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Related Concept Videos

Abnormal Proliferation02:23

Abnormal Proliferation

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 daughter...
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

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.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
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DNA Damage Can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
DNA Damage can Stall the Cell Cycle02:36

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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.
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Replicative Cell Senescence

Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds the telomeric...

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Updated: May 19, 2026

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Selective Elimination of TP53 Mutant Cells by Transcript-Activated Chromatin Shredding.

Jingkun Zeng1,2,3, Zhiyuan Cheng1,2, Huadong Chen4

  • 1Gladstone Institute of Data Science and Biotechnology, San Francisco, CA, USA, 94158.

Biorxiv : the Preprint Server for Biology
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Summary

Scientists reprogrammed CRISPR-Cas12a2 to target cancer-specific RNA, inducing DNA damage and cell death. This transcript-activated chromatin shredding offers a new way to treat cancers with undruggable mutations.

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10:44

In Vitro Selection of Engineered Transcriptional Repressors for Targeted Epigenetic Silencing

Published on: May 5, 2023

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Genetics

Background:

  • Genetic mutations in tumor suppressor proteins, like p53, drive cancer development.
  • Current cancer therapies struggle to target these mutations due to a lack of drug-binding pockets.
  • Restoring the function of mutated tumor suppressor proteins remains a significant challenge in cancer treatment.

Purpose of the Study:

  • To develop a novel method for selectively killing cancer cells by targeting cancer-specific transcripts.
  • To investigate the potential of CRISPR-Cas12a2 in treating cancers with undruggable mutations.
  • To establish transcript-activated chromatin shredding as a new therapeutic paradigm.

Main Methods:

  • Programmed CRISPR-Cas12a2, an RNA-guided nuclease, to target cancer-specific RNA sequences.
  • Utilized the trans-nucleolytic cleavage activity of Cas12a2 to induce chromatin cleavage.
  • Triggered DNA damage and subsequent cell death in cancer cells through targeted chromatin shredding.

Main Results:

  • Demonstrated that RNA-guided Cas12a2 can selectively identify and target cancer-specific RNA signatures.
  • Showcased the ability of Cas12a2 to induce trans chromatin cleavage, leading to DNA damage and cancer cell death.
  • Validated transcript-activated chromatin shredding as a viable strategy for targeting previously undruggable mutations.

Conclusions:

  • CRISPR-Cas12a2 can be programmed to selectively eliminate cancer cells by targeting their unique RNA.
  • Transcript-activated chromatin shredding represents an innovative approach for precision medicine.
  • This method holds promise for developing novel treatments for cancers with undruggable genetic mutations.