Evidence map›Paper›PMID 41071262›Full record

ArticleJournal of cachexia, sarcopenia and muscle2025

Pancreatic Damage in Ovarian Cancer-Associated Cachexia Is Driven by Activin A Signalling.

Amirhossein Abazarikia, Wonmi So, Yi Luan, Chandramohan Kattamuri, Thomas B Thompson, So-Youn Kim

Abstract read
In one paragraph

Article in Journal of cachexia, sarcopenia and muscle, 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

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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.

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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

6 authors.

Amirhossein AbazarikiaOlson Center for Women's Health, Department of Obstetrics and Gynecology, College of Medicine, University of Nebraska Medical Center, Omaha, Nebraska, USA.
Wonmi SoOlson Center for Women's Health, Department of Obstetrics and Gynecology, College of Medicine, University of Nebraska Medical Center, Omaha, Nebraska, USA.
Yi LuanOlson Center for Women's Health, Department of Obstetrics and Gynecology, College of Medicine, University of Nebraska Medical Center, Omaha, Nebraska, USA.
Chandramohan KattamuriDepartment of Molecular and Cellular Biosciences, College of Medicine, University of Cincinnati, Cincinnati, Ohio, USA.
Thomas B ThompsonDepartment of Molecular and Cellular Biosciences, College of Medicine, University of Cincinnati, Cincinnati, Ohio, USA.
So-Youn KimOlson Center for Women's Health, Department of Obstetrics and Gynecology, College of Medicine, University of Nebraska Medical Center, Omaha, Nebraska, USA.ORCID 0000-0003-1013-6852

Funding

UNMC/EPPLEY CANCER CENTER SUPPORT GRANTP30CA036727 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI James Eudy · 1985 to 2026
$55.0M
Development of mechanism-based ovarian reserve protecting adjuvant therapies against gonadotoxic therapeutic agentsR01HD096042 · NICHD · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI KIM, SO-YOUN · 2019 to 2023
$1.6M
Buffett Cancer Center CA036727Granulosa Cell Tumor Research FoundationNCI NIH HHS P30 CA036727NICHD NIH HHS R01 HD096042NIH HHS R01HD096042
6 · The paper itself

Abstract

backgroundCancer-associated cachexia (CAC) is a severe metabolic disorder characterized by involuntary weight loss, skeletal muscle atrophy and adipose tissue depletion. It is a major contributor to morbidity and mortality in the advanced stages of various cancers. However, the impact of CAC on the pancreas remains largely unexplored.

methodsWe used mice with constitutively active PI3K in oocytes, generated through a Cre-inducible Pik3ca* knock-in allele driven by Gdf9-icre and performed histological and molecular analyses of the pancreas during cachexia development. Additionally, we examined pancreatic changes following ovariectomy and administration of Follistatin 288 (FST288).

resultsMice that developed cachexia symptoms associated with granulosa cell tumour (GCT) growth exhibited significant pancreatic atrophy compared to controls (Cre+ vs. Cre- at PD83, p < 0.0001), including reduced size of individual acinar cells (102.99 ± 12.19 μm

conclusionsThese findings demonstrate pancreatic damage occurs during CAC development and highlight the critical role of activin A in this process. Targeting activin A signalling may represent a promising therapeutic strategy to mitigate cachexia in cancer patients and preserve pancreatic function.

Indexed as

ActivinsCachexiaOvarian NeoplasmsPancreasAnimalsDisease Models, AnimalFemaleHumansMiceSignal Transductionactivin AActivinsacinar cell atrophyactivin Aamylasecachexiafollistatin 288

Identifiers

PMID41071262
PMCPMC12512902

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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.