Document Type

Article

Publication Date

2020

Comments

This article is the author's final published version in Annals of Pancreatic Cancer, Volume 3, June 2020, Article number A91.

The published version is available at https://doi.org/10.21037/apc.2020.03.02

Copyright © 2021 Annals of Pancreatic Cancer. All rights reserved.

This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0.

Abstract

Recent advances in next generation sequencing (NGS) and molecular subtyping of tumors have opened the door to clinically available targeted therapies. Although the treatment of many solid tumors still rely on a steady regimen of non-targeted chemotherapeutic agents, it is becoming increasingly more apparent that certain tumors with defects in DNA damage repair (DDR) genes may be exquisitely sensitive to DNA damaging agents or therapies targeting key elements of this pathway such PARP1, ATR, or ATM. Still, for tumors with DDR defects the challenges are multi-fold including: (I) identifying these tumors in patients in time for a window of opportunity of treatment; (II) ensuring that these tumors are still reliant or addicted to this pathway; and (III) making sure these tumors are matched with the precise treatment option. Herein, we will discuss the opportunities, challenges, and future of targeting a subset of DDR-defective tumors.

Creative Commons License

Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 4.0 License.

Language

English

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