Tumor counterattack: fact or fiction?

Igney, Frederik H.; Krammer, Peter H.

doi:10.1007/s00262-005-0680-7

Cited by 98Cancer Immunotherapy and BiomarkersCell death mechanisms and regulationT-cell and B-cell Immunology

The DOI matches its Crossref record; 103 of the 103 references it cites were found in a registry or an index.

Tumor counterattack: fact or fiction?

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Igney, Frederik H., Krammer, Peter H.·2005·Cancer Immunology, Immunotherapy

DOI 10.1007/s00262-005-0680-7PMC PMC11034178

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Abstract

Cancer development relies on a variety of mechanisms that facilitate tumor growth despite the presence of a functioning immune system. Understanding these mechanisms may foster novel therapeutic approaches for oncology and organ transplantation. By expression of the apoptosis-inducing protein CD95L (FasL, APO-1L, CD178), tumors may eliminate tumor-infiltrating lymphocytes and suppress anti-tumor immune responses, a phenomenon called "tumor counterattack". On the one hand, preliminary evidence of tumor counterattack in human tumors exists, and CD95L expression can prevent T-cell responses in vitro. On the other hand, CD95L-expressing tumors are rapidly rejected and induce inflammation in mice. Here, we summarize and discuss the consequences of CD95L expression of tumor cells and its contribution to immune escape.

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Fas/Fas ligand interplay is involved in immune evasion, with neoplasms showing resistance to Fas-mediated cytotoxicity and FasL expression potentially resulting in immune effector cell apoptosis.
“Additionally, evidence supports the involvement of Fas/Fas Ligand (FasL) interplay in immune evasion [77], with neoplasms showing resistance to Fas-mediated cytotoxicity and FasL expression potentially resulting in immune effector cells apoptosis [76,78].”
From Current and Future Trends of Colorectal Cancer Treatment: Exploring Advances in Immunotherapy (2024) · cites this paper as [78]
Cancer cells directly inhibit the immune system through molecules such as VEGF, prostaglandin E2, TGF-β, and IL-10, which suppress cytotoxic T-cell function.
“Cancer cells also directly inhibit the immune system through molecules like vascular endothelial growth factor (VEGF), prostaglandin E2, transforming growth factor-β (TGF- β), and interleukin-10 (IL-10), which suppress cytotoxic T-cell function [77,78,80,81,82,83].”
From Current and Future Trends of Colorectal Cancer Treatment: Exploring Advances in Immunotherapy (2024) · cites this paper as [78]

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Bischof, A. (2000) · doi:10.1002/1521-4141(200003)30:3
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Authors: Igney, F. H., & Krammer, P. H.
Affiliations: German Cancer Research Center (DE)
Corresponding author: Igney, Frederik H.
ORCID: Igney, Frederik H.
Krammer, Peter H.
Venue: Cancer Immunology, Immunotherapy
Publisher: Springer Science and Business Media LLC
Published: 2005-05-12
Volume: 54
Issue: 11
Pages: 1127-1136
ISSN: 0340-7004 (ISSN-L)
1432-0851
DOI: 10.1007/s00262-005-0680-7
PMC: PMC11034178
OpenAlex: W2009371357
Cited by: 98
References: 102
Citations by year: 2025: 1 · 2024: 2 · 2022: 1 · 2021: 3 · 2020: 2 · 2019: 3 · 2018: 2 · 2017: 5 · 2016: 4 · 2015: 5 · 2014: 4 · 2013: 4 · 2012: 4
FWCI: 1.06
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.springer.com/tdm (tdm)
Locations: Cancer Immunology Immunotherapy (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
Keywords: Fas ligand, tumor immune evasion, tumor-infiltrating lymphocytes, antitumor immunity, T cell depletion, tumor rejection, inflammation, organ transplantation, cancer immunotherapy
MeSH terms: Humans, Inflammation, Membrane Glycoproteins, Neoplasms, T-Lymphocytes, Apoptosis, fas Receptor, Tumor Escape, Fas Ligand Protein

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