Evidence map›Paper›PMID 32664328›Full record

ReviewCells2020

High Mobility Group Box 1 in Human Cancer.

Bernardo L Rapoport, Helen C Steel, Annette J Theron, Liezl Heyman, Teresa Smit, Yastira Ramdas, Ronald Anderson

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
5.7field-weighted citation impact, top 3% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

41 citing papers in PubMed, 59 citations in OpenAlex.

  1. Melatonin exerts anOncology letters · 2026
    Article
  2. Modulation of HMGB1, PRF1, TRAIL, and M-CSF after TARGIT-IORT in breast-conserving surgery: defining a unique acute immune landscape.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Article
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  11. Immune aberrations in thymic epithelial tumors.Mediastinum (Hong Kong, China) · 2025
    Review
  12. Involvement of role of HMGB1-NLRP3 pathway in systemic disorders.Frontiers in cell and developmental biology · 2025
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Bernardo L RapoportDepartment of Immunology, Faculty of Health Sciences, University of Pretoria, Pretoria 0001, South Africa.
Helen C SteelDepartment of Immunology, Faculty of Health Sciences, University of Pretoria, Pretoria 0001, South Africa.
Annette J TheronDepartment of Immunology, Faculty of Health Sciences, University of Pretoria, Pretoria 0001, South Africa.
Liezl HeymanThe Medical Oncology Centre of Rosebank, Johannesburg 2196, South Africa.
Teresa SmitThe Medical Oncology Centre of Rosebank, Johannesburg 2196, South Africa.
Yastira RamdasThe Breast Care Centre, Netcare Milpark, 9 Guild Road, Parktown, Johannesburg 2193, South Africa.
Ronald AndersonDepartment of Immunology, Faculty of Health Sciences, University of Pretoria, Pretoria 0001, South Africa.
The Medical Oncology Centre of Rosebank · ZAUniversity of Pretoria · ZA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

High mobility group box 1 (HMGB1) is an extremely versatile protein that is located predominantly in the nucleus of quiescent eukaryotic cells, where it is critically involved in maintaining genomic structure and function. During cellular stress, however, this multifaceted, cytokine-like protein undergoes posttranslational modifications that promote its translocation to the cytosol, from where it is released extracellularly, either actively or passively, according to cell type and stressor. In the extracellular milieu, HMGB1 triggers innate inflammatory responses that may be beneficial or harmful, depending on the magnitude and duration of release of this pro-inflammatory protein at sites of tissue injury. Heightened awareness of the potentially harmful activities of HMGB1, together with a considerable body of innovative, recent research, have revealed that excessive production of HMGB1, resulting from misdirected, chronic inflammatory responses, appears to contribute to all the stages of tumorigenesis. In the setting of established cancers, the production of HMGB1 by tumor cells per se may also exacerbate inflammation-related immunosuppression. These pro-inflammatory mechanisms of HMGB1-orchestrated tumorigenesis, as well as the prognostic potential of detection of elevated expression of this protein in the tumor microenvironment, represent the major thrusts of this review.

Indexed as

CytokinesHMGB1 ProteinHumansNeoplasmsReceptor for Advanced Glycation End ProductsSignal TransductionToll-Like ReceptorsCytokinesHMGB1 ProteinReceptor for Advanced Glycation End ProductsToll-Like Receptorscytokinesimmunosuppressionmyeloid-derived suppressor cellsprognostic factorreceptor for advanced glycation end-productsredox isoformsToll-like receptorsT regulatory cellstumorigenesistumor microenvironment

Identifiers

PMID32664328
PMCPMC7407638
OpenAlexW3042034110

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.