Evidence map›Paper›PMID 37291277›Full record

ArticleMedical oncology (Northwood, London, England)2023

Capicua (CIC) mutations in gliomas in association with MAPK activation for exposing a potential therapeutic target.

Sourat Darabi, Joanne Xiu, Timothy Samec, Santosh Kesari, Jose Carrillo, Sonikpreet Aulakh, Kyle M Walsh, Soma Sengupta, Ashley Sumrall, David Spetzler and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Medical oncology (Northwood, London, England), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

16 citing papers in PubMed, 18 citations in OpenAlex.

  1. Evaluating Debio 1347 in Patients with FGFR Fusion-Positive Advanced Solid Tumors from the FUZE Multicenter, Open-Label, Phase II Basket Trial.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024
    Trial
  2. Article
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  7. Genetic mechanisms of resistance to targeted KRAS inhibition.bioRxiv : the preprint server for biology · 2025
    Article
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  9. Review
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  12. Genomic Profiling in Glioma Patients to Explore Clinically Relevant Markers.International journal of molecular sciences · 2024
    Article
  13. Article
  14. Advanced Age in Humans and Mouse Models of Glioblastoma Show Decreased Survival from Extratumoral Influence.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023
    Article
  15. Article
  16. 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

12 authors at 8 institutions in 1 country.

Sourat DarabiHoag Family Cancer Institute, Newport Beach, CA, USA.
Joanne XiuCaris Life Sciences, Phoenix, AZ, USA.
Timothy SamecCaris Life Sciences, Phoenix, AZ, USA. tsamec@carisls.com.ORCID http://orcid.org/0000-0003-3468-7165
Santosh KesariHoag Family Cancer Institute, Newport Beach, CA, USA.
Jose CarrilloHoag Family Cancer Institute, Newport Beach, CA, USA.
Sonikpreet AulakhWest Virginia University, Morgantown, WV, USA.
Kyle M WalshDuke University School of Medicine, Durham, NC, USA.
Soma SenguptaUniversity of Cincinnati College of Medicine, Cincinnati, OH, USA.
Ashley SumrallLevine Cancer Institute, Charlotte, NC, USA.
David SpetzlerCaris Life Sciences, Phoenix, AZ, USA.
Michael GlantzPenn State Hershey Medical Center, Hershey, PA, USA.
Michael J DemeureHoag Family Cancer Institute, Newport Beach, CA, USA.
Caris Life Sciences (United States) · USHoag Memorial Hospital Presbyterian · USDuke University · USLevine Cancer Institute · USPenn State Milton S. Hershey Medical Center · USTranslational Genomics Research Institute · USUniversity of Cincinnati Medical Center · USWest Virginia University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gliomas are the most prevalent neurological cancer in the USA and care modalities are not able to effectively combat these aggressive malignancies. Identifying new, more effective treatments require a deep understanding of the complex genetic variations and relevant pathway associations behind these cancers. Drawing connections between gene mutations with a responsive genetic target can help drive therapy selections to enhance patient survival. We have performed extensive molecular profiling of the Capicua gene (CIC), a tumor and transcriptional suppressor gene, and its mutation prevalence in reference to MAPK activation within clinical glioma tissue. CIC mutations occur far more frequently in oligodendroglioma (52.1%) than in low-grade astrocytoma or glioblastoma. CIC-associated mutations were observed across all glioma subtypes, and MAPK-associated mutations were most prevalent in CIC wild-type tissue regardless of the glioma subtype. MAPK activation, however, was enhanced in CIC-mutated oligodendroglioma. The totality of our observations reported supports the use of CIC as a relevant genetic marker for MAPK activation. Identification of CIC mutations, or lack thereof, can assist in selecting, implementing, and developing MEK/MAPK-inhibitory trials to improve patient outcomes potentially.

Indexed as

Brain NeoplasmsGliomaOligodendrogliomaHumansMutationRepressor ProteinsTreatment OutcomeRepressor ProteinsCapicuaClinical oncologyGliomaMAPKMolecular oncologyTargeted medicine

Identifiers

PMID37291277
PMCPMC10250263
OpenAlexW4379792438

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.