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Updated: May 10, 2026

The Colon-26 Carcinoma Tumor-bearing Mouse as a Model for the Study of Cancer Cachexia

The Colon-26 Carcinoma Tumor-bearing Mouse as a Model for the Study of Cancer Cachexia

Published on: November 30, 2016

Muscle wasting in cancer.

N Johns¹, N A Stephens, K C H Fearon

¹Department of Clinical and Surgical Sciences, University of Edinburgh, Edinburgh EH16 4SB, UK.

The International Journal of Biochemistry & Cell Biology

|June 18, 2013

Summary

This summary is machine-generated.

Cancer cachexia causes significant skeletal muscle loss, impacting patient outcomes. Understanding the molecular mechanisms of muscle wasting, whether through reduced protein synthesis or increased degradation, is crucial for developing effective human cancer cachexia treatments.

Keywords:

ACTRIIB APC APPR ARC ATP C-26 CHO COPD CRPc CSA Cachexia Cancer Chinese hamster ovary DGC DM DNA Degradation EDL EIF3F F-box protein 40 F-bxo40 FCSA FOXO ICU IFN IGF IL IRS JAK Janus associated kinase LBM LLC Lewis lung carcinoma MA MAC16 MAFbx MAPK MCR MRI MSH MURF-1 Muscle MyHC NFκB NPY NSCLC PBMC PI3K POMC QoL RNA STAT Synthesis T helper T(h)TA TAM TGF TNF TWEAK UPP Ub activin receptor type-2B acute phase protein response adenomatosis polyposis coli adenosine-5′-triphosphate arcuate nucleus chronic obstructive pulmonary disease colon-26 adenocarcinoma mouse model cross sectional area deoxyribonucleic acid diabetes mellitus dystrophin glycoprotein complex eukaryotic translation initiation factor 3 subunit F extensor digitorum longus fibre cross sectional area forkhead box class O transcription factor insulin receptor substrate insulin-like growth factor intensive care unit interferon interleukin lean body mass mAb mRNA mTOR magnetic resonance imaging mammalian target of rapamycin megestrol acetate melanocortin receptor melanocyte-stimulating hormone messenger ribonucleic acid mitogen activated kinase monoclonal antibody murine adenocarcinoma 16 mouse model muscle-specific F-box (also known as atrogin-1)muscle-specific RING finger-1 myosin heavy chain neuropeptide Y non-small cell lung cancer nuclear factor-κβ peripheral blood mononuclear cell phosphatidylinositol 3-kinase pro-opiomelanocortin quality of life reactive protein ribonucleic acid signal transducer and activator of transcription tibialis anterior transforming growth factor tumour necrosis factor tumour necrosis factor-like weak inducer of apoptosis tumour-associated macrophage ubiquitin ubiquitin-proteasome pathway

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Non-invasive Skeletal Muscle Quantification in Small Animals Using Micro-computed Tomography

Non-invasive Skeletal Muscle Quantification in Small Animals Using Micro-computed Tomography

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Last Updated: May 10, 2026

The Colon-26 Carcinoma Tumor-bearing Mouse as a Model for the Study of Cancer Cachexia

The Colon-26 Carcinoma Tumor-bearing Mouse as a Model for the Study of Cancer Cachexia

Published on: November 30, 2016

Non-invasive Skeletal Muscle Quantification in Small Animals Using Micro-computed Tomography

Non-invasive Skeletal Muscle Quantification in Small Animals Using Micro-computed Tomography

Published on: November 8, 2024

Area of Science:

Oncology
Molecular Biology
Physiology

Background:

Skeletal muscle loss is a critical clinical event in cancer cachexia, strongly linked to poor patient prognosis.
The precise molecular mechanisms driving muscle wasting in cancer cachexia remain debated, with ongoing discussion regarding the relative contributions of decreased protein synthesis and increased protein degradation.
Existing animal models exhibit variability in key mediators and activated pathways, complicating direct translation to human disease.

Purpose of the Study:

To review the current understanding of molecular mechanisms underlying skeletal muscle wasting in cancer cachexia.
To highlight the limitations of current animal models in recapitulating human cancer cachexia.
To emphasize the need for human data and robust clinical trials for therapeutic advancement.

Main Methods:

Review of existing literature on cancer cachexia and skeletal muscle wasting.
Analysis of different experimental models and their molecular pathways.
Discussion of the paucity of human data at both descriptive and molecular levels.

Main Results:

Skeletal muscle wasting is a hallmark of cancer cachexia with significant clinical implications.
Both reduced protein synthesis and increased protein degradation, particularly via the ubiquitin proteasome pathway (UPP), are implicated in muscle loss.
Murine models often display acute atrophy, differing from chronic human wasting, and show model-specific molecular mediators.

Conclusions:

Further research is needed to elucidate the specific molecular mechanisms of muscle wasting in human cancer cachexia.
Progress in treating cancer cachexia requires well-designed clinical trials with validated biomarkers.
Understanding the molecular basis of muscle wasting is essential for developing targeted therapies for cancer cachexia.