ArticleAmerican journal of cancer research2013
Life after death: targeting high mobility group box 1 in emergent cancer therapies.
Article in American journal of cancer research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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
49 citing papers in PubMed, 73 citations in OpenAlex.
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- Natural compounds and programmed necrosis: pioneering a new frontier in cancer treatments.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Research progress on risk factors for in-stent restenosis following cerebrovascular stent implantation.Frontiers in neurology · 2025Review
- A new strategy for treating colorectal cancer: Regulating the influence of intestinal flora and oncolytic virus on interferon.Molecular therapy oncolytics · 2023Review
- Research progress on exosomal proteins as diagnostic markers of gastric cancer (review article).Clinical and experimental medicine · 2023Review
- The expression of high mobility group protein 3 (American journal of cancer research · 2023Article
- Time-dependent expression of high-mobility group box-1 and toll-like receptors proteins as potential determinants of skin wound age in rats: Forensic implication.International journal of legal medicine · 2022Article
- MicroRNA-23a-3p targeting of HMGB1 inhibits LPS-induced inflammation in murine macrophagesExperimental and therapeutic medicine · 2022Article
- Damage-Associated Molecular Patterns (DAMPs) in Retinal Disorders.International journal of molecular sciences · 2022Review
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- HMGB1 promotes tumor progression and invasion through HMGB1/TNFR1/NF-κB axis in castration-resistant prostate cancer.American journal of cancer research · 2021Article
- Data Driven Mathematical Model of Colon Cancer Progression.Journal of clinical medicine · 2020Article
- Triangular Relationship between p53, Autophagy, and Chemotherapy Resistance.International journal of molecular sciences · 2020Review
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- Modulated Electro-Hyperthermia-Induced Tumor Damage Mechanisms Revealed in Cancer Models.International journal of molecular sciences · 2020Review
- The association between high mobility group box 1 chromatin protein and mitotic chromosomes in glioma cells.Oncology letters · 2020Article
- STAT3 Contributes To Oncolytic Newcastle Disease Virus-Induced Immunogenic Cell Death in Melanoma Cells.Frontiers in oncology · 2019Article
- Enhanced Antitumor Immune Response in 2'-5' Oligoadenylate Synthetase-Like 1- (OASL1-) Deficient Mice upon Cisplatin Chemotherapy and Radiotherapy.Journal of immunology research · 2019Article
- HMGB1 protein as a novel target for cancer.Toxicology reports · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
High mobility group box 1 (HMGB1), an evolutionarily highly conserved and abundant nuclear protein also has roles within the cytoplasm and as an extracellular damage-associated molecular pattern (DAMP) molecule. Extracellular HMGB1 is the prototypic endogenous 'danger signal' that triggers inflammation and immunity. Recent findings suggest that posttranslational modifications dictate the cellular localization and secretion of HMGB1. HMGB1 is actively secreted from immune cells and stressed cancer cells, or passively released from necrotic cells. During cancer development or administration of therapeutic agents including chemotherapy, radiation, epigenetic drugs, oncolytic viruses, or immunotherapy, the released HMGB1 may either promote or limit cancer growth, depending on the state of progression and vascularization of the tumor. Extracellular HMGB1 enhances autophagy and promotes persistence of surviving cancer cells following initial activation. When oxidized, it chronically suppresses the immune system to promote cancer growth and progression, thereby enhancing resistance to cancer therapeutics. In its reduced form, it can facilitate and elicit innate and adaptive anti-tumor immunity, recruiting and activating immune cells, in conjunction with cytotoxic agents, particularly in early transplantable tumor models. We hypothesize that HMGB1 also functions as an epigenetic modifier, mainly through regulation of NF-kB-dependent signaling pathways, to modulate the behavior of surviving cancer cells as well as the immune cells found within the tumor microenvironment. This has significant implications for developing novel cancer therapeutics.
Indexed as
Identifiers
23359863PMC3555201W177603265What 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.