Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

7.4K
Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
7.4K
The Tumor Microenvironment02:17

The Tumor Microenvironment

8.1K
Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...
8.1K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

5.1K
The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
5.1K
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

10.1K
Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
10.1K
Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

15.5K
Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
15.5K
Cancer Stem Cells and Tumor Maintenance02:40

Cancer Stem Cells and Tumor Maintenance

6.4K
Early diagnosis and treatment can often cure cancer. However, even with treatment, residual cells called cancer stem cells (CSC) might remain, often causing tumor recurrence. These cancer stem cells possess the potential for self-renewal and multi-lineage differentiation and are often responsible for the therapeutic resistance displayed in most cancers.
Cancer stem cells are thought to originate from tissue-specific normal stem cells or progenitor cells. The normal stem cells usually reside in...
6.4K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Tumor-muscle communication in cancer-associated cachexia (Review).

Oncology letters·2026
Same author

Skeletal muscle atrophy and dysfunction in obesity and type-2 diabetes mellitus: Myocellular mechanisms involved.

Reviews in endocrine & metabolic disorders·2025
Same author

Neuregulin 4 Downregulation Alters Mitochondrial Morphology and Induces Oxidative Stress in 3T3-L1 Adipocytes.

International journal of molecular sciences·2024
Same author

Anabolic deficits and divergent unfolded protein response underlie skeletal and cardiac muscle growth impairments in the Yoshida hepatoma tumor model of cancer cachexia.

Physiological reports·2024
Same author

Formoterol reduces muscle wasting in mice undergoing doxorubicin chemotherapy.

Frontiers in oncology·2024
Same author

Effects of S-pindolol in mouse pancreatic and lung cancer cachexia models.

Journal of cachexia, sarcopenia and muscle·2023

Related Experiment Video

Updated: Mar 30, 2026

The Colon-26 Carcinoma Tumor-bearing Mouse as a Model for the Study of Cancer Cachexia
08:55

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

Published on: November 30, 2016

17.4K

Nonmuscle Tissues Contribution to Cancer Cachexia.

Josep M Argilés1, Britta Stemmler2, Francisco J López-Soriano1

  • 1Cancer Research Group, Departament de Bioquímica i Biologia Molecular, Facultat de Biologia, Universitat de Barcelona, 08028 Barcelona, Spain ; Institut de Biomedicina de la Universitat de Barcelona, Barcelona, Spain.

Mediators of Inflammation
|November 3, 2015
PubMed
Summary

Cancer cachexia involves more than just muscle wasting; it is a complex syndrome affecting multiple organs. This review explores the significant impact of non-muscle tissues on cancer cachexia progression.

More Related Videos

Author Spotlight: Detection of Mitophagy in Caenorhabditis elegans and Mammalian Cells Using Organelle-Specific Dyes
11:59

Author Spotlight: Detection of Mitophagy in Caenorhabditis elegans and Mammalian Cells Using Organelle-Specific Dyes

Published on: May 19, 2023

3.3K
Dual Effects of Melanoma Cell-derived Factors on Bone Marrow Adipocytes Differentiation
07:00

Dual Effects of Melanoma Cell-derived Factors on Bone Marrow Adipocytes Differentiation

Published on: August 23, 2018

6.6K

Related Experiment Videos

Last Updated: Mar 30, 2026

The Colon-26 Carcinoma Tumor-bearing Mouse as a Model for the Study of Cancer Cachexia
08:55

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

Published on: November 30, 2016

17.4K
Author Spotlight: Detection of Mitophagy in Caenorhabditis elegans and Mammalian Cells Using Organelle-Specific Dyes
11:59

Author Spotlight: Detection of Mitophagy in Caenorhabditis elegans and Mammalian Cells Using Organelle-Specific Dyes

Published on: May 19, 2023

3.3K
Dual Effects of Melanoma Cell-derived Factors on Bone Marrow Adipocytes Differentiation
07:00

Dual Effects of Melanoma Cell-derived Factors on Bone Marrow Adipocytes Differentiation

Published on: August 23, 2018

6.6K

Area of Science:

  • Oncology
  • Metabolic Diseases
  • Physiology

Background:

  • Cachexia is a cancer-associated syndrome marked by weight loss, muscle and adipose tissue wasting, and inflammation.
  • While muscle wasting is prominent, other organs are increasingly recognized as key players.

Purpose of the Study:

  • To review the impact of non-muscle tissues on cancer cachexia.
  • To highlight cachexia as a multiorgan syndrome.

Main Methods:

  • Literature review of recent developments in cancer cachexia research.
  • Analysis of the role of adipose, brain, liver, gut, and heart tissues.

Main Results:

  • Non-muscle tissues, including adipose, brain, liver, gut, and heart, are directly implicated in the cachectic process.
  • These organs contribute significantly to overall muscle wasting in cancer patients.

Conclusions:

  • Cancer cachexia is a complex multiorgan syndrome, not solely a muscle-wasting condition.
  • Understanding the role of non-muscle tissues is crucial for developing effective therapeutic strategies.