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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...
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...
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase

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...
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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Related Experiment Video

Updated: Jun 25, 2026

Yeast As a Chassis for Developing Functional Assays to Study Human P53
14:57

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

Published on: August 4, 2019

Targeting p53 for enhanced radio- and chemo-sensitivity.

Chao Lu1, Wafik S El-Deiry

  • 1Department of Medicine, Laboratory of Molecular Oncology and Cell Cycle Regulation, The Institute for Translational Medicine and Therapeutics, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.

Apoptosis : an International Journal on Programmed Cell Death
|March 5, 2009
PubMed
Summary

The tumor suppressor protein p53 is crucial for cellular stress response and cancer suppression. Restoring wild-type p53 function enhances chemotherapy and radiation sensitivity in cancer cells.

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Procedure and Key Optimization Strategies for an Automated Capillary Electrophoretic-based Immunoassay Method
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Procedure and Key Optimization Strategies for an Automated Capillary Electrophoretic-based Immunoassay Method

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Last Updated: Jun 25, 2026

Yeast As a Chassis for Developing Functional Assays to Study Human P53
14:57

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

Published on: August 4, 2019

Procedure and Key Optimization Strategies for an Automated Capillary Electrophoretic-based Immunoassay Method
09:32

Procedure and Key Optimization Strategies for an Automated Capillary Electrophoretic-based Immunoassay Method

Published on: September 10, 2017

Area of Science:

  • Molecular Biology
  • Oncology
  • Cellular Biology

Background:

  • The p53 protein is a key mediator of cellular responses to stress.
  • Loss of p53 function through mutation is common in human cancers, impairing its growth-suppressive role.
  • Wild-type p53 enhances tumor cell sensitivity to chemotherapy and radiation therapy.

Purpose of the Study:

  • To review the role of p53 in enhancing sensitivity to chemotherapy and radiation.
  • To discuss current therapeutic strategies targeting p53 for cancer treatment.

Main Methods:

  • Review of accumulated evidence on wild-type p53's role in treatment efficacy.
  • Analysis of structural and functional insights into p53 mutations.
  • Examination of p53 degradation pathways involving MDM2 and p53 family proteins.

Main Results:

  • Wild-type p53 activity is essential for the effectiveness of radiation and chemotherapy.
  • Understanding p53 mutations, degradation, and family proteins provides a basis for drug design.
  • Strategies to restore normal p53 function in tumors are of significant interest.

Conclusions:

  • Restoring p53 function in tumors with defective p53 signaling is a promising therapeutic avenue.
  • Targeting p53 pathways offers potential for improving cancer treatment outcomes.
  • Further drug development based on p53 biology is warranted.