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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...
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...
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
Treatment Resistent Cancers02:56

Treatment Resistent Cancers

Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
Treatment Resistant Cancers02:56

Treatment Resistant Cancers

Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...

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PARP-2 depletion results in lower radiation cell survival but cell line-specific differences in poly(ADP-ribose) levels.

Cellular and molecular life sciences : CMLS·2014
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Variations in the mRNA expression of poly(ADP-ribose) polymerases, poly(ADP-ribose) glycohydrolase and ADP-ribosylhydrolase 3 in breast tumors and impact on clinical outcome.

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The impact of cyclin-dependent kinase 5 depletion on poly(ADP-ribose) polymerase activity and responses to radiation.

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Related Experiment Video

Updated: Jul 11, 2026

Identifying PD-1/PD-L1 Inhibitors with Surface Plasmon Resonance Technology
07:04

Identifying PD-1/PD-L1 Inhibitors with Surface Plasmon Resonance Technology

Published on: May 2, 2025

PARP inhibitor development for systemic cancer targeting.

Tomasz Zaremba1, Nicola Jane Curtin

  • 1Newcastle University, Northern Institute for Cancer Research, Paul O'Gorman Building, Medical School, Framlington Place, Newcastle upon Tyne, NE2 4HH, UK.

Anti-Cancer Agents in Medicinal Chemistry
|September 28, 2007
PubMed
Summary

Poly(ADP-ribose) polymerase 1 (PARP-1) inhibitors enhance cancer therapy by targeting DNA repair mechanisms. These potent inhibitors show promise in clinical trials, particularly for BRCA-deficient cancers.

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Cell Death Associated with Abnormal Mitosis Observed by Confocal Imaging in Live Cancer Cells
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Last Updated: Jul 11, 2026

Identifying PD-1/PD-L1 Inhibitors with Surface Plasmon Resonance Technology
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Published on: May 2, 2025

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Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts

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Cell Death Associated with Abnormal Mitosis Observed by Confocal Imaging in Live Cancer Cells
15:53

Cell Death Associated with Abnormal Mitosis Observed by Confocal Imaging in Live Cancer Cells

Published on: August 21, 2013

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Pharmacology

Background:

  • Poly(ADP-ribose) polymerase 1 (PARP-1) is a crucial DNA-binding enzyme activated by DNA breaks.
  • PARP-1 signaling involves poly(ADP-ribosyl)ation, leading to chromatin relaxation and DNA repair facilitation.
  • PARP inhibitors are developed to study PARP-1 function and overcome cancer therapy resistance.

Purpose of the Study:

  • To investigate the role of PARP-1 in cell biology and DNA repair.
  • To develop potent PARP inhibitors for cancer therapy.
  • To evaluate the efficacy of novel PARP inhibitors in combination treatments and specific genetic contexts.

Main Methods:

  • Development of potent PARP inhibitors through structure-activity relationships and crystal structure-based drug design.
  • Pre-clinical studies combining novel PARP inhibitors with DNA-methylating agents (temozolomide), topoisomerase poisons, and ionizing radiation.
  • Evaluation of PARP inhibitor efficacy in cancer cells with homozygous defects in BRCA1 and BRCA2 genes.

Main Results:

  • Identification of PARP inhibitors approximately 1,000 times more potent than early benzamide inhibitors.
  • Demonstrated enhancement of anti-tumor activity when novel PARP inhibitors are combined with standard cytotoxic therapies.
  • Selective killing of cancer cells and tumors with BRCA1/BRCA2 deficiencies by PARP inhibitors.

Conclusions:

  • Novel PARP inhibitors represent a significant advancement in targeting DNA repair pathways for cancer treatment.
  • These inhibitors enhance the efficacy of existing chemotherapies and radiation.
  • PARP inhibitors offer a targeted therapeutic strategy for BRCA-mutated cancers.