Evidence map›Paper›PMID 37280516›Full record

ArticleBMC cancer2023

S100A8, S100A9 and S100A8/A9 heterodimer as novel cachexigenic factors for pancreatic cancer-induced cachexia.

Wei-Chih Liao, Chih-Ta Chen, You-Shu Tsai, Xin-Ya Wang, Yen-Tzu Chang, Ming-Shiang Wu, Lu-Ping Chow

Open access · goldAbstract read
In one paragraph

Article in BMC cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

13 citing papers in PubMed, 15 citations in OpenAlex.

  1. S100A8/S100A9 released by CD11bExperimental & molecular medicine · 2026
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  5. Adipose-Derived Extracellular Vesicles and Intercellular Crosstalk With Skeletal Muscle: Implications for Sarcopenic Obesity and Metabolic Dysregulation.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2026
    Review
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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

7 authors at 2 institutions in 1 country.

Wei-Chih LiaoDivision of Gastroenterology and Hepatology, Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan.
Chih-Ta ChenGraduate Institute of Biochemistry and Molecular Biology, College of Medicine, National Taiwan University, No.1, Jen-Ai Road Section 1, Taipei, 10051, Taiwan.
You-Shu TsaiGraduate Institute of Biochemistry and Molecular Biology, College of Medicine, National Taiwan University, No.1, Jen-Ai Road Section 1, Taipei, 10051, Taiwan.
Xin-Ya WangGraduate Institute of Biochemistry and Molecular Biology, College of Medicine, National Taiwan University, No.1, Jen-Ai Road Section 1, Taipei, 10051, Taiwan.
Yen-Tzu ChangGraduate Institute of Biochemistry and Molecular Biology, College of Medicine, National Taiwan University, No.1, Jen-Ai Road Section 1, Taipei, 10051, Taiwan.
Ming-Shiang WuDivision of Gastroenterology and Hepatology, Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan.
Lu-Ping ChowGraduate Institute of Biochemistry and Molecular Biology, College of Medicine, National Taiwan University, No.1, Jen-Ai Road Section 1, Taipei, 10051, Taiwan. chowip@ntu.edu.tw.
National Taiwan University · TWNational Taiwan University Hospital · TW

Funding

Ministry of Science and Technology, Taiwan MOST 110-2320-B-002-059National Taiwan University Hospital 110-P01, 111-IF0008
6 · The paper itself

Abstract

backgroundCancer cachexia, occurring in ~ 80% pancreatic cancer (PC) patients overall, is a paraneoplastic syndrome mediated by cancer-induced systemic inflammation and characterized by weight loss and skeletal muscle wasting. Identifying clinically relevant PC-derived pro-inflammatory factors with cachexigenic potential may provide novel insights and therapeutic strategies.

methodsPro-inflammatory factors with cachexigenic potential in PC were identified by bioinformatic analysis. The abilities of selected candidate factors in inducing skeletal muscle atrophy were investigated. Expression levels of candidate factors in tumors and sera was compared between PC patients with and without cachexia. Associations between serum levels of the candidates and weight loss were assessed in PC patients.

resultsS100A8, S100A9, and S100A8/A9 were identified and shown to induce C2C12 myotube atrophy. Tumors of PC patients with cachexia had markedly elevated expression of S100A8 (P = 0.003) and S100A9 (P < 0.001). PC patients with cachexia had significantly higher serum levels of S100A8, S100A9 and S100A8/A9. Serum levels of these factors positively correlated with percentage of weight loss [correlation coefficient: S100A8: 0.33 (P < 0.001); S100A9: 0.30 (P < 0.001); S100A8/A9: 0.24 (P = 0.004)] and independently predicted the occurrence of cachexia [adjusted odds ratio (95% confidence interval) per 1ng/ml increase: S100A8 1.11 (1.02-1.21), P = 0.014; S100A9 1.10 (1.04-1.16), P = 0.001; per 1 µg/ml increase: S100A8/A9 1.04 (1.01-1.06), P = 0.009].

conclusionsAtrophic effects of S100A8, S100A9, and S100A8/A9 indicated them as potential pathogenic factors of PC-induced cachexia. In addition, the correlation with the degree of weight loss and prediction of cachexia in PC patients implicated their potential utility in the diagnosis of PC-induced cachexia.

Indexed as

CachexiaPancreatic NeoplasmsCalgranulin ACalgranulin BHumansCalgranulin ACalgranulin BS100A8 protein, humanS100A9 protein, humanBiomarkerCachexiaMuscle atrophyPancreatic cancerS100A8S100A9

Identifiers

PMID37280516
PMCPMC10242984
OpenAlexW4379536566

What OpenQuestion holds

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LicenceCC BY
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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 OpenQuestion graph.