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Immune Checkpoint Blockade Delays Cancer Development and Extends Survival in DNA Polymerase Mutator Syndromes
Akshada Sawant1,2, Fuqian Shi1, Eduardo Cararo Lopes1
1Rutgers Cancer Institute, Rutgers University, New Brunswick, New Jersey.
Abstract:
Mutations in the exonuclease domains of the replicative nuclear DNA polymerases POLD1 and POLE are associated with increased cancer incidence, elevated tumor mutation burden (TMB), and enhanced response to immune checkpoint blockade (ICB). Although ICB is approved for treatment of several cancers, not all tumors with elevated TMB respond, highlighting the need for a better understanding of how TMB affects tumor biology and subsequently immunotherapy response. To address this, we generated mice with germline and conditional mutations in the exonuclease domains of Pold1 and Pole. Engineered mice with Pold1 and Pole mutator alleles presented with spontaneous cancers, primarily lymphomas, lung cancer, and intestinal tumors, whereas Pold1 mutant mice also developed tail skin carcinomas. These cancers had highly variable tissue type-dependent increased TMB with mutational signatures associated with POLD1 and POLE mutations found in human cancers. The Pold1 mutant tail tumors displayed increased TMB; however, only a subset of established tumors responded to ICB. Similarly, introducing the mutator alleles into mice with lung cancer driven by mutant Kras and Trp53 deletion did not improve survival, whereas passaging these tumor cells in vitro without immune editing and subsequently implanting them into immunocompetent mice caused tumor rejection in vivo. These results demonstrated the efficiency by which cells with antigenic mutations are eliminated in vivo. Finally, ICB treatment of mutator mice earlier, before observable tumors had developed delayed cancer onset, improved survival and selected for tumors without aneuploidy, suggesting the potential of ICB in high-risk individuals for cancer prevention. Significance: Treating high-mutation burden mice with immunotherapy prior to cancer onset significantly improves survival, raising the possibility of utilizing immune checkpoint blockade for cancer prevention, especially in individuals with increased risk.
Insights
Mutations in DNA polymerases POLD1 and POLE increase cancer risk and tumor mutation burden (TMB). Early immune checkpoint blockade (ICB) in high-risk mice prevents cancer, suggesting potential for cancer prevention in individuals with increased risk.
Area of Science:
- Genetics
- Immunology
- Cancer Biology
Background:
- Mutations in DNA polymerases POLD1 and POLE are linked to increased cancer incidence, elevated tumor mutation burden (TMB), and improved response to immune checkpoint blockade (ICB).
- Understanding how TMB influences tumor biology and immunotherapy response is crucial, as not all TMB-high tumors respond to ICB.
Purpose of the Study:
- To investigate the impact of POLD1 and POLE mutations on cancer development, TMB, and response to ICB in a mouse model.
- To explore the potential of ICB as a cancer prevention strategy in individuals at high risk.
Main Methods:
- Generated mice with germline and conditional mutations in the exonuclease domains of Pold1 and Pole.
- Analyzed spontaneous cancers for TMB and mutational signatures.
- Assessed tumor response to ICB in established tumors and in a preventative setting.
Main Results:
- Engineered mice developed spontaneous cancers (lymphomas, lung, intestinal, skin) with increased TMB and human-relevant mutational signatures.
- Pold1 mutant tail tumors showed high TMB but only partial ICB response; ICB did not improve survival in Kras/Trp53-driven lung cancer models.
- Early ICB treatment in mutator mice delayed cancer onset and improved survival, selecting for tumors without aneuploidy.
Conclusions:
- POLD1 and POLE mutations drive cancer with high TMB, but established tumors may not fully respond to ICB due to factors like immune editing.
- Early administration of ICB shows promise as a cancer prevention strategy for high-risk individuals, delaying cancer onset and improving survival.
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