ArticleNeuro-oncology2025
BCOR loss promotes both retinoblastoma growth and susceptibility to IGF1R inhibition.
Article in Neuro-oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
backgroundBCL-6 corepressor (BCOR) loss-of-function alterations are common in clinically aggressive retinoblastoma. The study aim was to determine if BCOR loss promotes the growth and dissemination of retinoblastoma cells, and identify the pathways it regulates in these retinal tumors of childhood.
methodsGain- and loss-of-function strategies were used to modulate BCOR levels in a panel of retinoblastoma cell lines, and the effects on proliferation, clonogenicity, apoptosis, and migration were assessed in vitro and in murine xenograft models.
resultsBCOR knockdown or knockout in retinoblastoma lines with high protein levels increased tumor growth, invasion, clonogenicity, and chemoresistance in vitro, while increased expression in low BCOR lines slowed growth. Growth of retinoblastoma xenografts was similarly sensitive to BCOR gain or loss. BCOR reduction resulted in upregulation of IGF1 and activation of IGF1 receptor (IGF1R) signaling, and the effects of IGF1R inhibition were dependent on BCOR level. In vitro, reduction of retinoblastoma growth and induction of apoptosis by the IGF1R inhibitors linsitinib and AEW541 were also significantly stronger in cells with low BCOR as compared to controls. Both linsitinib and AEW541 suppressed colony formation in a dose-dependent manner in BCOR knockout or knockdown cells. Finally, high BCOR levels rendered retinoblastoma xenografts insensitive to linsitinib.
conclusionsLoss of BCOR function is associated with more aggressive retinoblastoma cell line growth and chemoresistance, at least in part due to increased IGF1R signaling. Inhibiting IGF1R pharmacologically had a marked anti-tumor effect in aggressive retinoblastoma lacking BCOR, suggesting it as a new therapeutic target, although this still needs to be confirmed in clinical samples with BCOR mutations.
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.