Evidence map›Paper›PMID 40304035›Full record

ArticleDisease models & mechanisms2025

Oncogenic signaling in the Drosophila prostate-like accessory gland activates a pro-tumorigenic program in the absence of proliferation.

S Jaimian Church, Ajai J Pulianmackal, Joseph A Dixon, Luke V Loftus, Sarah R Amend, Kenneth Pienta, Frank C Cackowski, Laura A Buttitta

Abstract read
In one paragraph

Article in Disease models & mechanisms, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Review
  3. Evidence for Transcriptomic Conservation Between the Main Cells of thebioRxiv : the preprint server for biology · 2025
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors.

S Jaimian ChurchMolecular, Cellular and Developmental Biology, University of Michigan, Ann Arbor, MI 48109, USA.
Ajai J PulianmackalMolecular, Cellular and Developmental Biology, University of Michigan, Ann Arbor, MI 48109, USA.
Joseph A DixonMolecular, Cellular and Developmental Biology, University of Michigan, Ann Arbor, MI 48109, USA.
Luke V LoftusCancer Ecology Center, The Brady Urological Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Sarah R AmendCancer Ecology Center, The Brady Urological Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.ORCID 0000-0002-5606-1262
Kenneth PientaCancer Ecology Center, The Brady Urological Institute, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.
Frank C CackowskiKarmanos Cancer Institute and Wayne State University, Department of Oncology, Detroit, MI 48201, USA.
Laura A ButtittaMolecular, Cellular and Developmental Biology, University of Michigan, Ann Arbor, MI 48109, USA.ORCID 0000-0002-5064-0650

Funding

Tumor microvesicle-mediated modulation of the bone microenvironmentP01CA093900 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KELLER, EVAN T · 2004 to 2024
$29.6M
Resource Component: Acquisition, maintenance and distribution of Drosophila stocksP40OD018537 · OD · TRUSTEES OF INDIANA UNIVERSITY · PI Annette L. Parks · 2014 to 2026
$13.5M
Probing the flexibility of G0R35GM149273 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Laura A Buttitta · 2023 to 2026
$1.6M
Chromatin remodeling at cell cycle exitR01GM127367 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BUTTITTA, LAURA A · 2018 to 2022
$1.6M
American Cancer Society RSG-15-161-01-DDCNCI NIH HHS CA093900NCI NIH HHS P01 CA093900NIGMS NIH HHS GM127367NIGMS NIH HHS R01 GM127367NIGMS NIH HHS R35 GM149273NIH HHS P40 OD018537Prostate Cancer Foundation 16CHAL05University of MichiganU.S. Department of Defense W81XWH-20-10353
6 · The paper itself

Abstract

Drosophila models for tumorigenesis have revealed conserved mechanisms of signaling involved in mammalian cancer. Many of these models use highly mitotically active Drosophila tissues. Few Drosophila tumorigenesis models use adult tissues, when most cells are terminally differentiated and postmitotic. The Drosophila accessory glands are prostate-like tissues, and a model for prostate tumorigenesis using this tissue has been explored. In this prior model, oncogenic signaling was induced during the proliferative stages of accessory gland development, raising the question of how oncogenic activity impacts the terminally differentiated, postmitotic adult tissue. Here, we show that oncogenic signaling in the adult Drosophila accessory gland leads to activation of a conserved pro-tumorigenic program, similar to that of mitotic tissues, but in the absence of proliferation. In our experiments, oncogenic signaling in the adult gland led to tissue hypertrophy with nuclear anaplasia, in part through endoreduplication. Oncogene-induced gene expression changes in the adult Drosophila prostate-like model overlapped with those in polyploid prostate cancer cells after chemotherapy, which potentially mediate tumor recurrence. Thus, the adult accessory glands provide a useful model for aspects of prostate cancer progression that lack cellular proliferation.

Indexed as

CarcinogenesisDrosophila melanogasterOncogenesProstateSignal TransductionAnimalsCell ProliferationDisease Models, AnimalDrosophila ProteinsEndoreduplicationGene Expression Regulation, NeoplasticHypertrophyMaleProstatic NeoplasmsDrosophila ProteinsDrosophila accessory glandEndoreduplicationOncogenic signalingPolyploidyPostmitoticProstateTumorigenesis

Identifiers

PMID40304035
PMCPMC12067084

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Registered trials

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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.