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Related Experiment Video

Updated: May 11, 2026

Laser Microirradiation to Study In Vivo Cellular Responses to Simple and Complex DNA Damage

Laser Microirradiation to Study In Vivo Cellular Responses to Simple and Complex DNA Damage

Published on: January 31, 2018

Poly(ADP-ribosyl)ation in carcinogenesis.

Mitsuko Masutani¹, Hiroaki Fujimori

¹Division of Genome Stability Research, National Cancer Center Research Institute, Japan.

Molecular Aspects of Medicine

|May 30, 2013

Summary

Poly(ADP-ribosyl)ation plays a dual role in cancer, acting as a tumor suppressor by maintaining genomic stability and a promoter in specific cancer types. Targeting this process offers potential for cancer prevention and treatment.

Area of Science:

Molecular Biology
Genetics
Cancer Research

Background:

Cancer arises from multi-step genetic and epigenetic alterations.
Poly(ADP-ribosyl)ation (PAR) is a post-translational modification involved in cellular processes.

Purpose of the Study:

To review the multifaceted role of poly(ADP-ribosyl)ation in various carcinogenesis pathways.
To explore the implications of PAR in cancer prevention and treatment strategies.

Main Methods:

Review of molecular and cellular studies.
Analysis of animal models and human genetic data.
Examination of PARP inhibition's synthetic lethality in cancer.

Main Results:

Poly(ADP-ribosyl)ation is crucial for DNA damage repair and genomic stability, suggesting a tumor-suppressive role.

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Published on: March 20, 2018

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Last Updated: May 11, 2026

Laser Microirradiation to Study In Vivo Cellular Responses to Simple and Complex DNA Damage

Laser Microirradiation to Study In Vivo Cellular Responses to Simple and Complex DNA Damage

Published on: January 31, 2018

Formation of Covalent DNA Adducts by Enzymatically Activated Carcinogens and Drugs In Vitro and Their Determination by 32P-postlabeling

Formation of Covalent DNA Adducts by Enzymatically Activated Carcinogens and Drugs In Vitro and Their Determination by ³²P-postlabeling

Published on: March 20, 2018

PARP inhibition demonstrates synthetic lethality in DNA repair-deficient cancer cells.

PARP family members influence diverse pathways including epigenetics, inflammation, and epithelial-mesenchymal transition, indicating context-dependent roles in carcinogenesis.

Conclusions:

Poly(ADP-ribosyl)ation exhibits both tumor-suppressive and tumor-promoting functions in carcinogenesis.
Targeting poly(ADP-ribosyl)ation pathways presents opportunities for novel cancer prevention and therapeutic interventions.