Evidence map›Paper›PMID 40429877›Full record

ReviewInternational journal of molecular sciences2025

Different Mechanisms in Doxorubicin-Induced Neurotoxicity: Impact of BRCA Mutations.

Kriti S Bhatt, Aman Singh, Gursharan S Marwaha, Naresh Ravendranathan, Inderbir S Sandhu, Kristen Kim, Eesha Singh, Jefferson C Frisbee, Krishna K Singh

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PubMed Full text at PMC Publisher
In one paragraph

Review in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
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

9 citing papers in PubMed.

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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

9 authors.

Kriti S BhattDepartment of Medical Biophysics, Schulich School of Medicine and Dentistry, University of Western Ontario, London, ON N6A 5C1, Canada.ORCID 0009-0001-2627-8065
Aman SinghDepartment of Medical Biophysics, Schulich School of Medicine and Dentistry, University of Western Ontario, London, ON N6A 5C1, Canada.
Gursharan S MarwahaDepartment of Medical Biophysics, Schulich School of Medicine and Dentistry, University of Western Ontario, London, ON N6A 5C1, Canada.
Naresh RavendranathanDepartment of Medical Biophysics, Schulich School of Medicine and Dentistry, University of Western Ontario, London, ON N6A 5C1, Canada.
Inderbir S SandhuDepartment of Medical Biophysics, Schulich School of Medicine and Dentistry, University of Western Ontario, London, ON N6A 5C1, Canada.
Kristen KimDepartment of Medical Biophysics, Schulich School of Medicine and Dentistry, University of Western Ontario, London, ON N6A 5C1, Canada.
Eesha SinghLondon Central Secondary School, London, ON N6B 2P8, Canada.
Jefferson C FrisbeeDepartment of Medical Biophysics, Schulich School of Medicine and Dentistry, University of Western Ontario, London, ON N6A 5C1, Canada.
Krishna K SinghDepartment of Medical Biophysics, Schulich School of Medicine and Dentistry, University of Western Ontario, London, ON N6A 5C1, Canada.ORCID 0000-0002-6097-8401

Funding

Heart and Stroke Foundation of Canada G-22-0032104
6 · The paper itself

Abstract

The genotoxic drug doxorubicin (Dox) remains one of the most powerful chemotherapeutic options available for a wide range of cancers including breast, ovarian, and other cancers. However, emerging evidence links Dox treatment with chemotherapy-induced cognitive impairment, a condition that is popularly referred to as Dox-induced neurotoxicity or "chemobrain", which limits the use of the drug. There are no specific treatments for Dox-induced neurotoxicity, only interventions to mitigate the neurotoxic effects of the drug. Accumulating evidence indicates that DNA damage, oxidative stress, dysregulation of autophagy and neurogenesis, inflammation, and apoptosis play central roles in Dox-induced neurotoxicity. Additionally, germline mutations in the tumour suppressor genes breast cancer susceptibility genes 1 and 2 (BRCA1 and BRCA2) increase the risk of breast, ovarian, and related cancers. BRCA1 and BRCA2 are distinct proteins that play crucial, unique roles in homologous recombination-mediated double-stranded break repair. Furthermore, BRCA1 and 2 mitigate oxidative stress in both neural cells and brain microvascular endothelial cells, which suggests that they have a critical role as regulators of pathways central to the development of Dox-induced neurotoxicity. Despite research on the effects of Dox on cognitive function, there is a gap in knowledge about the role of BRCA1 and BRCA2 in Dox-induced neurotoxicity. In this review, we discuss existing findings about the role of different mechanisms and the role of BRCA1 and BRCA2 in Dox-induced neurotoxicity, along with future perspectives.

Indexed as

Antibiotics, AntineoplasticBRCA1 ProteinBRCA2 ProteinDoxorubicinMutationNeurotoxicity SyndromesAnimalsDNA DamageFemaleHumansOxidative StressAntibiotics, AntineoplasticBRCA1 ProteinBRCA1 protein, humanBRCA2 ProteinBRCA2 protein, humanDoxorubicinBRCA1BRCA2cognitive impairmentdoxorubicinneurodegeneration

Identifiers

PMID40429877
PMCPMC12111927

What OpenQuestion holds

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Registered trials

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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.