ReviewCells2021
Role of Complement in Regulating Inflammation Processes in Renal and Prostate Cancers.
Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Organokines in COVID-19: A Systematic Review.Cells · 2023Pooled it
- Oxidative Stress and Mitochondrial Dysfunction in Chronic Kidney Disease: From Molecular Mechanisms to Biomarkers and Targeted Therapies.Antioxidants (Basel, Switzerland) · 2026Review
- Decoding Lupus Diagnosis, Pathogenesis and Therapy: From Systemic Autoimmunity to Renal Damage.Diagnostics (Basel, Switzerland) · 2026Review
- Molecular mechanisms and recent advances in cellular senescence.Cell & bioscience · 2026Review
- A non-complement role for C1R rewires integrin and death-receptor signaling to drive renal cancer metastasis.Molecular cancer · 2026Article
- Article
- Progress in the study of the role of C5a-induced tubular cell senescence in the progression of diabetic kidney disease.Annals of medicine · 2025Review
- Review
- Enigmatic Roles of Complement Anaphylatoxin Signaling in Health and Disease.Immune network · 2025Review
- Identification of prostate cancer potential therapeutic targets and virtual drug screening through combined Mendelian randomization study, Bayesian colocalization and molecular docking.Discover oncology · 2025Article
- Article
- Improving drug repositioning with negative data labeling using large language models.Journal of cheminformatics · 2025Article
- Exploring Potential Complement Modulation Strategies for Ischemia-Reperfusion Injury in Kidney Transplantation.Antioxidants (Basel, Switzerland) · 2025Review
- Target repositioning using multi-layer networks and machine learning: The case of prostate cancer.Computational and structural biotechnology journal · 2024Article
- Distinct mesenchymal cell states mediate prostate cancer progression.Nature communications · 2024Article
- Plasma proteome fingerprint in kidney diseases.Frontiers in molecular biosciences · 2024Article
- The Janus-faced nature of complement in hemodialysis: interplay between complement, inflammation, and bioincompatibility unveiling a self-amplifying loop contributing to organ damage.Frontiers in nephrology · 2024Article
- Cellular senescence: the good, the bad and the unknown.Nature reviews. Nephrology · 2022Review
- Construction of 2DE Patterns of Plasma Proteins: Aspect of Potential Tumor Markers.International journal of molecular sciences · 2022Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
For decades, the complement system, the central pillar of innate immune response, was recognized as a protective mechanism against cancer cells and the manipulation of complement effector functions in cancer setting offered a great opportunity to improve monoclonal antibody-based cancer immunotherapies. Similarly, cellular senescence, the process of cell cycle arrest that allow DNA and tissue repair has been traditionally thought to be able to suppress tumor progression. However, in recent years, extensive research has identified the complement system and cellular senescence as two main inducers of tumour growth in the context of chronic, persistent inflammation named inflammaging. Here, we discuss the data describing the ambivalent role of senescence in cancer with a particular focus on tumors that are strongly dependent on complement activation and can be understood by a new, senescence-related point of view: prostate cancer and renal cell carcinoma.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.