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Related Concept Videos

Mismatch Repair01:20

Mismatch Repair

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Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
The Mutator Protein Family Plays a Key Role in DNA Mismatch Repair
The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic...
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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.
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Cancers Originate from Somatic Mutations in a Single Cell

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Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
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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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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.
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Cancer-Critical Genes II: Tumor Suppressor Genes

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Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
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Related Experiment Video

Updated: Jul 4, 2025

Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer
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Degradation trumps mutations in cancer.

R Eric Davis1, Jason R Westin1

  • 1Department of Lymphoma and Myeloma, MD Anderson Cancer Center, Houston, TX, USA.

Science (New York, N.Y.)
|February 1, 2024
PubMed
Summary

Targeted protein degradation is a novel strategy to overcome acquired drug resistance. This approach redirects specific proteins for cellular breakdown, offering a new therapeutic avenue.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Pharmacology

Background:

  • Acquired drug resistance is a major challenge in cancer therapy.
  • Targeted protein degradation offers a promising strategy to combat resistance.

Purpose of the Study:

  • To investigate the potential of redirecting targeted proteins for degradation as a method to overcome acquired drug resistance.
  • To explore novel therapeutic strategies for drug-resistant cancers.

Main Methods:

  • Utilizing proteolysis-targeting chimeras (PROTACs) to induce targeted protein degradation.
  • Employing biochemical assays and cell-based models to assess drug efficacy.

Main Results:

  • Demonstrated successful degradation of targeted proteins in drug-resistant cancer cells.

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  • Showcased restoration of drug sensitivity through targeted protein degradation.

    • Conclusions:

    • Redirecting targeted proteins for degradation is a viable strategy to overcome acquired drug resistance.
    • This approach holds significant promise for developing new treatments for refractory cancers.