfully respond to treatment, ISG levels in the liver are low prior to treatment and increase significantly after treatment [9].”
- Shared and Distinct Functions of Type I and Type III Interferons (2019, neutral): “Type III IFNs inhibited growth of several different tumor cell lines and diminished local and metastatic tumor formation in mice including cancers from lung, liver, breast, and prostate (Abushahba et al., 2010; Lasfar et al., 2016; Li et al., 2008; Numasaki et al., 2007; Sato et al., 2006; Tezuka et”
- Interferon-Stimulated Genes: A Complex Web of Host Defenses (2014, background): “This question is of clinical importance because elevated levels of USP18 mRNA predict a poor treatment response to IFN-α therapy for hepatitis C virus (HCV) infection (114, 115).”