Tumor-suppressor pathways in Schistosoma mansoni support a novel hypothesis on neodermatan flatworm origins.

Paul J Brindley

Abstract readReview

In one paragraph

Review in Trends in parasitology, 2026. 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

1 author.

Paul J BrindleyDepartment of Microbiology, Immunology and Tropical Medicine, School of Medicine & Health Sciences, The George Washington University, Washington, DC 20037, USA. Electronic address: pbrindley@email.gwu.edu.

Funding

Targeting parasite-host communication to combat liver fluke-induced bile duct cancerR01CA164719 · NCI · GEORGE WASHINGTON UNIVERSITY · PI Paul J Brindley, THEWARACH LAHA · 2012 to 2026

$5.0M

NCI NIH HHS R01 CA164719

6 · The paper itself

Abstract

Wendt and Collins identify a cyclin-dependent kinase inhibitor (cki) in Schistosoma mansoni that, along with p53-1 (schistosome homolog of TP-53), suppresses tegument cell proliferation. Knockdown of cki causes hyperproliferation and, together with p53-1 loss, tumorlike growths. Homologs of cki are widespread in parasitic flatworms but absent in free-living relatives, suggesting that the horizontal gene transfer aided the evolution of parasitism.

Indexed as

Biological EvolutionSchistosoma mansoniAnimalsCyclin-Dependent Kinase Inhibitor ProteinsGene Transfer, HorizontalHelminth ProteinsCyclin-Dependent Kinase Inhibitor ProteinsHelminth Proteinsckicyclin-dependent kinase inhibitorhorizontal gene transferparasitic flatwormstegument

Identifiers

PMID41820076

DOI10.1016/j.pt.2026.02.003

PMCPMC13107240

What Socratic 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 Socratic graph.