Resources

Resources

Funding information, project links, documents, and references for GLIOBREAK.

Project resources

Funding, links and public materials

Horizon Europe

Funding

GLIOBREAK is supported by Horizon Europe EIC Transition funding and builds on tumour-host and single-cell multi-omics expertise associated with the ongoing EU-funded GLIOMATCH project at KU Leuven.[CORDIS GLIOMATCH]


Public materials

Approved information and future placeholders

This area distinguishes material that is already public from categories that will be populated only when approved items become available.

Available

Funding acknowledgement

The official EU funding acknowledgement is provided on this page.

View acknowledgement

Available

EU disclaimer

The official funder disclaimer is provided with the funding acknowledgement.

View disclaimer

Available

Project factsheet

The European Commission CORDIS record provides the current public GLIOBREAK project factsheet.

Open CORDIS factsheet

When available

Press releases

Approved public press releases will be linked from News when available.

Visit News

When available

Publications

GLIOBREAK project publications will be listed when available and approved for public release. The reference library below is a separate collection of supporting sources.

Browse supporting references

When available

Presentations

Approved public presentations and posters will be added when available.

Current information

Plain-language resources

The patient and family page provides current plain-language project status and independent support resources. Further approved materials will be added when available.

For Patients and Families

Scientific references

Selected evidence and guidance

Claim-level links throughout the site point to these sources. Peer-reviewed evidence, official project records, regulatory guidance, and company-reported preclinical findings are identified separately. None constitutes clinical evidence for BEA-17, which remains investigational.

Glioblastoma disease context

  1. Stupp R et al. Radiotherapy plus concomitant and adjuvant temozolomide for glioblastoma. New England Journal of Medicine (2005).

    Landmark clinical evidence establishing radiotherapy with concomitant and adjuvant temozolomide as a standard treatment approach.

  2. Wen PY et al. Glioblastoma in adults: a SNO and EANO consensus review on current management and future directions. Neuro-Oncology (2025).

    Updated consensus review of adult glioblastoma classification, standard management, therapeutic challenges, and investigational approaches.

  3. Price M et al. CBTRUS Statistical Report: Primary Brain and Other Central Nervous System Tumors Diagnosed in the United States in 2017-2021. Neuro-Oncology (2024).

    US registry source for glioblastoma incidence (3.27 per 100,000 annually) and five-year relative survival (7.1%).

  4. Weller M et al. EANO guideline on the diagnosis and treatment of adult astrocytic and oligodendroglial gliomas. The Lancet Oncology (2017).

    Clinical guideline context for the diagnosis and treatment of adult diffuse gliomas, including glioblastoma.

LSD1 biology and tumour immunity

  1. Shi Y et al. Histone demethylation mediated by the nuclear amine oxidase homolog LSD1. Cell (2004).

    Foundational description of LSD1 as a histone demethylase and epigenetic regulator.

  2. SuvĂ  ML et al. Reconstructing and reprogramming the tumor-propagating potential of glioblastoma stem-like cells. Cell (2014).

    Preclinical evidence implicating the RCOR2/LSD1 complex in glioblastoma stem-like tumour-propagating cells.

  3. Sheng W et al. LSD1 ablation stimulates anti-tumor immunity and enables checkpoint blockade. Cell (2018).

    Preclinical evidence linking LSD1 loss with anti-tumour immune responses and checkpoint blockade activity.

  4. Qin Y et al. Inhibition of histone lysine-specific demethylase 1 elicits breast tumor immunity and enhances antitumor efficacy of immune checkpoint blockade. Oncogene (2019).

    Preclinical breast-cancer evidence that LSD1 inhibition can increase T-cell-attracting chemokines and CD8-positive T-cell tumour infiltration.

  5. Chagraoui J et al. UM171 preserves epigenetic marks that are reduced in ex vivo culture of human HSCs via potentiation of the CLR3-KBTBD4 complex. Cell Stem Cell (2021).

    Preclinical evidence that targeted degradation can perturb LSD1/CoREST components in a haematopoietic stem-cell context.

  6. Xiong Y et al. Inhibiting the coregulator CoREST impairs Foxp3-positive Treg function and promotes antitumor immunity. Journal of Clinical Investigation (2020).

    Preclinical mouse and human-cell evidence linking RCOR1 loss or CoREST inhibition with lower FoxP3 expression and impaired regulatory-T-cell suppressive function.

  7. Yeo MJR et al. UM171 glues asymmetric CRL3-HDAC1/2 assembly to degrade CoREST corepressors. Nature (2025).

    Mechanistic preclinical evidence that a molecular glue can induce degradation of LSD1/CoREST-family corepressors, including RCOR2 reporter constructs.

  8. Bao L et al. Tumoral RCOR2 promotes tumor development through dual epigenetic regulation of tumor plasticity and immunogenicity. Journal of Clinical Investigation (2025).

    Preclinical evidence that RCOR2 loss can restore CIITA/MHC-II expression and MHC-II-mediated antigen presentation in non-GBM tumour models.

  9. Mamun MA et al. LSD1: an emerging face in altering the tumor microenvironment and enhancing immune checkpoint therapy. Journal of Biomedical Science (2023).

    Review of evidence connecting LSD1 biology, the tumour microenvironment, and immunotherapy.

GBM heterogeneity and tumour microenvironment

  1. Neftel C et al. An integrative model of cellular states, plasticity, and genetics for glioblastoma. Cell (2019).

    Single-cell framework for glioblastoma cellular states, heterogeneity, and plasticity relevant to biomarker development.

  2. Weng L et al. Distinct tumor immune microenvironmental landscapes drive divergent immunotherapy responses in glioblastoma. Neuro-Oncology (2026).

    Human and murine single-cell evidence for distinct glioblastoma immune microenvironment states and divergent preclinical treatment responses.

Protein-complex destabilisation analogue

  1. Xu Y et al. A cell-based high-content screen identifies isocotoin as a small-molecule inhibitor of the meiosis-specific MEIOB-SPATA22 complex. Biology of Reproduction (2020).

    Mechanistic analogue in a different biological system: isocotoin disrupted the MEIOB-SPATA22 interaction and promoted degradation of both proteins.

Development and regulatory guidance

  1. International Council for Harmonisation. S7A and S7B safety pharmacology guidelines for human pharmaceuticals.

    International guidance on core safety pharmacology and non-clinical evaluation of delayed ventricular repolarisation risk.

  2. International Council for Harmonisation. M3(R2): Non-clinical safety studies for the conduct of human clinical trials and marketing authorisation for pharmaceuticals.

    International standards for non-clinical studies intended to support clinical trials and marketing-authorisation applications.

  3. European Medicines Agency. Guideline on strategies to identify and mitigate risks for first-in-human and early clinical trials with investigational medicinal products.

    Regulatory guidance for risk assessment, dose selection, and planning before and during early clinical trials.

  4. Regulation (EU) 2017/746 on in vitro diagnostic medical devices.

    European regulatory framework relevant to the future development and validation of an in vitro companion diagnostic.

Public project and development records

  1. European Commission CORDIS. GLIOBREAK project factsheet, Grant Agreement 101292011.

    Official public record for project partners, funding, duration, objectives, work programme, and stated development targets.

  2. European Innovation Council. EIC Transition 2025 call results: 40 projects selected from 611 submissions (2026).

    Official source for the EIC Transition selection figures and programme purpose.

  3. European Commission CORDIS. GLIOMATCH project factsheet, Grant Agreement 101136670.

    Official public record for the ongoing GLIOMATCH project and its spatial, single-cell, imaging, and patient-stratification work.

  4. Beactica Therapeutics. FDA Orphan Drug Designation for BEA-17 for the treatment of glioblastoma (2023).

    Company announcement supporting BEA-17's FDA Orphan Drug Designation and reported development status.

  5. Emond WB et al. Potentiation of Immunotherapy by LSD1 Modulation. AACR Annual Meeting abstract 705 (2023).

    Company-reported preclinical evidence that BEA-17 binds an allosteric site on LSD1 and reduces cellular levels of LSD1 and CoREST.

  6. Beactica Therapeutics. Scientific advisory meeting regarding the preclinical development of BEA-17 (2025).

    Company-reported source for preclinical model, oral-availability, blood-brain-barrier, and regulatory-planning statements.

EU acknowledgement

Funding acknowledgement and disclaimer

Funded by the European Union. Views and opinions expressed are however those of the author(s) only and do not necessarily reflect those of the European Union or European Innovation Council and SMEs Executive Agency (EISMEA). Neither the European Union nor the granting authority can be held responsible for them.

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