Evidence map›Paper›PMID 27135739›Full record

ArticleNature medicine2016

Excessive fatty acid oxidation induces muscle atrophy in cancer cachexia.

Tomoya Fukawa, Benjamin Chua Yan-Jiang, Jason Chua Min-Wen, Elwin Tan Jun-Hao, Dan Huang, Chao-Nan Qian, Pauline Ong, Zhimei Li, Shuwen Chen, Shi Ya Mak and 12 more

Abstract read
PubMed Publisher
In one paragraph

Article in Nature medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 137 papers.

0numbers the graph read from it
0cells of the map it votes in
137citing papers in PubMed
12.7field-weighted citation impact, top 1% 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

137 citing papers in PubMed, 207 citations in OpenAlex.

  1. Trial
  2. Article
  3. Subcutaneous adipose tissue outperforms muscle strength as an indicator of survival and quality of life in patients with cancer: a multicenter cohort study.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2026
    Observational
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  17. Cancer Cachexia.Advances in experimental medicine and biology · 2025
    Review
  18. Article
  19. Overexpression of CPT1A disrupts the maintenance and regenerative function of muscle stem cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
  20. Article

77 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

22 authors at 7 institutions in 3 countries.

Tomoya FukawaLaboratory of Cancer Therapeutics, Program in Cancer and Stem Cell Biology, Duke-National University of Singapore Medical School, Singapore.
Benjamin Chua Yan-JiangGenome Institute of Singapore, Agency for Science Technology and Research, Singapore.
Jason Chua Min-WenGenome Institute of Singapore, Agency for Science Technology and Research, Singapore.
Elwin Tan Jun-HaoGenome Institute of Singapore, Agency for Science Technology and Research, Singapore.
Dan HuangLaboratory of Cancer Epigenome, Division of Medical Science, National Cancer Centre Singapore, Singapore.
Chao-Nan QianSun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, China.
Pauline OngLaboratory of Cancer Therapeutics, Program in Cancer and Stem Cell Biology, Duke-National University of Singapore Medical School, Singapore.
Zhimei LiLaboratory of Cancer Epigenome, Division of Medical Science, National Cancer Centre Singapore, Singapore.
Shuwen ChenBioprocessing Technology Institute, Agency for Science Technology and Research, Singapore.
Shi Ya MakBioprocessing Technology Institute, Agency for Science Technology and Research, Singapore.
Wan Jun LimDivision of Medical Oncology, National Cancer Centre Singapore, Singapore.
Hiro-Omi KanayamaDepartment of Urology, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima, Japan.
Rosmin Elsa MohanSchool of Mechanical and Aerospace Engineering, Nanyang Technological University, Singapore.
Ruiqi Rachel WangSchool of Mechanical and Aerospace Engineering, Nanyang Technological University, Singapore.
Jiunn Herng LaiDepartment of Colorectal Surgery, Singapore General Hospital, Singapore.
Clarinda ChuaGenome Institute of Singapore, Agency for Science Technology and Research, Singapore.
Hock Soo OngDepartment of Upper Gastrointestinal and Bariatric Surgery, Singapore General Hospital, Singapore.
Ker-Kan TanDepartment of Surgery, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.
Ying Swan HoBioprocessing Technology Institute, Agency for Science Technology and Research, Singapore.
Iain Beehuat TanGenome Institute of Singapore, Agency for Science Technology and Research, Singapore.
Bin Tean TehLaboratory of Cancer Therapeutics, Program in Cancer and Stem Cell Biology, Duke-National University of Singapore Medical School, Singapore.
Ng Shyh-ChangGenome Institute of Singapore, Agency for Science Technology and Research, Singapore.ORCID 0000-0003-3138-9525
Agency for Science, Technology and Research · SGNational Cancer Centre Singapore · SGNational University of Singapore · SGNanyang Technological University · SGSingapore General Hospital · SGSun Yat-sen University · CNTokushima University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cachexia is a devastating muscle-wasting syndrome that occurs in patients who have chronic diseases. It is most commonly observed in individuals with advanced cancer, presenting in 80% of these patients, and it is one of the primary causes of morbidity and mortality associated with cancer. Additionally, although many people with cachexia show hypermetabolism, the causative role of metabolism in muscle atrophy has been unclear. To understand the molecular basis of cachexia-associated muscle atrophy, it is necessary to develop accurate models of the condition. By using transcriptomics and cytokine profiling of human muscle stem cell-based models and human cancer-induced cachexia models in mice, we found that cachectic cancer cells secreted many inflammatory factors that rapidly led to high levels of fatty acid metabolism and to the activation of a p38 stress-response signature in skeletal muscles, before manifestation of cachectic muscle atrophy occurred. Metabolomics profiling revealed that factors secreted by cachectic cancer cells rapidly induce excessive fatty acid oxidation in human myotubes, which leads to oxidative stress, p38 activation and impaired muscle growth. Pharmacological blockade of fatty acid oxidation not only rescued human myotubes, but also improved muscle mass and body weight in cancer cachexia models in vivo. Therefore, fatty acid-induced oxidative stress could be targeted to prevent cancer-induced cachexia.

Indexed as

Oxidation-ReductionAgedAnimalsBlotting, WesternCachexiaCell LineCell Line, TumorCytokinesDisease Models, AnimalEnzyme InhibitorsEpoxy CompoundsFatty AcidsFemaleGene Expression ProfilingHumansImmunohistochemistryCytokinesEnzyme InhibitorsEpoxy CompoundsetomoxirFatty Acidsp38 Mitogen-Activated Protein Kinases

Identifiers

PMID27135739
OpenAlexW2345985540

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.