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Related Concept Videos

Canonical Wnt Signaling Pathway02:54

Canonical Wnt Signaling Pathway

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The gene encoding the main signaling molecules of the Wnt signaling pathways (the Wnt proteins) was discovered almost four decades ago by Nüsslein-Volhard and Wieschaus. They identified and originally named the gene "wingless" (wg) after a phenotype discovered during their landmark genetic screen in Drosophila for body pattern defects. At around the same time, another researcher named Harold Varmus found that a murine tumor virus activates the mammalian wg homolog, Int-1, which...
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Wnt is a zygotic effect gene that is expressed during very early embryonic development. It regulates various processes in animals starting from early development through the adult stage, such as organogenesis in the embryo and maintenance of neuronal and blood stem cells. Wnt proteins can induce a wide variety of intracellular pathways depending upon the specific abilities of different Wnt ligands to form a complex with shared and cognate receptors in the presence of different co-receptors. The...
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Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
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The Notch signaling pathway is a major intracellular signaling pathway that is highly conserved over a broad spectrum of metazoan species. It stands unique from other intracellular signaling mechanisms in animals because notch protein itself acts as the receptor as well as the primary signaling molecule.
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Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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Related Experiment Video

Updated: May 21, 2025

A Mouse Model of Incompletely Resected Soft Tissue Sarcoma for Testing Neoadjuvant Therapies
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Deciphering WNT Signalling Vulnerabilities in Soft Tissue Sarcoma.

Marina Pérez-Capó1,2,3, Esther Martinez-Font4,5,6, Elena Prados4,7

  • 1Group of Advanced Therapies and Biomarkers in Clinical Oncology, Health Research Institute of the Balearic Islands (IdISBa), Palma, Spain, marina.perez@ssib.es.

Pathobiology : Journal of Immunopathology, Molecular and Cellular Biology
|March 20, 2025
PubMed
Summary

Soft tissue sarcomas (STSs) show WNT/β-catenin pathway activation. Genetic analysis revealed variants in key pathways, including PI3K/AKT/mTOR-MAPK, offering potential therapeutic targets.

Keywords:
Personalized treatmentPrimary cultureSoft tissue sarcomaWNT signallingβ-catenin

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Soft tissue sarcomas (STSs) are rare cancers with few treatment options.
  • The WNT/β-catenin pathway is implicated in STS development and other cancers.

Purpose of the Study:

  • To investigate WNT/β-catenin pathway activation in STS.
  • To identify genetic alterations and potential therapeutic targets in STS.

Main Methods:

  • Characterization of eight patient-derived STS primary cultures.
  • Analysis of WNT/β-catenin activation using immunohisto(cyto)chemistry.
  • Next-generation sequencing of STS tumors for genetic variants.

Main Results:

  • All STS cultures exhibited elevated active phospho-β-catenin and nuclear localization.
  • Genomic analysis revealed pathogenic variants in WNT, DNA damage repair, and PI3K/AKT/mTOR-MAPK pathways.
  • 50% of STS tumors had clinically significant variants in PIK3CA and PTEN, serving as predictive biomarkers.

Conclusions:

  • WNT signaling is a key vulnerability in STS.
  • Identified genetic variants can guide targeted therapy development.
  • Biomarkers for personalized treatment of STS patients were discovered.