Related Experiment Video

Updated: Apr 8, 2026

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

15.7K

PARP inhibitors and more

Chinmoy K Bose1, Nirban Basu2

  • 1Department of Gynecological Oncolgy, Division of Clinical Trial, Netaji Subhas Chandra Bose Cancer Research Institute, West Bengal, India.

Journal of the Turkish German Gynecological Association
|June 23, 2015
PubMed

Insights

Polyadenosine diphosphate (ADP) ribose polymerase (PARP) inhibitors target cancer cell DNA repair. Resistance to these PARP inhibitors is a growing clinical challenge, necessitating further research into alternative damage repair strategies.

Area of Science:

  • Molecular Biology
  • Genetics
  • Oncology

Background:

  • Polyadenosine diphosphate (ADP) ribose polymerase (PARP) enzymes are crucial for maintaining genomic integrity against cellular DNA damage.
  • PARP functions in concert with tumor suppressors like breast cancer (BRCA) 1 and 2.
  • PARP inhibitors exploit synthetic lethality to eliminate tumor cells, with applications in ovarian cancer treatment.

Purpose of the Study:

  • To explore the mechanisms underlying resistance to PARP inhibitors.
  • To understand the clinical implications of PARP inhibitor resistance.
  • To investigate alternative DNA damage repair approaches in the context of resistance.

Main Methods:

  • The study reviews existing literature on PARP inhibitors and resistance mechanisms.
  • It analyzes the interplay between PARP, BRCA, and DNA repair pathways.
  • Clinical data on patients treated with PARP inhibitors is examined.

Main Results:

  • PARP inhibitors induce synthetic lethality in cancer cells with compromised DNA repair pathways.
  • Acquired resistance to PARP inhibitors can arise through various genetic and non-genetic alterations.
  • Understanding these resistance mechanisms is critical for optimizing cancer therapy.

Conclusions:

  • PARP inhibitors represent a significant advancement in cancer treatment, particularly for BRCA-mutated cancers.
  • Mechanisms of resistance to PARP inhibitors are diverse and clinically relevant.
  • Further research into overcoming resistance and exploring combination therapies is warranted.
Keywords:
BRCAPARP inhibitorsolaparibovarian cancersynthetic lethality

More Related Videos

Author Spotlight: Developing Parmodulins to Target Protease-Activated Receptors for Inflammation Control07:13

Author Spotlight: Developing Parmodulins to Target Protease-Activated Receptors for Inflammation Control

Published on: May 24, 2024

1.1K
Silencing of BRCA2 to Identify Novel BRCA2-regulated Biological Functions in Cultured Human Cells09:24

Silencing of BRCA2 to Identify Novel BRCA2-regulated Biological Functions in Cultured Human Cells

Published on: August 12, 2015

9.7K

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...
9.1K
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...
6.2K
Negative Regulator Molecules01:23

Negative Regulator Molecules

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
39.1K
Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors01:20

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors

Antiplatelet drugs emerge as frontline defenders against the insidious threat of thromboembolic diseases, where abnormal clots obstruct vital blood vessels. These drugs stand as bulwarks, inhibiting platelet aggregation and clot formation, thereby mitigating the risk of life-threatening conditions like myocardial infarction, coronary artery disease, and thrombotic strokes.
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
1.5K
Dipeptidyl Peptidase 4 Inhibitors01:23

Dipeptidyl Peptidase 4 Inhibitors

Dipeptidyl peptidase 4 (DPP-4) is a serine protease widely distributed in the body. It's involved in the inactivation of GLP-1 and GIP hormones, which are crucial for insulin regulation. DPP-4 inhibitors, such as sitagliptin (Januvia), saxagliptin (Onglyza), linagliptin (Tradjenta), alogliptin (Nesina), and vildagliptin (Galvus), help increase the proportion of active GLP-1, enhancing insulin secretion. These inhibitors work by competitively binding to DPP-4. This binding causes a...
1.1K
Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists01:23

Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists

Prostacyclin receptor agonists are a class of therapeutic agents integral to managing pulmonary arterial hypertension (PAH). These drugs operate by mimicking the action of prostaglandin I2, or PGI2, a naturally occurring compound in the body.
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...
615