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Related Concept Videos

mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

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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...
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PI3K/mTOR/AKT Signaling Pathway01:22

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The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
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Tumor Immunotherapy01:27

Tumor Immunotherapy

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Immunotherapy is a treatment that boosts or manipulates the immune system to fight diseases, including cancer. For instance, by stimulating an immune response through vaccinations against viruses that cause cancers, like hepatitis B virus and human papillomavirus, these diseases can be prevented. Nonetheless, some cancer cells can avoid the immune system due to their rapid mutation and division. The immune response to many cancers involves three phases: elimination, equilibrium, and escape.
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Tumor Progression02:07

Tumor Progression

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Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
Colon cancer is one of the best-documented examples of tumor progression. Early mutation in the APC gene in colon cells causes a small growth on the colon wall called a polyp. With time, this polyp grows into a benign, pre-cancerous tumor. Further...
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The Tumor Microenvironment02:17

The Tumor Microenvironment

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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...
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Cancer Stem Cells and Tumor Maintenance02:40

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

Adrian P Duval1, Cheryl Jeanneret2, Tania Santoro3

  • 1Department of Visceral Surgery, Lausanne University Hospital, 1011 Lausanne, Switzerland. adrian.duval@chuv.ch.

International Journal of Molecular Sciences
|August 1, 2018
PubMed
Summary
This summary is machine-generated.

Cancer cachexia causes significant weight loss in advanced cancer patients. This review explores how the mechanistic target of rapamycin (mTOR) pathway influences muscle and fat depletion in cancer cachexia.

Keywords:
lipolysismTORmetabolismproteolysissignallingtumour cachexia

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Area of Science:

  • Oncology
  • Molecular Biology
  • Metabolism

Background:

  • Cancer cachexia is a complex metabolic syndrome characterized by involuntary weight loss, primarily affecting muscle and adipose tissue.
  • It significantly increases morbidity and mortality in patients with advanced cancers.
  • Understanding the molecular mechanisms driving cachexia is crucial for developing effective therapeutic interventions.

Purpose of the Study:

  • To review the role of the mechanistic target of rapamycin (mTOR) pathway in the cellular processes underlying cancer cachexia.
  • To highlight existing research demonstrating the involvement of mTOR in the development and progression of cancer cachexia.

Main Methods:

  • Literature review of studies investigating the mechanistic target of rapamycin (mTOR) pathway.
  • Analysis of research on mTOR's role in protein and lipid synthesis.
  • Synthesis of evidence linking mTOR signaling to muscle and adipose tissue depletion in cancer.

Main Results:

  • The mechanistic target of rapamycin (mTOR) is a key intracellular signaling pathway regulating cell growth, protein, and lipid synthesis.
  • Emerging evidence indicates that mTOR signaling and its inhibitors play a significant role in modulating cancer cachexia.
  • Dysregulation of mTOR contributes to the catabolic state observed in cancer cachexia.

Conclusions:

  • The mechanistic target of rapamycin (mTOR) pathway is implicated in the pathogenesis of cancer cachexia.
  • Targeting mTOR signaling represents a potential therapeutic strategy for managing cancer cachexia.
  • Further research is warranted to fully elucidate the complex interplay between mTOR and cancer cachexia.