MétaCan
Menu
Back to cohort
Record W2911216374 · doi:10.1158/0008-5472.can-18-1602

MNK1/NODAL Signaling Promotes Invasive Progression of Breast Ductal Carcinoma <i>In Situ</i>

2019· article· en· W2911216374 on OpenAlexafffund
Qianyu Guo, Vivian Z. Li, Jessica N. Nichol, Fan Huang, William Yang, Samuel E.J. Preston, Zahra Talat, Hanne Lefrère, Henry Yu, Guihua Zhang, Mark Basik, Christophe Gonçalves, Dany Plourde, Jie Su, José Torres, Maud Marques, Sara Al Habyan, Krikor Bijian, Frédéric Amant, Michael Witcher, Fariba Behbod, Luke McCaffrey, Moulay A. Alaoui‐Jamali, Nadia V. Giannakopoulos, Muriel Brackstone, Lynne‐Marie Postovit, Sonia V. del Rincón, Wilson H. Miller

Bibliographic record

VenueCancer Research · 2019
Typearticle
Languageen
FieldMedicine
TopicCancer Cells and Metastasis
Canadian institutionsWestern UniversityUniversity of AlbertaMcGill University Health CentreNorthern Alberta Institute of TechnologyMcGill UniversityJewish General Hospital
FundersCanadian Cancer SocietyRéseau de cancérologie RossyCanadian Institutes of Health ResearchCancer Research SocietyNational Cancer InstituteGovernment of CanadaIsrael Cancer Research Fund
KeywordsDuctal carcinomaNodal signalingCancer researchNODALTumor progressionMetastasisCancerBreast cancerBiologyMedicineOncologyInternal medicine

Abstract

fetched live from OpenAlex

Abstract The mechanisms by which breast cancers progress from relatively indolent ductal carcinoma in situ (DCIS) to invasive ductal carcinoma (IDC) are not well understood. However, this process is critical to the acquisition of metastatic potential. MAPK-interacting serine/threonine-protein kinase 1 (MNK1) signaling can promote cell invasion. NODAL, a morphogen essential for embryogenic patterning, is often reexpressed in breast cancer. Here we describe a MNK1/NODAL signaling axis that promotes DCIS progression to IDC. We generated MNK1 knockout (KO) or constitutively active MNK1 (caMNK1)-expressing human MCF-10A–derived DCIS cell lines, which were orthotopically injected into the mammary glands of mice. Loss of MNK1 repressed NODAL expression, inhibited DCIS to IDC conversion, and decreased tumor relapse and metastasis. Conversely, caMNK1 induced NODAL expression and promoted IDC. The MNK1/NODAL axis promoted cancer stem cell properties and invasion in vitro. The MNK1/2 inhibitor SEL201 blocked DCIS progression to invasive disease in vivo. In clinical samples, IDC and DCIS with microinvasion expressed higher levels of phospho-MNK1 and NODAL versus low-grade (invasion-free) DCIS. Cumulatively, our data support further development of MNK1 inhibitors as therapeutics for preventing invasive disease. Significance: These findings provide new mechanistic insight into progression of ductal carcinoma and support clinical application of MNK1 inhibitors to delay progression of indolent ductal carcinoma in situ to invasive ductal carcinoma.

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)0.001
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 score0.104
Threshold uncertainty score0.901

Codex and Gemma teacher scores by category

CategoryCodexGemma
Metaresearch0.0010.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0000.001
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.000
Research integrity0.0000.000
Insufficient payload (model declined to judge)0.0010.000

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 head0.056
GPT teacher head0.389
Teacher spread0.333 · 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

Citations36
Published2019
Admission routes2
Has abstractyes

Explore more

Same venueCancer ResearchSame topicCancer Cells and MetastasisFrench-language works237,207