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Related Concept Videos

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Cancer

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Cancers arise due to mutations in genes involved in the regulation of cell division, which leads to unrestricted cell proliferation. Modern science and medicine have made great strides in the understanding and treatment of cancer, including eradicating cancer in some patients. However, there is still no cure for cancer. This is largely due to the fact that cancer is a large group of many diseases.
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Cells with similar structure and function are grouped into tissues. A group of tissues with a specialized function is called an organ. There are four main types of tissue in vertebrates: epithelial, connective, muscle, and nervous.
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The Colon-26 Carcinoma Tumor-bearing Mouse as a Model for the Study of Cancer Cachexia
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Adipose tissue dysfunction in cancer cachexia.

Sahar I Daas1,2, Balsam R Rizeq3,4, Gheyath K Nasrallah4,5

  • 1Department of Biomedical and Biological Sciences, Hamad Bin Khalifa University, Doha, Qatar.

Journal of Cellular Physiology
|August 6, 2018
PubMed
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Cancer cachexia causes extreme weight loss through inflammation and metabolic issues. White adipose tissue (WAT) browning increases energy expenditure, contributing to this wasting syndrome.

Keywords:
WAT browningbrown adipocytescancer cachexiainflammationwhite adipocytes

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Area of Science:

  • Biochemistry
  • Metabolism
  • Oncology

Background:

  • Cancer cachexia is a complex metabolic disorder characterized by inflammation and extreme weight loss.
  • Adipose tissue, comprising white adipose tissue (WAT) and brown adipose tissue, is a key metabolic and secretory organ implicated in cancer cachexia.
  • Secretory products from adipose tissue, such as adipokines and cytokines, influence various organs, including skeletal muscle, brain, pancreas, and liver.

Purpose of the Study:

  • To review the characteristics of cancer cachexia and WAT browning.
  • To elucidate the mechanisms of adipose tissue inflammation in cancer.
  • To highlight the molecular mechanisms underlying WAT dysfunction and browning in cancer cachexia.

Main Methods:

  • Literature review summarizing current understanding of cancer cachexia and WAT browning.
  • Analysis of the role of secreted macromolecules, cytokines, hormones, and tumor mediators in adipose tissue dysfunction.
  • Examination of inflammatory responses, energy utilization defects, and molecular pathways involved in WAT dysfunction.

Main Results:

  • Cancer cachexia involves metabolic alterations and systemic inflammation, leading to adipose tissue wasting.
  • WAT undergoes a browning process during cancer cachexia, enhancing lipid mobilization and energy expenditure.
  • Adipose tissue dysfunction is influenced by a combination of factors, including inflammation, lipolysis, apoptosis, and reduced lipogenesis.

Conclusions:

  • Understanding adipose tissue dysfunction and browning in cancer cachexia is crucial.
  • Further research into the mechanisms of adipose tissue loss may lead to novel therapeutic strategies.
  • Targeting adipose tissue dysfunction could offer new approaches to treat cancer cachexia.