Evidence map›Paper›PMID 41808999›Full record

ArticlebioRxiv : the preprint server for biology2026

Pancreatic cancer-associated organ dysfunction promotes muscle autophagy and contributes to peripheral tissue wasting.

Yetiş Gültekin, Sharanya Sivanand, Kian M Eghbalian, Anna M Barbeau, Keene L Abbott, George Eng, Victoria L Tavernier, Brian T Do, Heaji Shin, Elif Özçelik and 13 more

Abstract readPreprint
PubMed Full text at PMC Publisher
In one paragraph

Article in bioRxiv : the preprint server for biology, 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

23 authors.

Yetiş GültekinKoch Institute for Integrative Cancer Research at Massachusetts Institute of Technology, Cambridge, MA, USA.
Sharanya SivanandKoch Institute for Integrative Cancer Research at Massachusetts Institute of Technology, Cambridge, MA, USA.ORCID 0000-0002-2559-9270
Kian M EghbalianKoch Institute for Integrative Cancer Research at Massachusetts Institute of Technology, Cambridge, MA, USA.
Anna M BarbeauKoch Institute for Integrative Cancer Research at Massachusetts Institute of Technology, Cambridge, MA, USA.
Keene L AbbottKoch Institute for Integrative Cancer Research at Massachusetts Institute of Technology, Cambridge, MA, USA.ORCID 0000-0002-6166-704X
George EngKoch Institute for Integrative Cancer Research at Massachusetts Institute of Technology, Cambridge, MA, USA.
Victoria L TavernierKoch Institute for Integrative Cancer Research at Massachusetts Institute of Technology, Cambridge, MA, USA.
Brian T DoKoch Institute for Integrative Cancer Research at Massachusetts Institute of Technology, Cambridge, MA, USA.
Heaji ShinKoch Institute for Integrative Cancer Research at Massachusetts Institute of Technology, Cambridge, MA, USA.ORCID 0000-0001-5208-5999
Elif ÖzçelikKoch Institute for Integrative Cancer Research at Massachusetts Institute of Technology, Cambridge, MA, USA.
Sabrina HuKoch Institute for Integrative Cancer Research at Massachusetts Institute of Technology, Cambridge, MA, USA.
Tenzin KunchokKoch Institute for Integrative Cancer Research at Massachusetts Institute of Technology, Cambridge, MA, USA.
Millenia WaiteKoch Institute for Integrative Cancer Research at Massachusetts Institute of Technology, Cambridge, MA, USA.
William M RideoutKoch Institute for Integrative Cancer Research at Massachusetts Institute of Technology, Cambridge, MA, USA.
Yiğit K KizlierKoch Institute for Integrative Cancer Research at Massachusetts Institute of Technology, Cambridge, MA, USA.
Daniel A SharyginKoch Institute for Integrative Cancer Research at Massachusetts Institute of Technology, Cambridge, MA, USA.
William A Freed-PastorKoch Institute for Integrative Cancer Research at Massachusetts Institute of Technology, Cambridge, MA, USA.
Tyler JacksKoch Institute for Integrative Cancer Research at Massachusetts Institute of Technology, Cambridge, MA, USA.
Eileen WhiteRutgers Cancer Institute, Rutgers University, New Brunswick, New Jersey, USA.
Ömer H YilmazKoch Institute for Integrative Cancer Research at Massachusetts Institute of Technology, Cambridge, MA, USA.
Jonathan A NowakDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
Brian M WolpinDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.
Matthew G Vander HeidenKoch Institute for Integrative Cancer Research at Massachusetts Institute of Technology, Cambridge, MA, USA.ORCID 0000-0002-6702-4192

Funding

VIRUS PRODUCTION COREP30CA014051 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI MATTHEW G. VANDER HEIDEN · 1985 to 2026
$93.9M
Medical Scientist Training ProgramT32GM007753 · NIGMS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI WALENSKY, LOREN DAVID · 1985 to 2021
$50.0M
PRE-DOCTORAL TRAINING IN THE BIOLOGICAL SCIENCEST32GM007287 · NIGMS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI BELL, STEPHEN P., KEATING, AMY E · 1985 to 2019
$40.8M
Understanding the role of metabolism in cancerR35CA242379 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI VANDER HEIDEN, MATTHEW G. · 2019 to 2025
$5.8M
Elucidating the molecular and cellular mechanisms of immune evasion in pancreatic cancerK08CA259621 · NCI · DANA-FARBER CANCER INST · PI WILLIAM A FREED-PASTOR · 2022 to 2026
$1.1M
Molecular determinants of fetal hemoglobin induction by hydroxyurea to treat sickle cell diseaseF30HL156404 · NHLBI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI DO, BRIAN TSHAO · 2021 to 2023
$155k
Exploiting metabolic vulnerabilities of breast cancer brain metastases for therapyF31CA271787 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI ABBOTT, KEENE · 2022 to 2023
$94k
NCI NIH HHS F31 CA271787NCI NIH HHS K08 CA259621NCI NIH HHS P30 CA014051NCI NIH HHS R35 CA242379NHLBI NIH HHS F30 HL156404NIGMS NIH HHS T32 GM007287NIGMS NIH HHS T32 GM007753
6 · The paper itself

Abstract

Normal pancreas function supports both digestion and the hormonal regulation of whole-body metabolism. We find pancreatic ductal adenocarcinoma (PDAC) disrupts the normal function of the remaining pancreas, leading to altered systemic metabolism and peripheral tissue wasting that begins early in disease progression. Using mouse models of PDAC, we find small pancreas tumors lead to both endocrine and exocrine pancreatic dysfunction that results in systemic nutrient depletion and loss of both muscle and fat tissue. Providing free glucose in the diet that is absorbed despite pancreatic exocrine dysfunction causes hyperglycemia and blunts fat wasting without affecting muscle loss. Muscle mass can be restored by free dietary amino acids or pancreatic enzyme supplementation. Exocrine dysfunction causing reduced dietary protein digestion promotes muscle proteolysis and autophagy. Autophagy is a major driver of muscle wasting in PDAC, as muscle-specific deletion of the core autophagy gene

Identifiers

PMID41808999
PMCPMC12970336

What OpenQuestion holds

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LicenceCC BY-NC-ND
Read underepoch 390

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.