ReviewJournal of cellular and molecular medicine2008
Death receptors as targets for anti-cancer therapy.
Review in Journal of cellular and molecular medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 64 citations in OpenAlex.
- Chemotherapy-induced cardiotoxicity in breast cancer: mechanisms, diagnostic advances, and emerging protective strategies.American journal of physiology. Heart and circulatory physiology · 2025Review
- Pro-apoptotic and anti-apoptotic regulation mediated by deubiquitinating enzymes.Cellular and molecular life sciences : CMLS · 2022Review
- Review
- Aquaporin 1 suppresses apoptosis and affects prognosis in esophageal squamous cell carcinoma.Oncotarget · 2018Article
- Inactivation of BRCA2 in human cancer cells identifies a subset of tumors with enhanced sensitivity towards death receptor-mediated apoptosis.Oncotarget · 2016Article
- Embelin-Induced Apoptosis of Human Prostate Cancer Cells Is Mediated through Modulation of Akt and β-Catenin Signaling.PloS one · 2015Article
- Article
- Isolation and chemopreventive evaluation of novel naphthoquinone compounds from Alkanna tinctoria.Anti-cancer drugs · 2013Article
- Moutan Cortex Radicis inhibits inflammatory changes of gene expression in lipopolysaccharide-stimulated gingival fibroblasts.Journal of natural medicines · 2013Article
- Delivery of sTRAIL variants by MSCs in combination with cytotoxic drug treatment leads to p53-independent enhanced antitumor effects.Cell death & disease · 2013Article
- Enhanced antitumor activity of the photosensitizer meso-Tetra(N-methyl-4-pyridyl) porphine tetra tosylate through encapsulation in antibody-targeted chitosan/alginate nanoparticles.Biomacromolecules · 2013Article
- CD95 is part of a let-7/p53/miR-34 regulatory network.PloS one · 2012Article
- Glycogen synthase kinase-3 inhibition sensitizes pancreatic cancer cells to TRAIL-induced apoptosis.PloS one · 2012Article
- Anoikis mediators in oral squamous cell carcinoma.Oral diseases · 2011Review
- APO010, a synthetic hexameric CD95 ligand, induces human glioma cell death in vitro and in vivo.Neuro-oncology · 2011Article
- Differential effects of alpha-particle radiation and x-irradiation on genes associated with apoptosis.Radiology research and practice · 2011Article
- Quercetin induced apoptosis in association with death receptors and fludarabine in cells isolated from chronic lymphocytic leukaemia patients.British journal of cancer · 2010Article
- Inhibition of nuclear factor-kappa B differentially affects thyroid cancer cell growth, apoptosis, and invasion.Molecular cancer · 2010Article
- Acquired activation of the Akt/cyclooxygenase-2/Mcl-1 pathway renders lung cancer cells resistant to apoptosis.Molecular pharmacology · 2010Article
- Early growth response-1 is a regulator of DR5-induced apoptosis in colon cancer cells.British journal of cancer · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human tumour cells are characterized by their ability to avoid the normal regulatory mechanisms of cell growth, division and death. The classical chemotherapy aims to kill tumour cells by causing DNA damage-induced apoptosis. However, as many tumour cells possess mutations in intracellular apoptosis-sensing molecules like p53, they are not capable of inducing apoptosis on their own and are therefore resistant to chemotherapy. With the discovery of the death receptors the opportunity arose to directly trigger apoptosis from the outside of tumour cells, thereby circumventing chemotherapeutic resistance. Death receptors belong to the tumour necrosis factor receptor superfamily, with tumour necrosis factor (TNF) receptor-1, CD95 and TNF-related apoptosis-inducing ligand-R1 and -R2 being the most prominent members. This review covers the current knowledge about these four death receptors, summarizes pre-clinical approaches engaging these death receptors in anti-cancer therapy and also gives an overview about their application in clinical trials conducted to date.
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.