Evidence map›Paper›PMID 41173942›Full record

ArticleScientific reports2025

Pan-cancer Myc modulator that targets Myc-α-tubulin interaction to drive selective mitotic catastrophe.

Jessica Teitel, Margaret Farah, Michele L Dziubinski, Pil Lee, Andrew White, Alexander Sobeck, Jose Colina, John Takyi-Williams, Bo Wen, Elmar Nurmemmedov and 10 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

20 authors.

Jessica TeitelDepartment of Pathology, University of Michigan, Ann Arbor, MI, 48109, USA.
Margaret FarahRogel Cancer Center, University of Michigan, Ann Arbor, MI, 48109, USA.
Michele L DziubinskiRogel Cancer Center, University of Michigan, Ann Arbor, MI, 48109, USA.
Pil LeeCollege of Pharmacy, University of Michigan, Ann Arbor, MI, 48109, USA.
Andrew WhiteCollege of Pharmacy, University of Michigan, Ann Arbor, MI, 48109, USA.
Alexander SobeckRogel Cancer Center, University of Michigan, Ann Arbor, MI, 48109, USA.
Jose ColinaDepartment of Pathology, University of Michigan, Ann Arbor, MI, 48109, USA.
John Takyi-WilliamsTherapeutic Systems Research Laboratories (TSRL), Inc, Ann Arbor, MI, 48105, USA.
Bo WenPharmacokinetics Core, University of Michigan, Ann Arbor, MI, 48109, USA.
Elmar NurmemmedovCellarisBio, San Diego, CA, 92121, USA.
Ivan BabicCellarisBio, San Diego, CA, 92121, USA.
Andre Monteiro da RochaFrankel Cardiovascular Center Cardiovascular Regeneration Core Laboratory, University of Michigan, Ann Arbor, MI, 48109, USA.
Karan BediDepartment of Biostatistics, University of Michigan, Ann Arbor, MI, 48109, USA.
Aaron RobidaCenter for Chemical Genomics, University of Michigan, Ann Arbor, MI, 48109, USA.
Grace McIntyreDepartment of Pathology, University of Michigan, Ann Arbor, MI, 48109, USA.
Takashi HottaDepartment of Cell and Developmental Biology, University of Michigan, Ann Arbor, MI, 48109, USA.
Yinzhi LinDepartment of Pathology, University of Michigan, Ann Arbor, MI, 48109, USA.
Sreeja C SekharDepartment of Pathology, University of Michigan, Ann Arbor, MI, 48109, USA.
Ryoma OhiDepartment of Cell and Developmental Biology, University of Michigan, Ann Arbor, MI, 48109, USA.
Analisa DiFeoDepartment of Pathology, University of Michigan, Ann Arbor, MI, 48109, USA. adifeo@med.umich.edu.

Funding

XenograftP30CA046592 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI THEODORE S LAWRENCE · 1988 to 2026
$178.2M
NCI NIH HHS P30 CA046592
6 · The paper itself

Abstract

MYC overexpression is a well-established cancer vulnerability, yet direct therapeutic targeting of Myc remains a challenge. Here, we identify DL78 as a potent antimitotic agent with selective anticancer activity through its regulation of Myc. DL78 demonstrated broad efficacy by inhibiting growth across nine cancer types and significantly reducing tumor burden in an in vivo model of platinum-resistant high-grade serous ovarian cancer, with no overt toxicity. DL78 preferentially targets chromosomally unstable, MYC-overexpressing cancer cells, a hallmark of high-grade serous ovarian cancer. Mechanistically, DL78 exploits Myc's role in mitotic entry by disrupting its interaction with α-tubulin, leading to sustained mitotic arrest, mitotic catastrophe, and apoptosis while sparing nonmalignant cells. This study establishes a novel paradigm for Myc-targeted therapy by introducing DL78, which induces cancer-selective mitotic catastrophe by disrupting Myc's interaction with α-tubulin rather than its transcriptional activity.

Indexed as

Antineoplastic AgentsMitosisNeoplasmsProto-Oncogene Proteins c-mycTubulinAnimalsApoptosisCell Line, TumorFemaleGene Expression Regulation, NeoplasticHumansMiceOvarian NeoplasmsXenograft Model Antitumor AssaysAntineoplastic AgentsMYC protein, humanProto-Oncogene Proteins c-mycTubulinc-MycG2-M arrestHigh-grade serous ovarian cancerMitotic catastropheα-tubulin

Identifiers

PMID41173942
PMCPMC12578881

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.