Evidence map›Paper›PMID 31449084›Full record

ReviewCurrent opinion in oncology2019

Emerging mechanistic underpinnings and therapeutic targets for chemotherapy-related cognitive impairment.

Erin M Gibson, Michelle Monje

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.1field-weighted citation impact, top 7% 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

25 citing papers in PubMed, 54 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Observational
  7. Review
  8. Article
  9. Hormonal basis of brain fog in cancer treatment.The Journal of experimental medicine · 2024
    Article
  10. Article
  11. Review
  12. The neural addiction of cancer.Nature reviews. Cancer · 2023
    Review
  13. Chemobrain: An accelerated aging process linking adenosine AInternational review of neurobiology · 2023
    Review
  14. Review
  15. Article
  16. Distinct sleep disturbance and cognitive dysfunction profiles in oncology outpatients receiving chemotherapy.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2022
    Article
  17. Review
  18. Review
  19. Article
  20. Article
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

2 authors at 1 institution in 2 countries.

Erin M GibsonDepartment of Neurology and Neurological Sciences.
Michelle MonjeDepartment of Neurology and Neurological Sciences.
California Institute for Regenerative Medicine · US

Funding

Glioma Circuitry: Bridging Systems Neuroscience and CancerDP1NS111132 · NINDS · STANFORD UNIVERSITY · PI MONJE-DEISSEROTH, MICHELLE · 2018 to 2022
$5.7M
Neuronal activity-regulated mechanisms of glioma growthR01NS092597 · NINDS · STANFORD UNIVERSITY · PI MONJE-DEISSEROTH, MICHELLE · 2016 to 2021
$2.1M
NINDS NIH HHS DP1 NS111132NINDS NIH HHS R01 NS092597
6 · The paper itself

Abstract

purpose of reviewModern innovations in cancer therapy have dramatically increased the number of cancer survivors. An unfortunately frequent side-effect of cancer treatment is enduring neurological impairment. Persistent deficits in attention, concentration, memory, and speed of information processing afflict a substantial fraction of cancer survivors following completion of these life-saving therapies. Here, we highlight chemotherapy-related cognitive impairment (CRCI) and discuss the current understanding of mechanisms underlying CRCI. RECENT

findingsNew studies emphasize the deleterious impact of chemotherapeutic agents on glial-glial and neuron-glial interactions that shape the form, function and plasticity of the central nervous system. An emerging theme in cancer therapy-related cognitive impairment is therapy-induced microglial activation and consequent dysfunction of both neural precursor cells and mature neural cell types. Recent work has highlighted the complexity of dysregulated intercellular interactions involving oligodendrocyte lineage cells, microglia, astrocytes, and neurons following exposure to traditional cancer therapies such as methotrexate. This new understanding of the mechanistic underpinnings of CRCI has elucidated potential therapeutic interventions, including colony-stimulating factor 1 receptor inhibition, TrkB agonism, and aerobic exercise. SUMMARY: Traditional cancer therapies induce lasting alterations to multiple neural cell types. Therapy-induced microglial activation is a critical component of the cause of CRCI, contributing to dysregulation of numerous processes of neural plasticity. Therapeutic targeting of microglial activation or the consequent dysregulation of neural plasticity mechanisms are emerging.

Indexed as

AnimalsCognitive DysfunctionExerciseHumansMicrogliaNeoplasmsNeural Stem CellsNeuronal Plasticity

Identifiers

PMID31449084
PMCPMC7205182
OpenAlexW2969513413

What OpenQuestion holds

Textmetadata
LicenceTDM
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.