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Abstract PR07: Oncogene addition to MYB-NFIB in adenoid cystic carcinomas induced in transgenic mice

2023· article· en· W4386784603 on OpenAlexaboutno aff
Vicente Escamilla‐Rivera, Yuan Hu, S. H. Cho, Adel K. El‐Naggar, Han Luo, Carlos Caulı́n

Bibliographic record

VenueClinical Cancer Research · 2023
Typearticle
Languageen
FieldMedicine
TopicSalivary Gland Tumors Diagnosis and Treatment
Canadian institutionsnot available
Fundersnot available
KeywordsMYBCancer researchBiologyAdenoid cystic carcinomaOncogeneCancerCarcinomaCell cycleTranscription factorGeneticsGene

Abstract

fetched live from OpenAlex

Abstract Adenoid cystic carcinoma (ACC) is a slow-growing salivary gland malignancy. The frequent occurrence of chromosome t(6;9) translocations, resulting in MYB-NFIB fusions, is a hallmark of ACC. Approximately, 50% of all ACCs studied to date have been shown to express MYB-NFIB chimeric transcripts, suggesting a prominent role in ACC tumorigenicity. However, the potential relevance of chimeric MYB-NFIB proteins in the development and progression of ACC remains poorly understood. To assess the role of MYB-NFIB in ACC development, we generated transgenic mice in which MYB-NFIB is overexpressed in salivary and mammary glands, using a doxycycline-inducible system. Importantly, a subset of these mice developed ACCs, suggesting that MYB-NFIB is an oncogenic driver of ACC. Using this reversible inducible model, we investigated whether MYB-NFIB was required to maintain established tumors. We found that suppression of the MYB-NFIB transgene upon exposure to doxycycline (Dox) promoted a rapid tumor regression. Tumoral volumes decreased by more than 50 % after only 10 days of starting Dox. This reduction in volume was accompanied by a transition towards a more organized cellular structure and a reduction in the number of cells positive for Ki-67 and MYB-NFIB. To identify mechanisms involved in tumor regression, we compared the transcriptomes from biopsies collected from salivary tumors prior to MYB-NFIB suppression with those from the same tumors after Dox-induced regression. We found that tumor regression upregulated immune-related pathways and promoted T cell infiltration. Additionally, several pathways were downregulated by MYB-NFIB suppression; particularly NOTCH signaling, Cyclin D1-CDK4/6, and Wnt/beta-catenin signaling. We then confirmed, by immunohistochemistry, that tumor biopsies taken before Dox had a higher number of cells positive for Cdk6, CyclinD1, and nuclear beta-catenin. Our results suggest that proteins in these pathways could be used as potential therapeutic targets in MYB-NFIB-driven ACCs. Citation Format: Vicente Escamilla-Rivera, Yuan Hu, Sungman Cho, Adel El-Naggar, Han Luo, Carlos Caulin. Oncogene addition to MYB-NFIB in adenoid cystic carcinomas induced in transgenic mice [abstract]. In: Proceedings of the AACR-AHNS Head and Neck Cancer Conference: Innovating through Basic, Clinical, and Translational Research; 2023 Jul 7-8; Montreal, QC, Canada. Philadelphia (PA): AACR; Clin Cancer Res 2023;29(18_Suppl):Abstract nr PR07.

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame machine prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.000
Version: metacan-v3-hybrid-931329e0061cValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Bench or experimental · Consensus signal: Bench or experimental
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.004
Threshold uncertainty score0.013

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0000.000
Meta-epidemiology (narrow)0.0010.001
Meta-epidemiology (broad)0.0000.001
Bibliometrics0.0010.000
Science and technology studies0.0000.001
Scholarly communication0.0010.000
Open science0.0010.000
Research integrity0.0010.003
Insufficient payload (model declined to judge)0.0040.002

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.398
GPT teacher head0.557
Teacher spread0.160 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
Study designBench or experimental
Domainnot available
GenreEmpirical

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

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Citations0
Published2023
Admission routes1
Has abstractyes

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