TY - JOUR
T1 - Targeting homologous recombination addicted tumors
T2 - Challenges and opportunities
AU - Golan, Talia
AU - Brody, Jonathan R.
N1 - Funding Information:
Funding: JRB is supported by NIH-NCI R01 CA212600, the National Cancer Institute of the National Institutes of Health under Award Number P30CA056036 SKCC Core Grant (TJU). 2015 Pancreatic Cancer Action Network American Association for Cancer Research Acceleration Network Grant (15-90-25-BROD). Also the generous support of the W. Kim Foster Pancreatic Cancer Research Endowment. TG is supported by ICRF 2018-2019, MOST-DFZK 2019-2020, Investigator. Initiative Grant Astra Zeneca 2016-2019, Investigator. Initiative Grant Merck MSD 2017-2020, and Soyka Pancreatic Cancer Fund.
Publisher Copyright:
© 2021 Annals of Pancreatic Cancer. All rights reserved.
PY - 2020/6
Y1 - 2020/6
N2 - 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.
AB - 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.
KW - DNA damaging repair genes
KW - Pancreatic adenocarcinoma
KW - Precision medicine
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U2 - 10.21037/apc.2020.03.02
DO - 10.21037/apc.2020.03.02
M3 - Review article
AN - SCOPUS:85110982087
SN - 2616-2741
VL - 3
JO - Annals of Pancreatic Cancer
JF - Annals of Pancreatic Cancer
M1 - A91
ER -