ReviewCold Spring Harbor perspectives in biology2020
Death Receptors and Their Ligands in Inflammatory Disease and Cancer.
Review in Cold Spring Harbor perspectives in biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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
28 citing papers in PubMed, 60 citations in OpenAlex.
- Article
- Acupuncture-induced HSP70 upregulation in neuroprotection: mitochondrial and anti-apoptotic mechanisms.American journal of translational research · 2026Review
- Targeting cuproptosis in liver cancer: Molecular mechanisms and therapeutic implications.Apoptosis : an international journal on programmed cell death · 2025Review
- Loss of Beclin 1 primes colorectal cancer cells for Immunogenic necroptosis via transcriptional de-repression of RIPK1/RIPK3/MLKL axis.Molecular biology reports · 2025Article
- Necroptosis in cancer: insight from epigenetic, post-transcriptional and post-translational modifications.Journal of hematology & oncology · 2025Review
- PTPN23-dependent ESCRT machinery functions as a cell death checkpoint.Nature communications · 2024Article
- Strong activation of p53 by actinomycin D and nutlin-3a overcomes the resistance of cancer cells to the pro-apoptotic activity of the FAS ligand.Apoptosis : an international journal on programmed cell death · 2024Article
- Apoptosis, a Metabolic "Head-to-Head" between Tumor and T Cells: Implications for Immunotherapy.Cells · 2024Review
- Caspase 8 deletion causes infection/inflammation-induced bone marrow failure and MDS-like disease in mice.Cell death & disease · 2024Article
- IRE1 RNase controls CD95-mediated cell death.EMBO reports · 2024Article
- Review
- The Function of Necroptosis and Its Treatment Target in IBD.Mediators of inflammation · 2024Review
- Review
- Targeting regulated cell death pathways in cancers for effective treatment: a comprehensive review.Frontiers in cell and developmental biology · 2024Review
- Progress of natural sesquiterpenoids in the treatment of hepatocellular carcinoma.Frontiers in oncology · 2024Review
- Characterizing the regulatory Fas (CD95) epitope critical for agonist antibody targeting and CAR-T bystander function in ovarian cancer.Cell death and differentiation · 2023Article
- Cleavage of cFLIP restrains cell death during viral infection and tissue injury and favors tissue repair.Science advances · 2023Article
- DR5 Up-Regulation Induced by Dichloroacetate Sensitizes Tumor Cells to Lipid Nanoparticles Decorated with TRAIL.Journal of clinical medicine · 2023Article
- Endothelial Caspase-8 prevents fatal necroptotic hemorrhage caused by commensal bacteria.Cell death and differentiation · 2023Article
- Regulation of apoptosis by ubiquitination in liver cancer.American journal of cancer research · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
On binding to their cognate ligands, death receptors can initiate a cascade of events that can result in two distinct outcomes: gene expression and cell death. The study of three different death receptor-ligand systems, the tumor necrosis factor (TNF)-TNF receptor 1 (TNFR1), the CD95L-CD95, and the TNF-related apoptosis-inducing ligand (TRAIL)-TRAIL-R1/2 system, has drawn the attention of generations of scientists over the past 50 years. This scientific journey, as often happens in science, has been anything but a straight line to success and discoveries in this field were often made by serendipity, catching the scientists by surprise. However, as Louis Pasteur pointed out, luck prefers the prepared mind. It is therefore not surprising that the most impactful discovery of the field to date, the fact that TNF inhibition serves as an effective treatment for several inflammatory and autoimmune diseases, has been like this. Luckily, the scientists who made this discovery were prepared and, most importantly, determined to harness their discovery for therapeutic benefit. Today's research on these death receptor-ligand systems has led to the discovery of a causal link between cell death induced by a variety of these systems and inflammation. In this review, we explain why we predict that therapeutic exploitation of this discovery may profoundly impact the future treatment of inflammatory disease and cancer.
Indexed as
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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.