Evidence map›Paper›PMID 40721295›Full record

ReviewGenes & development2025

Modeling and targeting general and chromosome-specific aneuploidy in cancer.

Aleah Goldberg, Maria Trifas, Teresa Davoli

Abstract readReview
In one paragraph

Review in Genes & development, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. 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

3 authors.

Aleah GoldbergInstitute for Systems Genetics, Department of Biochemistry and Molecular Pharmacology, New York University Grossman School of Medicine, New York, New York 10016, USA.
Maria TrifasInstitute for Systems Genetics, Department of Biochemistry and Molecular Pharmacology, New York University Grossman School of Medicine, New York, New York 10016, USA teresa.davoli@nyulangone.org tdavoli@gmail.com.
Teresa DavoliInstitute for Systems Genetics, Department of Biochemistry and Molecular Pharmacology, New York University Grossman School of Medicine, New York, New York 10016, USA teresa.davoli@nyulangone.org tdavoli@gmail.com.

Funding

Why do Down Syndrome patients have high risk of Hirschsprung disease?R01DK135089 · NIDDK · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI ARAVINDA CHAKRAVARTI, Sumantra Chatterjee · 2022 to 2026
$4.2M
MutSensor System: A Set of Highly Sensitive Mutation Reporters to Dissect Genome Stability in Health and DiseaseR01HG012590 · NHGRI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI Jef D BOEKE, Teresa Davoli · 2023 to 2026
$3.1M
Deconstructing and targeting aneuploidy in human cancer - Resubmission - 1R37CA248631 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI Teresa Davoli · 2021 to 2026
$2.9M
Studying the Role of Aneuploidy in Cancer Immune EvasionR00CA212621 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI DAVOLI, TERESA · 2018 to 2020
$704k
NCI NIH HHS R00 CA212621NCI NIH HHS R37 CA248631NHGRI NIH HHS R01 HG012590NIDDK NIH HHS R01 DK135089
6 · The paper itself

Abstract

Throughout the last century, aneuploidy has been cemented as a hallmark of cancer. Although the association of aneuploidy with tumorigenesis has been well established, the role of these genetic imbalances in tumor formation has only recently begun to be elucidated. Advancements in genomics have revealed the complexity and context dependence of the effect of aneuploidy on cancer growth, while developments in genetic editing have allowed for proper modeling of specific aneuploidies. In this review, we discuss the key factors to consider when studying the role of aneuploidy in cancer and the tools that are available to do so. We then highlight recent studies that establish phenotypic contributions of aneuploidy to tumorigenicity. In particular, we highlight how general aneuploidy and chromosomal instability affect the tumor microenvironment and how specific chromosomal alterations, including the loss of chromosome 9p and the gain of chromosomes 8q and 1q, influence tumor behavior and therapeutic responses. Finally, we emphasize the potential of targeting aneuploidy-induced vulnerabilities to improve cancer treatment outcomes.

Indexed as

AneuploidyNeoplasmsAnimalsChromosomal InstabilityHumansTumor Microenvironmentaneuploidycancer genomicscell biologychromosomegenome instability

Identifiers

PMID40721295
PMCPMC12487708

What OpenQuestion holds

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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.