Evidence map›Paper›PMID 40745137›Full record

ReviewAdvances in experimental medicine and biology2025

The Power of Drosophila in Modeling Cancer Cachexia.

Chen Cheng, Ying Liu, Yuchen Chen, Jiaying Li, Weiqi Xu, Norbert Perrimon, Wei Song

Abstract readReview
PubMed Publisher
In one paragraph

Review in Advances in experimental medicine and biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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.

Chen ChengDepartment of Geriatrics, Frontier Science Center for Immunology and Metabolism, Medical Research Institute, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, Hubei, China.
Ying LiuDepartment of Genetics, Blavatnik Institute, Harvard Medical School, Boston, MA, USA. ying_liu@hms.harvard.edu.ORCID https://orcid.org/0000-0002-6419-1980
Yuchen ChenDepartment of Geriatrics, Frontier Science Center for Immunology and Metabolism, Medical Research Institute, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, Hubei, China.
Jiaying LiDepartment of Geriatrics, Frontier Science Center for Immunology and Metabolism, Medical Research Institute, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, Hubei, China.
Weiqi XuDepartment of Geriatrics, Frontier Science Center for Immunology and Metabolism, Medical Research Institute, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, Hubei, China.
Norbert PerrimonDepartment of Genetics, Blavatnik Institute, Harvard Medical School, Boston, MA, USA. perrimon@genetics.med.harvard.edu.ORCID https://orcid.org/0000-0001-7542-472X
Wei SongDepartment of Geriatrics, Frontier Science Center for Immunology and Metabolism, Medical Research Institute, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, Hubei, China. songw@whu.edu.cn.ORCID https://orcid.org/0000-0002-7007-5281

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Late-stage cancer patients often exhibit cachexia, a wasting syndrome characterized by the loss of muscle and adipose tissues. However, the extent to which these wasting effects directly contribute to mortality remains unclear. Drosophila, a well-conserved model organism, has been instrumental in demonstrating systemic energy wasting and mortality in the context of tumors, similar to mice and humans. Research in Drosophila has elucidated the underlying mechanisms by which tumor-associated secreted proteins cause muscle atrophy and lipid loss, ultimately leading to energy wasting. Nevertheless, emerging evidence in both Drosophila and mammals challenges the notion that blocking energy loss in muscle or fat is sufficient to improve tumor-associated mortality, suggesting the existence of additional pathogenic factors in cancer cachexia. This raises two critical questions: how do tumors disrupt the physiological functions of other organs besides muscle and fat, and to what extent do these organ dysfunctions contribute to tumor-induced mortality? In this chapter, we summarize current knowledge regarding how fly tumors interact with host organs or tissues through the production of cachectic secreted proteins, and how they influence disease progression. We also discuss the power of Drosophila models in uncovering the mechanisms and principles of tumor-induced wasting and mortality and exploring therapeutic opportunities using various leading technologies.

Indexed as

CachexiaDisease Models, AnimalDrosophila melanogasterNeoplasmsAnimalsDrosophilaEnergy MetabolismHumansBlood-brain barrier disruptionCancer cachexiaCoagulopathyExcessive hepatic gluconeogenesisHost interactionHost wastingKidney injuryLipid lossMortalityMuscle atrophyPathogenic organsSignaling pathwaysTumorTumor-secreted proteins

Identifiers

PMID40745137

What OpenQuestion holds

Textmetadata
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.