Evidence map›Paper›PMID 30666818›Full record

ArticleJournal of cachexia, sarcopenia and muscle2019

MyD88 signalling is critical in the development of pancreatic cancer cachexia.

Xinxia Zhu, Kevin G Burfeind, Katherine A Michaelis, Theodore P Braun, Brennan Olson, Katherine R Pelz, Terry K Morgan, Daniel L Marks

Open access · goldAbstract read
In one paragraph

Article in Journal of cachexia, sarcopenia and muscle, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 6% of its field
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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.

  1. Pooled it
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  7. Exploring heterogeneity: a dive into preclinical models of cancer cachexia.American journal of physiology. Cell physiology · 2024
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  13. The roles of P-selectin in cancer cachexia.Medical oncology (Northwood, London, England) · 2023
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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

8 authors at 1 institution in 1 country.

Xinxia ZhuPapé Family Pediatric Research Institute, Oregon Health & Science University, Portland, OR, 97239, USA.
Kevin G BurfeindPapé Family Pediatric Research Institute, Oregon Health & Science University, Portland, OR, 97239, USA.
Katherine A MichaelisPapé Family Pediatric Research Institute, Oregon Health & Science University, Portland, OR, 97239, USA.
Theodore P BraunKnight Cancer Institute, Oregon Health & Science University, Portland, USA.
Brennan OlsonPapé Family Pediatric Research Institute, Oregon Health & Science University, Portland, OR, 97239, USA.
Katherine R PelzPapé Family Pediatric Research Institute, Oregon Health & Science University, Portland, OR, 97239, USA.
Terry K MorganDepartment of Pathology, Oregon Health & Science University, Portland, USA.
Daniel L MarksPapé Family Pediatric Research Institute, Oregon Health & Science University, Portland, OR, 97239, USA.
Oregon Health & Science University · US

Funding

(PQD6) Hypothalamic Inflammation in the Initiation of CachexiaR01CA184324 · NCI · OREGON HEALTH & SCIENCE UNIVERSITY · PI MARKS, DANIEL L. · 2014 to 2017
$1.8M
The Role of Leukocytes in the Hypothalamus in Cancer CachexiaF30CA213745 · NCI · OREGON HEALTH & SCIENCE UNIVERSITY · PI BURFEIND, KEVIN GLENN · 2018 to 2021
$151k
NCI NIH HHS R01 CA184324
6 · The paper itself

Abstract

backgroundUp to 80% of pancreatic cancer patients suffer from cachexia, a devastating condition that exacerbates underlying disease, reduces quality of life, and increases treatment complications and mortality. Tumour-induced inflammation is linked to this multifactorial wasting syndrome, but mechanisms and effective treatments remain elusive. Myeloid differentiation factor (MyD88), a key component of the innate immune system, plays a pivotal role in directing the inflammatory response to various insults. In this study, we tested whether MyD88 signalling is essential in the development of pancreatic cancer cachexia using a robust mouse tumour model.

methodsSex, age, and body weight-matched wide type (WT) and MyD88 knockout (MyD88 KO) mice were orthotopically or intraperitoneally implanted with a pancreatic tumour cell line from a syngeneic C57BL/6 KRAS

resultsBlocking MyD88 signalling greatly ameliorated pancreatic ductal adenocarcinoma-associated anorexia and fatigue, attenuated lean mass loss, reduced muscle catabolism and atrophy, diminished systemic and central nervous system inflammation, and ultimately improved survival. Our data demonstrate that MyD88 signalling plays a critical role in mediating pancreatic cancer-induced inflammation that triggers cachexia development and therefore represents a promising therapeutic target.

conclusionsMyD88-dependent inflammation is crucial in the pathophysiology of pancreatic cancer progression and contributes to high mortality. Our findings implicate the importance of innate immune signalling pathways in pancreatic cancer cachexia and a novel therapeutic target.

Indexed as

Signal TransductionAnimalsBody CompositionCachexiaCell Line, TumorDisease Models, AnimalEnergy MetabolismFemaleHumansMaleMiceMice, KnockoutMotor ActivityMuscle, SkeletalMyeloid Differentiation Factor 88Pancreatic NeoplasmsMYD88 protein, humanMyeloid Differentiation Factor 88CachexiaInflammationMyD88Orthotopic modelPancreatic cancer

Identifiers

PMID30666818
PMCPMC6463469
OpenAlexW2911239965

What OpenQuestion holds

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LicenceCC BY-NC
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.