Maciejowski Lab

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

Extrachromosomal DNA

Oncogenes amplified on circular DNA that has no centromere, and how those circles survive cell division anyway.

APOBEC3A mutagenesis

An enzyme responsible for a large share of the point mutations in human cancer, and the rare cell state that switches it on.

Recent work

All publications →

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