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Related Concept Videos

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...
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...
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...
DNA Damage can Stall the Cell Cycle02:36

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

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...
Combination Therapies and Personalized Medicine02:50

Combination Therapies and Personalized Medicine

Combining two or more treatment methods increases the life span of cancer patients while reducing damage to vital organs or tissue from the overuse of a single treatment. Combination therapy also targets different cancer-inducing pathways, thus reducing the chances of developing resistance to treatment.
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...

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Updated: Jun 13, 2026

Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence
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Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence

Published on: December 30, 2025

p53-based cancer therapy.

David P Lane1, Chit Fang Cheok, Sonia Lain

  • 1p53 Laboratory (A-Star) 8A Biomedical Grove Immunos Singapore 138648. dplane@p53lab.a-star.edu.sg

Cold Spring Harbor Perspectives in Biology
|May 14, 2010
PubMed
Summary
This summary is machine-generated.

Cancer therapies targeting the p53 tumor suppressor are advancing rapidly. Research explores gene therapy, oncolytic viruses, RNA interference, and small molecules to restore p53 function and combat cancer effectively.

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Yeast As a Chassis for Developing Functional Assays to Study Human P53
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Purification of Ubiquitinated p53 Proteins from Mammalian Cells
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Purification of Ubiquitinated p53 Proteins from Mammalian Cells

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Last Updated: Jun 13, 2026

Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence
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Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence

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Yeast As a Chassis for Developing Functional Assays to Study Human P53
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Yeast As a Chassis for Developing Functional Assays to Study Human P53

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Purification of Ubiquitinated p53 Proteins from Mammalian Cells
10:55

Purification of Ubiquitinated p53 Proteins from Mammalian Cells

Published on: March 21, 2022

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Therapeutics

Background:

  • The tumor suppressor protein p53 is inactivated in most human cancers.
  • This widespread p53 dysfunction presents a significant target for novel cancer therapies.

Purpose of the Study:

  • To review current and emerging p53-based cancer therapeutic strategies.
  • To highlight the diverse approaches being developed to restore or leverage p53 function in cancer treatment.

Main Methods:

  • Gene therapy utilizing wild-type p53 delivered via adenovirus vectors.
  • Development of oncolytic viruses targeting p53-deficient cancer cells.
  • RNA interference (siRNA, antisense RNA) to inhibit p53 negative regulators (Mdm2, MdmX, HPV E6).
  • p53-based vaccines to elicit anti-tumor immune responses (T-cell and B-cell).
  • Small molecule inhibitors targeting p53-Mdm2 interactions.
  • Drug combinations enhancing chemotherapy selectivity and safety.

Main Results:

  • Adenovirus-mediated p53 gene therapy is in clinical use.
  • Oncolytic viruses and RNA-based therapies are under development.
  • p53-based vaccines are in clinical trials.
  • Small molecule inhibitors, particularly p53-Mdm2 inhibitors, have reached clinical stages.
  • Combination therapies aim to improve chemotherapy efficacy and reduce toxicity.

Conclusions:

  • Multiple p53-based therapeutic strategies are progressing towards clinical application.
  • Restoring or exploiting p53 function offers a promising avenue for cancer treatment.
  • Future directions include optimizing drug combinations for enhanced selectivity and safety.