Evidence map›Paper›PMID 41923464›Full record

ArticleHead & neck2026

AKT, ATR, and Notch Inhibitors Radiosensitize a Preclinical Model of Adenoid Cystic Carcinoma.

Shivani Thoidingjam, Sushmitha Sriramulu, Asya Haider Muratoglu, Stephen Brown, Oudai Hassan, Benjamin Movsas, Haythem Ali, Steven Chang, Patrick Ha, Farzan Siddiqui and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Head & neck, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

11 authors.

Shivani ThoidingjamDepartment of Radiation Oncology, Henry Ford Cancer Institute, Henry Ford Health, Detroit, Michigan, USA.
Sushmitha SriramuluDepartment of Radiation Oncology, Henry Ford Cancer Institute, Henry Ford Health, Detroit, Michigan, USA.
Asya Haider MuratogluDepartment of Radiation Oncology, Henry Ford Cancer Institute, Henry Ford Health, Detroit, Michigan, USA.
Stephen BrownDepartment of Radiation Oncology, Henry Ford Cancer Institute, Henry Ford Health, Detroit, Michigan, USA.
Oudai HassanDepartment of Surgical Pathology, Henry Ford Cancer Institute, Henry Ford Health, Detroit, Michigan, USA.
Benjamin MovsasDepartment of Radiation Oncology, Henry Ford Cancer Institute, Henry Ford Health, Detroit, Michigan, USA.
Haythem AliDepartment of Hematology/Oncology, Henry Ford Health, Detroit, Michigan, USA.
Steven ChangDepartment of Otolaryngology, Henry Ford Health, Detroit, Michigan, USA.
Patrick HaDepartment of Otolaryngology, University of California, San Francisco, California, USA.ORCID https://orcid.org/0000-0003-0306-6147
Farzan SiddiquiDepartment of Radiation Oncology, Henry Ford Cancer Institute, Henry Ford Health, Detroit, Michigan, USA.ORCID https://orcid.org/0000-0003-1547-835X
Shyam NyatiDepartment of Radiation Oncology, Henry Ford Cancer Institute, Henry Ford Health, Detroit, Michigan, USA.

Funding

Henry Ford Health System Department of Radiation OncologyHenry Ford Health System Game on Cancer AwardHenry Ford Health System Henry Ford-Research AdministrationHenry Ford Health System Near Miss Award
6 · The paper itself

Abstract

backgroundAdenoid Cystic Carcinoma (ACC) is a rare and lethal type of head and neck cancer. Standard therapy involves surgery followed by radiation therapy. The majority of ACC has MYB overexpression and MYB-NFIB gene fusions, while Notch mutations are associated with aggressive behavior. Targeted therapies against these drivers or their downstream targets have been incompletely explored, especially in combination with radiation.

methodscBioPortal was used for genomic and survival analyses. MYB, AKT, ATR, NOTCH, and NFIB expression was assessed via RNA-seq, qRT-PCR, and western blot. Radiation sensitization was evaluated by clonogenic assays while the effect on DNA damage was tested using γH2AX and RAD51 foci assays.

resultsMYB, ATR, AKT1, Notch1, Notch2, and NFIB are overexpressed in ACC tumors, PDX, and cell lines. ACC patients with ATR, AKT, MYB, and NFIB alterations have poor overall survival. ATR, AKT, and Notch inhibitors sensitized UM-HACC2A cells to radiation. Drugs and radiation combination reduced target mRNA expression.

conclusionATR, AKT, and Notch inhibitors radiosensitize a preclinical model of ACC.

Indexed as

Ataxia Telangiectasia Mutated ProteinsCarcinoma, Adenoid CysticHead and Neck NeoplasmsProto-Oncogene Proteins c-aktRadiation ToleranceReceptors, NotchAnimalsCell Line, TumorHumansNFI Transcription FactorsProto-Oncogene Proteins c-mybReceptor, Notch1Receptor, Notch2AKT1 protein, humanAtaxia Telangiectasia Mutated ProteinsATR protein, humanMYB protein, humanNFIB protein, humanNFI Transcription FactorsNOTCH1 protein, humanNOTCH2 protein, humanProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-mybReceptor, Notch1Receptor, Notch2Receptors, Notchadenoid cystic carcinomaAKTATRcombination therapymolecular targeted therapyMYB‐NFIBNOTCH signalingradiation therapy

Identifiers

PMID41923464
PMCPMC13432354

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LicenceCC BY-NC-ND
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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.