Evidence map›Paper›PMID 40464797›Full record

ArticleMolecular biology of the cell2025

Loss of negative regulation by HDAC1 and REST contributes to MAD1 overexpression in breast cancer.

Sarah E Copeland, Boya Chen, Avtar Roopra, Beth A Weaver

Abstract read
In one paragraph

Article in Molecular biology of the cell, 2025. 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. International journal of molecular sciences · 2026
    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

4 authors.

Sarah E CopelandMolecular and Cellular Pharmacology Graduate Training Program, University of Wisconsin-Madison, Madison 53705, WI.
Boya ChenMolecular and Cellular Pharmacology Graduate Training Program, University of Wisconsin-Madison, Madison 53705, WI.
Avtar RoopraDepartment of Neuroscience, University of Wisconsin-Madison, Madison 53705, WI.
Beth A WeaverDepartment of Cell and Regenerative Biology, University of Wisconsin-Madison, Madison 53705, WI.

Funding

UW COMPREHENSIVE CANCER CENTER SUPPORTP30CA014520 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI Justine Yang Bruce · 1985 to 2026
$142.6M
Non-canonical roles of Mitotic Arrest Deficient 1 (Mad1) in tumor promotionR01CA270133 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI Beth A Weaver · 2022 to 2026
$2.3M
NCI NIH HHS P30 CA014520NCI NIH HHS R01 CA270133
6 · The paper itself

Abstract

Mitotic arrest deficient 1 (MAD1), an essential component of the mitotic spindle assembly checkpoint, is commonly overexpressed in breast cancers where it serves as a marker of poor prognosis. MAD1 overexpression is sufficient to permit nontransformed cells to form orthotopic mammary tumors and to promote tumorigenesis in a recently described mouse model with inducible expression of endogenous Mad1. However, the mechanism of MAD1 up-regulation in cancer is unclear. Here, we report a 440-bp region of the

Indexed as

Breast NeoplasmsCell Cycle ProteinsHistone Deacetylase 1Nuclear ProteinsRepressor ProteinsAnimalsCell Line, TumorFemaleGene Expression Regulation, NeoplasticHumansMicePromoter Regions, GeneticRE1-Silencing Transcription FactorTranscription, GeneticCell Cycle ProteinsHDAC1 protein, humanHistone Deacetylase 1MAD1L1 protein, humanNuclear ProteinsRE1-Silencing Transcription FactorRepressor Proteins

Identifiers

PMID40464797
PMCPMC12367301

What OpenQuestion holds

Textmetadata
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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.