FACT inhibitor CBL0137, administered in an optimized schedule, potentiates radiation therapy for glioblastoma by suppressing DNA damage repair

No abstract is available for this paper.

• Publication year

  2024

• Venue

  Journal of Neuro-Oncology

• Publication date

  2024-09-09

• Fields of study

  Biology, Medicine, Chemistry

• Identifiers
  DOI 10.1007/s11060-024-04819-8PMID 39251545PMCID PMC12704690
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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  2023influential reference
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  2018cited by this paper
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  2018cited by this paper
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  2017cited by this paper
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  2017cited by this paper
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• HaloJ

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  2013cited by this paper
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  2013cited by this paper
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• Journal

  2008cited by this paper
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