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Related Concept Videos

Tumor Progression02:07

Tumor Progression

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...
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against specific...
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Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...

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Related Experiment Video

Updated: Jun 25, 2026

Artificial Antigen Presenting Cell (aAPC) Mediated Activation and Expansion of Natural Killer T Cells
13:18

Artificial Antigen Presenting Cell (aAPC) Mediated Activation and Expansion of Natural Killer T Cells

Published on: December 29, 2012

The APC tumour suppressor has a nuclear export function.

R Rosin-Arbesfeld1, F Townsley, M Bienz

  • 1Laboratory of Molecular Biology, Cambridge, UK.

Nature
|September 13, 2000
PubMed
Summary
This summary is machine-generated.

Mutations in the adenomatous polyposis coli (APC) protein disrupt its nuclear export, leading to beta-catenin accumulation and contributing to colorectal tumor formation. Restoring APC

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Killer Artificial Antigen Presenting Cells (KaAPC) for Efficient In Vitro Depletion of Human Antigen-specific T Cells
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Production of Monoclonal Antibodies Targeting Aminopeptidase N in the Porcine Intestinal Mucosal Epithelium
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Production of Monoclonal Antibodies Targeting Aminopeptidase N in the Porcine Intestinal Mucosal Epithelium

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Last Updated: Jun 25, 2026

Artificial Antigen Presenting Cell (aAPC) Mediated Activation and Expansion of Natural Killer T Cells
13:18

Artificial Antigen Presenting Cell (aAPC) Mediated Activation and Expansion of Natural Killer T Cells

Published on: December 29, 2012

Killer Artificial Antigen Presenting Cells (KaAPC) for Efficient In Vitro Depletion of Human Antigen-specific T Cells
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Killer Artificial Antigen Presenting Cells (KaAPC) for Efficient In Vitro Depletion of Human Antigen-specific T Cells

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Production of Monoclonal Antibodies Targeting Aminopeptidase N in the Porcine Intestinal Mucosal Epithelium
09:45

Production of Monoclonal Antibodies Targeting Aminopeptidase N in the Porcine Intestinal Mucosal Epithelium

Published on: May 18, 2021

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • Adenomatous polyposis coli (APC) protein mutations are prevalent in colorectal tumors, often resulting in truncated proteins.
  • Mutant APC in cancer cells stabilizes beta-catenin, promoting its nuclear translocation and acting as a transcriptional co-activator.
  • APC normally facilitates beta-catenin degradation via the Axin complex and proteasome pathway, a process with poorly understood regulatory roles.

Purpose of the Study:

  • To investigate the regulatory role of APC in beta-catenin destabilization.
  • To identify the mechanism by which APC exits the nucleus and its impact on beta-catenin.
  • To determine the significance of APC nuclear export for its tumor suppressor function.

Main Methods:

  • Identification and analysis of conserved nuclear export signals (NES) in the APC protein.
  • Comparison of APC nuclear export in normal versus APC mutant cancer cells.
  • Investigation of the correlation between APC nuclear export and beta-catenin nuclear accumulation.

Main Results:

  • Highly conserved nuclear export signals were identified 3' adjacent to the APC mutation cluster region.
  • APC's ability to exit the nucleus is lost in APC mutant cancer cells.
  • Evidence suggests that loss of APC nuclear export leads to beta-catenin accumulation in the nucleus.

Conclusions:

  • APC nuclear export, mediated by conserved NES, is crucial for its function.
  • Impaired nuclear export of APC in cancer cells contributes to beta-catenin stabilization and nuclear accumulation.
  • APC's ability to exit the nucleus is critical for its tumor suppressor activity in colorectal cancer.