ArticleJournal for immunotherapy of cancer2022
Complement downregulation promotes an inflammatory signature that renders colorectal cancer susceptible to immunotherapy.
Article in Journal for immunotherapy of cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- Complement system in cancer: friend or foe of immunotherapy.Journal for immunotherapy of cancer · 2026Review
- The role of the complement system in gastrointestinal-related diseases.Frontiers in immunology · 2026Review
- The cost of persistent alarm: temporal transcriptional reprogramming of macrophages from acute activation to chronic immune suppression by day 11.Frontiers in immunology · 2026Article
- A comprehensive analysis of supermere, exomere, and extracellular vesicle isolation and cargo in colorectal cancer.Cell reports · 2025Article
- The complement system in intestinal inflammation and cancer.The Journal of clinical investigation · 2025Review
- Gut complement system: a new frontier in microbiota-host communication and intestinal homeostasis.The Journal of clinical investigation · 2025Review
- Organ-specific cancer biomarker identification: a ten-year single-center study in southern China.BMC cancer · 2025Article
- Advances in research on the intestinal microbiota in the mechanism and prevention of colorectal cancer (Review).Molecular medicine reports · 2025Review
- New insights into the role of complement system in colorectal cancer (Review).Molecular medicine reports · 2025Review
- TLR4/MyD88 expression patterns and novel genetic variants: association with aggressive clinicopathological features in colorectal cancer.Frontiers in oncology · 2025Article
- Pan-cancer convergence of tumour-immune microenvironment motifs revealed by CyTOF and imaging mass cytometry.Frontiers in immunology · 2025Review
- Effect of colorectal cancer stem cells on the development and metastasis of colorectal cancer.World journal of gastrointestinal oncology · 2024Review
- Complement: you gutsy thing!Trends in immunology · 2024Article
- State-of-the-art cytometry in the search of novel biomarkers in digestive cancers.Frontiers in oncology · 2024Review
- The role of intestinal flora on tumorigenesis, progression, and the efficacy of PD-1/PD-L1 antibodies in colorectal cancer.Cancer biology & medicine · 2023Review
- Improving radiotherapy in immunosuppressive microenvironments by targeting complement receptor C5aR1.The Journal of clinical investigation · 2023Article
Corrections and comments
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Authors and funding
11 authors at 6 institutions in 5 countries.
Funding
Abstract
BACKGROUND AND
aimsThe role of inflammatory immune responses in colorectal cancer (CRC) development and response to therapy is a matter of intense debate. While inflammation is a known driver of CRC, inflammatory immune infiltrates are a positive prognostic factor in CRC and predispose to response to immune checkpoint blockade (ICB) therapy. Unfortunately, over 85% of CRC cases are primarily unresponsive to ICB due to the absence of an immune infiltrate, and even the cases that show an initial immune infiltration can become refractory to ICB. The identification of therapy supportive immune responses in the field has been partially hindered by the sparsity of suitable mouse models to recapitulate the human disease. In this study, we aimed to understand how the dysregulation of the complement anaphylatoxin C3a receptor (C3aR), observed in subsets of patients with CRC, affects the immune responses, the development of CRC, and response to ICB therapy.
methodsWe use a comprehensive approach encompassing analysis of publicly available human CRC datasets, inflammation-driven and newly generated spontaneous mouse models of CRC, and multiplatform high-dimensional analysis of immune responses using microbiota sequencing, RNA sequencing, and mass cytometry.
resultsWe found that patients' regulation of the complement C3aR is associated with epigenetic modifications. Specifically, downregulation of
conclusionsOur findings reveal that C3aR may act as a previously unrecognized checkpoint to enhance antitumor immunity in CRC. C3aR can thus be exploited to overcome ICB resistance in a larger group of patients with CRC.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.