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

6.8K
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,...
6.8K
Overview of Protein Metabolism01:21

Overview of Protein Metabolism

3.4K
Proteins are broken down into amino acids during digestion. Unlike fats and carbohydrates, which are stored for later use, proteins are not. Instead, amino acids are either used to produce ATP through oxidation or contribute to the creation of new proteins for the growth and repair of the body. Any surplus amino acids from the diet are converted into glucose or triglycerides rather than excreted.
Amino acids play various roles in the body once they are absorbed into cells. They are restructured...
3.4K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

4.5K
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...
4.5K
Metastasis02:30

Metastasis

6.3K
Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
6.3K
The Tumor Microenvironment02:17

The Tumor Microenvironment

7.5K
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...
7.5K
Chronic Kidney Disease II: Clinical Manifestations01:24

Chronic Kidney Disease II: Clinical Manifestations

475
Chronic Kidney Disease (CKD) progressively impairs multiple body systems due to the accumulation of uremic toxins, which disrupt cellular functions across various organs.Neurologic symptomsNeurologic symptoms often arise early in CKD, as uremic toxin buildup drives changes in cognitive and motor functions. Patients frequently experience fatigue, headache, confusion, difficulty concentrating, and, in severe cases, seizures. Peripheral neuropathy commonly manifests as burning sensations in the...
475

You might also read

Related Articles

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

Sort by
Same author

How to query administrative databases for heart failure epidemiological investigations? Rationale, design, and case definition criteria for the nation-wide HF-EPI-HUN Study.

European journal of heart failure·2026
Same author

Translation, cultural adaptation and psychometric evaluation of the Slovene version of the Heart Failure-Specific Health Literacy Scale in patients with heart failure.

Scientific reports·2026
Same author

Does the global prevalence of heart failure now exceed 600 million people? From guesswork to evidence.

European heart journal·2026
Same author

Population-based screening for cardiovascular diseases and type 2 diabetes risk among migrant origin and ethnic minority groups in Europe: a scoping review.

BMC public health·2026
Same author

The Global Epidemiology of Heart Failure: A Comprehensive and Contemporary Review.

European journal of heart failure·2026
Same author

You evaluation of the PARACHUTE-HF trial: role of sacubitril/valsartan compared to enalapril on outcomes in patients with heart failure from Chagas' disease.

Heart failure reviews·2026

Related Experiment Video

Updated: Dec 25, 2025

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

17.0K

Cancer Cachexia and Related Metabolic Dysfunction.

Guilherme Wesley Peixoto da Fonseca1,2, Jerneja Farkas3,4,5, Eva Dora6

  • 1Heart Institute (InCor), University of São Paulo Medical School, São Paulo SP 05403-900, Brazil.

International Journal of Molecular Sciences
|April 2, 2020
PubMed
Summary

Cancer cachexia causes severe muscle and fat loss, impacting cancer patients

Keywords:
cancer cachexiaclinical managementinflammationmetabolic dysfunctionmetabolism

More Related Videos

Exploring the Regulation of Lipid Droplet Catabolism through Lipophagy
07:20

Exploring the Regulation of Lipid Droplet Catabolism through Lipophagy

Published on: January 31, 2025

997
Body Composition and Metabolic Caging Analysis in High Fat Fed Mice
10:28

Body Composition and Metabolic Caging Analysis in High Fat Fed Mice

Published on: May 24, 2018

16.2K

Related Experiment Videos

Last Updated: Dec 25, 2025

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

17.0K
Exploring the Regulation of Lipid Droplet Catabolism through Lipophagy
07:20

Exploring the Regulation of Lipid Droplet Catabolism through Lipophagy

Published on: January 31, 2025

997
Body Composition and Metabolic Caging Analysis in High Fat Fed Mice
10:28

Body Composition and Metabolic Caging Analysis in High Fat Fed Mice

Published on: May 24, 2018

16.2K

Area of Science:

  • Oncology
  • Metabolism
  • Physiology

Background:

  • Cancer cachexia is a complex syndrome characterized by progressive skeletal muscle and fat mass depletion.
  • It affects up to 74% of cancer patients, leading to impaired physical function, reduced therapy response, and increased mortality.
  • Organs like muscle, adipose tissue, and the liver contribute to cachexia by modulating inflammatory responses and metabolic dysfunction.

Purpose of the Study:

  • To review the current understanding of cancer cachexia.
  • To highlight the limitations of single-agent therapies.
  • To propose a multimodal approach for managing cancer cachexia.

Main Methods:

  • Literature review of cancer cachexia mechanisms and therapeutic strategies.
  • Analysis of the role of organ systems and metabolic alterations in cachexia progression.
  • Evaluation of existing pharmacological interventions and their outcomes.

Main Results:

  • Cancer cachexia involves complex interactions between the tumor, host immune system, and metabolic pathways.
  • Current pharmacological treatments show limited efficacy in improving physical function.
  • Nutritional support alone is insufficient to reverse cachexia.

Conclusions:

  • Cancer cachexia is a multifactorial condition requiring a comprehensive management strategy.
  • A multimodal intervention combining pharmacological agents, nutritional support, and physical exercise is a promising approach.
  • Further research is needed to effectively prevent and treat body compartment wasting in cancer patients.