ArticleFrontiers in oncology2026
Synergistic antitumor effect of HMGB2 targeting combined with MDM2 inhibitor in diffuse intrinsic pontine glioma therapy.
Article in Frontiers in oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diffuse intrinsic pontine glioma (DIPG) is a brain malignancy in children with a dismal prognosis. The high mobility group box 2 (HMGB2) is a member of the HMGB family of chromatin-associated proteins, and is identified as a potential oncogene in various cancers. However, the effects of HMGB2 in DIPG remains unclear. In this study, we observed aberrant expression of HMGB2 in multiple cancer types, with its expression level being negatively correlated with clinical outcomes across pan-cancers. High expression of HMGB2 was determined in DIPG cells, but not in primary brainstem neural progenitor cells (PPCs). Knockdown of HMGB2 significantly inhibited the DIPG cell proliferation and induced cell apoptosis. Intriguingly, bulk RNA sequencing revealed that inhibition of HMGB2 upregulated p53 protein expression and enhanced the activity of p53-p21 axis. Combining HMGB2 inhibitor with a p53-MDM2 inhibitor RG7388 resulted in a synergistic suppression of DIPG cell growth and promoted cell apoptosis by activating the tumor suppressor p53 and p21 expressions
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.