ArticleCancer research2012
Cancer cell secretion of the DAMP protein HMGB1 supports progression in malignant mesothelioma.
Article in Cancer research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02044185 (Observational Study for Clinical Implications of HMGB1), which is not on this map. Cited by 158 papers, 3 of them syntheses 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.
Observational Study for Clinical Implications of HMGB1 (High-mobility Group Protein B1) in Patients Treated With Chemotherapy or Hematopoietic Stem Cell Transplantation
Who cites it
158 citing papers in PubMed, 3 syntheses or guidelines pooled it, 249 citations in OpenAlex.
- No association between HMGB1 polymorphisms and cancer risk: evidence from a meta-analysis.Bioscience reports · 2018Pooled it
- HMGB1 overexpression as a prognostic factor for survival in cancer: a meta-analysis and systematic review.Oncotarget · 2016Pooled it
- Pooled it
- HMGB1 directly activates BAP1 transcription to sustain tumor growth in mesothelioma.Cell death and differentiation · 2026Article
- Damage-Associated Molecular Patterns in Mesothelioma: Drivers of Inflammation and Therapeutic Targets.International journal of molecular sciences · 2026Review
- Dose-Response Relationships for Lung Tumor and Pleural Mesothelioma Induction by Repetitive Intratracheal Instillation of a Multiwalled Carbon Nanotube, MWCNT-7, in Rats: Comparison with Inhalation Carcinogenicity Based on Lung Burden.Nanomaterials (Basel, Switzerland) · 2026Article
- Context-dependent release of HMGB1: cell death mode, cell type and LPS stress drive monomer and heterocomplex formation.Molecular medicine (Cambridge, Mass.) · 2026Article
- Review
- HMGB1-Platelet Interactions: Mechanisms and Targeted Therapy Strategies.Thrombosis and haemostasis · 2026Review
- Mesothelioma location influences the tumour microenvironment and immune checkpoint therapy response in preclinical models.Scientific reports · 2026Article
- The SMAD-Pathway Mediates HMGB1-Induced Proliferation and Metastatic Progression in Cutaneous Squamous Cell Carcinoma Cells.Annals of dermatology · 2026Article
- Pathobiology and clinical significance of malignant pleural effusions.EMBO molecular medicine · 2026Review
- From biology to therapy: current standards and emerging strategies in pleural mesothelioma.Frontiers in oncology · 2026Review
- Review
- Comparative Carcinogenicity of Double-Walled Carbon Nanotubes of Different Lengths Administered by Intratracheal Installation into Rat Lungs.Nanomaterials (Basel, Switzerland) · 2025Article
- Pleural mesothelioma.Nature reviews. Disease primers · 2025Review
- HMGB1 Deficiency Occurs in a Broad Range of Human Cancers and Is Often Associated with Unfavorable Tumor Phenotype.Diagnostics (Basel, Switzerland) · 2025Article
- Metal-based immunogenic cell death inducers for cancer immunotherapy.Chemical science · 2025Review
- A pan-cancer analysis of the oncogenic function of HMGB1 in human tumors.Biochemistry and biophysics reports · 2024Article
- High Mobility Group Box 1 (HMGB1): Molecular Signaling and Potential Therapeutic Strategies.Cells · 2024Review
98 more citing papers are in PubMed but not listed here.
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 3 institutions in 2 countries.
Funding
Abstract
Human malignant mesothelioma is an aggressive and highly lethal cancer that is believed to be caused by chronic exposure to asbestos and erionite. Prognosis for this cancer is generally poor because of late-stage diagnosis and resistance to current conventional therapies. The damage-associated molecular pattern protein HMGB1 has been implicated previously in transformation of mesothelial cells. Here we show that HMGB1 establishes an autocrine circuit in malignant mesothelioma cells that influences their proliferation and survival. Malignant mesothelioma cells strongly expressed HMGB1 and secreted it at high levels in vitro. Accordingly, HMGB1 levels in malignant mesothelioma patient sera were higher than that found in healthy individuals. The motility, survival, and anchorage-independent growth of HMGB1-secreting malignant mesothelioma cells was inhibited in vitro by treatment with monoclonal antibodies directed against HMGB1 or against the receptor for advanced glycation end products, a putative HMGB1 receptor. HMGB1 inhibition in vivo reduced the growth of malignant mesothelioma xenografts in severe-combined immunodeficient mice and extended host survival. Taken together, our findings indicate that malignant mesothelioma cells rely on HMGB1, and they offer a preclinical proof-of-principle that antibody-mediated ablation of HMBG1 is sufficient to elicit therapeutic activity, suggesting a novel therapeutic approach for malignant mesothelioma treatment.
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.