John Maciejowski

This study identifies heterogeneous roles of APOBEC3A and APOBEC3B in lung adenocarcinoma mutagenesis using CRISPR-Cas9 and whole-genome sequencing of single-cell clones.

The paper identifies transient squamous-state excursions in cancer cells as a source of APOBEC3A mutagenesis, linking it to lineage-state plasticity rather than persistent inflammation.

The paper identifies BAF as a barrier that restricts TREX1 access to micronuclei, explaining the need for ER-tethering to enable TREX1 entry and suppress cGAS activation.

This study identifies APOBEC3B as the enzyme responsible for ssDNA breakage during replication catastrophe induced by ATR inhibition, revealing a mechanism for PARP1 trapping and synthetic lethality with PARP inhibitors.

The paper shows that ecDNA inheritance is ensured through mitotic transcription and chromosomal tethering via BRD4 and PVT1, preventing cytosolic mis-segregation and chromosomal integration.

This study shows that TREX1 mutations in the polyproline motif destabilize the protein, leading to excessive cGAS-STING signaling and autoimmune disease.

The paper identifies TREX1 as a suppressor of CRISPR-Cas9 HDR efficiency in human cells and shows that TREX1 removal or use of chemically protected templates can enhance HDR.

This study shows TREX1 limits cGAS recognition of micronuclear DNA by degrading it after micronuclear envelope rupture, and a TREX1 mutation disrupts this process, enhancing immune sensing.

This study identifies TREX1 and APOBEC3B as key drivers of chromothripsis and kataegis during telomere crisis in cancer.

The paper identifies three novel complex structural variation patterns in cancer genomes using genome graph analysis across 2,833 tumor WGS.