Evidence map›Paper›PMID 34057732›Full record

ReviewCellular oncology (Dordrecht, Netherlands)2021

DNA damage repair in glioblastoma: current perspectives on its role in tumour progression, treatment resistance and PIKKing potential therapeutic targets.

Mathew Lozinski, Nikola A Bowden, Moira C Graves, Michael Fay, Paul A Tooney

Abstract readReview
In one paragraph

Review in Cellular oncology (Dordrecht, Netherlands), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

15 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Role of BRCA1 in glioblastoma etiology.Cellular oncology (Dordrecht, Netherlands) · 2024
    Review
  9. Article
  10. Article
  11. Oncolytic viral vectors in the era of diversified cancer therapy: from preclinical to clinical.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022
    Review
  12. Article
  13. Article
  14. Article
  15. Review
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

5 authors at 1 institution in 1 country.

Mathew LozinskiSchool of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, University of Newcastle, Newcastle, NSW, Australia.ORCID http://orcid.org/0000-0001-7311-9430
Nikola A BowdenCentre for Drug Repurposing and Medicines Research, University of Newcastle, Newcastle, NSW, Australia.ORCID http://orcid.org/0000-0002-6047-1694
Moira C GravesCentre for Drug Repurposing and Medicines Research, University of Newcastle, Newcastle, NSW, Australia.ORCID http://orcid.org/0000-0002-3380-5417
Michael FayCentre for Drug Repurposing and Medicines Research, University of Newcastle, Newcastle, NSW, Australia.ORCID http://orcid.org/0000-0002-8519-315X
Paul A TooneySchool of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, University of Newcastle, Newcastle, NSW, Australia. paul.tooney@newcastle.edu.au.ORCID http://orcid.org/0000-0003-3745-4367
Hunter Medical Research Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe aggressive, invasive and treatment resistant nature of glioblastoma makes it one of the most lethal cancers in humans. Total surgical resection is difficult, and a combination of radiation and chemotherapy is used to treat the remaining invasive cells beyond the tumour border by inducing DNA damage and activating cell death pathways in glioblastoma cells. Unfortunately, recurrence is common and a major hurdle in treatment, often met with a more aggressive and treatment resistant tumour. A mechanism of resistance is the response of DNA repair pathways upon treatment-induced DNA damage, which enact cell-cycle arrest and repair of DNA damage that would otherwise cause cell death in tumour cells.

conclusionsIn this review, we discuss the significance of DNA repair mechanisms in tumour formation, aggression and treatment resistance. We identify an underlying trend in the literature, wherein alterations in DNA repair pathways facilitate glioma progression, while established high-grade gliomas benefit from constitutively active DNA repair pathways in the repair of treatment-induced DNA damage. We also consider the clinical feasibility of inhibiting DNA repair in glioblastoma and current strategies of using DNA repair inhibitors as agents in combination with chemotherapy, radiation or immunotherapy. Finally, the importance of blood-brain barrier penetrance when designing novel small-molecule inhibitors is discussed.

Indexed as

DNA DamageAntineoplastic Agents, AlkylatingBrain NeoplasmsCell Cycle CheckpointsDNA RepairDrug Resistance, NeoplasmGlioblastomaHumansModels, GeneticTemozolomideAntineoplastic Agents, AlkylatingTemozolomideBlood-brain barrierDNA damage response, DNA repairGlioblastomaPIKK inhibitorTreatment resistance

Identifiers

PMID34057732
PMCPMC12980763
OpenAlexW3165585889

What OpenQuestion holds

Textmetadata
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.