Data from Drug-Driven Synthetic Lethality: Bypassing Tumor Cell Genetics with a Combination of AsiDNA and PARP Inhibitors Article Swipe
Wael Jdey
,
Sylvain Thierry
,
Christophe Russo
,
Flavien Devun
,
Muthana Al Abo
,
Patricia Noguiez‐Hellin
,
Jian‐Sheng Sun
,
Emmanuel Barillot
,
Andreï Zinovyev
,
Inna Kuperstein
,
Yves Pommier
,
Marie Dutreix
·
YOU?
·
· 2023
· Open Access
·
· DOI: https://doi.org/10.1158/1078-0432.c.6526154
YOU?
·
· 2023
· Open Access
·
· DOI: https://doi.org/10.1158/1078-0432.c.6526154
Purpose: Cancer treatments using tumor defects in DNA repair pathways have shown promising results but are restricted to small subpopulations of patients. The most advanced drugs in this field are PARP inhibitors (PARPi), which trigger synthetic lethality in tumors with homologous recombination (HR) deficiency. Using AsiDNA, an inhibitor of HR and nonhomologous end joining, together with PARPi should allow bypassing the genetic restriction for PARPi efficacy.Experimental Design: We characterized the DNA repair inhibition activity of PARPi (olaparib) and AsiDNA by monitoring repair foci formation and DNA damage. We analyzed the cell survival to standalone and combined treatments of 21 tumor cells and three nontumor cells. In 12 breast cancer (BC) cell lines, correlation with sensitivity to each drug and transcriptome were statistically analyzed to identify resistance pathways.Results: Molecular analyses demonstrate that olaparib and AsiDNA respectively prevent recruitment of XRCC1 and RAD51/53BP1 repair enzymes to damage sites. Combination of both drugs increases the accumulation of unrepaired damage resulting in an increase of cell death in all tumor cells. In contrast, nontumor cells do not show an increase of DNA damage nor lethality. Analysis of multilevel omics data from BC cells highlighted different DNA repair and cell-cycle molecular profiles associated with resistance to AsiDNA or olaparib, rationalizing combined treatment. Treatment synergy was also confirmed with six other PARPi in development.Conclusions: Our results highlight the therapeutic interest of combining AsiDNA and PARPi to recapitulate synthetic lethality in all tumors independently of their HR status. Clin Cancer Res; 23(4); 1001–11. ©2016 AACR.
Related Topics
Concepts
Olaparib
Synthetic lethality
DNA damage
DNA repair
PARP inhibitor
RAD51
Cancer research
XRCC1
PARP1
Biology
Poly ADP ribose polymerase
Homologous recombination
Genome instability
Molecular biology
Genetics
DNA
Polymerase
Genotype
Gene
Single-nucleotide polymorphism
Metadata
- Type
- preprint
- Language
- en
- Landing Page
- https://doi.org/10.1158/1078-0432.c.6526154
- OA Status
- gold
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4361818171
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W4361818171Canonical identifier for this work in OpenAlex
- DOI
-
https://doi.org/10.1158/1078-0432.c.6526154Digital Object Identifier
- Title
-
Data from Drug-Driven Synthetic Lethality: Bypassing Tumor Cell Genetics with a Combination of AsiDNA and PARP InhibitorsWork title
- Type
-
preprintOpenAlex work type
- Language
-
enPrimary language
- Publication year
-
2023Year of publication
- Publication date
-
2023-03-31Full publication date if available
- Authors
-
Wael Jdey, Sylvain Thierry, Christophe Russo, Flavien Devun, Muthana Al Abo, Patricia Noguiez‐Hellin, Jian‐Sheng Sun, Emmanuel Barillot, Andreï Zinovyev, Inna Kuperstein, Yves Pommier, Marie DutreixList of authors in order
- Landing page
-
https://doi.org/10.1158/1078-0432.c.6526154Publisher landing page
- Open access
-
YesWhether a free full text is available
- OA status
-
goldOpen access status per OpenAlex
- OA URL
-
https://doi.org/10.1158/1078-0432.c.6526154Direct OA link when available
- Concepts
-
Olaparib, Synthetic lethality, DNA damage, DNA repair, PARP inhibitor, RAD51, Cancer research, XRCC1, PARP1, Biology, Poly ADP ribose polymerase, Homologous recombination, Genome instability, Molecular biology, Genetics, DNA, Polymerase, Genotype, Gene, Single-nucleotide polymorphismTop concepts (fields/topics) attached by OpenAlex
- Cited by
-
0Total citation count in OpenAlex
- Related works (count)
-
10Other works algorithmically related by OpenAlex
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| abstract_inverted_index.cells | 100, 170, 188 |
| abstract_inverted_index.death | 162 |
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| abstract_inverted_index.breast | 107 |
| abstract_inverted_index.cancer | 108 |
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| abstract_inverted_index.damage | 144, 155, 178 |
| abstract_inverted_index.lines, | 111 |
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| abstract_inverted_index.sites. | 145 |
| abstract_inverted_index.tumors | 38, 235 |
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| abstract_inverted_index.AsiDNA, | 45 |
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