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Record W4409652619 · doi:10.1158/1538-7445.am2025-7225

Abstract 7225: The secreted cytokine Chitinase 3-like-1 promotes breast cancer metastasis

2025· article· en· W4409652619 on OpenAlexaff
Tarek Taifour, Yu Gu, Virginie Sanguin‐Gendreau, Dongmei Zuo, Bin Xiao, Hailey Proud, Nancy U. Lin, Melissa E. Hughes, Kalie Smith, Rinath Jeselsohn, William J. Muller

Bibliographic record

VenueCancer Research · 2025
Typearticle
Languageen
FieldBiochemistry, Genetics and Molecular Biology
TopicStudies on Chitinases and Chitosanases
Canadian institutionsMcGill University
Fundersnot available
KeywordsMetastasisCancer researchBreast cancerMedicineBreast cancer metastasisChitinaseCytokineCancerInternal medicineOncologyBiologyCancer metastasisEnzymeBiochemistry

Abstract

fetched live from OpenAlex

Abstract Breast cancer is the second most common cancer and a major cause of mortality affecting women worldwide. Immunosuppression is a key hallmark of cancer progression, whereby cancer cells suppress the immune system that is programmed to fight the disease. This suppressed tumor immune microenvironment (TIME) facilitates cancer metastatic spread to distant organs, which is associated with treatment resistance, recurrence, and poor prognosis. The Signal transducer and activator of transcription 3 (Stat3) suppresses the immune system, drives cancer progression and metastasis. Genetic ablation of Stat3 in the murine inducible breast tumor model expressing polyoma virus middle T (PyMT), results in delayed tumor onset and reduced tumor growth and metastasis. We have also previously demonstrated that the secreted protein Chitinase 3-like-1 (Chi3l1) is a direct target of Stat3 which promotes immunosuppression through its actions on neutrophils. Chi3l1 recruits neutrophils and induces the formation of Neutrophil Extracellular Traps (NETs) that block T cells from infiltrating the tumor. Targeting both Chi3l1 or neutrophils resulted in increased T cell infiltration and delayed tumor onset. However, the roles of Chi3l1 during the metastatic cascade remained unclear. To further investigate the role of Chi3l1 in metastasis, we generated a novel inducible mouse model that overexpresses Chi3l1 specifically in the mammary epithelial cells. Overexpression of the Chi3l1 protein in the Stat3 knockout PyMT model showed a rescue of the delay in tumor onset. Consistent with our previous studies, Chi3l1 overexpression caused a dramatic influx of neutrophils and the generation of an immune suppressed TIME. In addition, we observe an increase in circulating tumor cells which correlated with a quicker onset and increased incidence of pulmonary metastasis. These results hint that in breast cancer, Chi3l1 overexpression creates a pro-tumorigenic TIME which favorizes tumor initiation and progression as well as induces intravasation of tumor cells into the blood stream, which leads to metastasis to distant sites. Our future studies will investigate whether this phenotype is driven through neutrophils and whether targeting neutrophils would inhibit Chi3l1-mediated metastasis. Citation Format: Adeline Masse, Tarek Taifour, Yu Gu, Virginie Sanguin-Gendreau, Dongmei Zuo, Bin Xiao, Hailey Proud, Nancy U. Lin, Melissa E. Hughes, Kalie Smith, Rinath Jeselsohn, William J. Muller. The secreted cytokine Chitinase 3-like-1 promotes breast cancer metastasis [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 7225.

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 distilled prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. Learned from the 10,348 direct Codex labels and 10,348 direct Gemma labels. Candidate is the union of thresholded teacher heads; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels or direct frontier model labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.000
Version: codex-gemma-dda1882f352aValidation 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 score0.140
Threshold uncertainty score0.588

Codex and Gemma teacher scores by category

CategoryCodexGemma
Metaresearch0.0000.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0000.001
Science and technology studies0.0010.000
Scholarly communication0.0000.000
Open science0.0010.000
Research integrity0.0000.000
Insufficient payload (model declined to judge)0.0000.000

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 head0.038
GPT teacher head0.387
Teacher spread0.350 · 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 teacher head, 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".

Quick stats

Citations0
Published2025
Admission routes1
Has abstractyes

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