ArticlebioRxiv : the preprint server for biology2025
Pan-cancer 3D genomic analysis revealed extremely long Polycomb loops as the biomarker for sensitivity to Polycomb inhibition.
Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Polycomb targeted loci form long-range chromatin interactions independent of CTCF-cohesion and are demarcated by low DNA methylation(1-3). Polycomb targets form extremely long-range loops (long Polycomb loops) that can separate anchors up to 60 Mb. These loops predominantly occur in cells of self-renewal status, such as human hematopoietic stem cells (HSC) and mouse embryonic stem cells (ESC), but rarely in cell lines. To identify long Polycomb loops in cancer, we initiated a pan-cancer survey of long Polycomb loops in a collection of 264 tumor samples (33 acute myeloid leukemias, 17 T cell lymphoblastic leukemia, 29 Breast cancer samples, 63 pediatric brain tumors, 70 prostate cancers, and 42 colon cancers). We found most cancers, including all prostate cancers and colon cancers, lack long Polycomb loops except pediatric brain tumors and certain AMLs. In pediatric brain tumors, we found 30% of the ependymoma PFA subtype (which shows globally depleted H3K27me3) notably displayed strong long Polycomb loop interactions. AML displayed more diverse levels of long Polycomb loop interactions. Most AMLs lost both long Polycomb loops with Polycomb binding loss at the loop anchors. Whereas 10% of AMLs retain long Polycomb loops as strong as in HSCs. These AMLs recurrently carry mutations in
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