The Maciejowski Lab, with the New York City skyline behind them

Sloan Kettering Institute · Memorial Sloan Kettering Cancer Center

Genomic instability puts DNA where it does not belong. Chromosomes are mis-segregated, telomeres fail, and broken chromosomes fuse and break again, and each of these leaves DNA in the wrong place or the wrong state inside the cell. From that common origin the lab follows two questions. The first is what happens when a cell finds its own DNA loose in the cytoplasm, where it reads as a sign of infection, and how tumors learn to suppress the response that follows. The second is what instability writes into the genome and leaves behind, from characteristic patterns of mutation to oncogenes amplified onto circles of DNA that float free of the chromosomes. Across both we want to understand how cancer cells exploit the consequences of their own instability, and to turn that understanding into something treatable.

Research

Recent work

All publications →
  1. Striepen J, Dananberg A, Ruzgaitė A, Hurley A, Toufektchan E, Nichols A, Rosenberg H, Cordero C, Mertz TM, Norman RX, Koche R, Roberts SA, Maciejowski J. Squamous-state excursions activate APOBEC3A in cancer. bioRxiv 2026.DOIPubMed 42244601
  2. Striepen J, Culibrk L, Dananberg A, Rozowsky JS, Petljak M, Maciejowski J. A context dependent hierarchy of APOBEC3A and APOBEC3B mutators in lung adenocarcinoma. bioRxiv 2026.DOI
  3. Chen Y, Norman RX, Toufektchan E, Luan X, Shim A, Rosenberg H, Kovacs MT, Nichols A, Hickling J, Cifani P, Kentsis A, Zhou W, Maciejowski J. ER-tethering directs TREX1 penetration of a BAF-dependent barrier at micronuclei. Molecular Cell 2026;86(6):1099–1115.DOIPubMed 41861785

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