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Clonal dominance defines metastatic dissemination in pancreatic cancer

Using patient-derived cells from a pancreatic ductal adenocarcinoma, we created orthotopic clonal replica tumors to trace in an unbiased fashion clonal lineage dynamics of unperturbed tumor expansion and dissemination over time. The model revealed the complex multifaced nature of tumor clonal expansion and uncovered brisk changes in fitness that lead to a continuous reshuffling of tumor clonal architecture and alternating clonal dominance as a distinct feature of cancer growth. Paired analysis of clonal lineages in primary and secondary sites revealed fitness in the primary tumor as a major contributor to dissemination, although other clonal intrinsic and extrinsic factors may contribute to metastatic process. Molecular characterization of lineages with differential metastatic potential identified actionable strategy to suppress dissemination at the subclonal level.

Click on a Dataset ID in the table below to learn more, and to find out who to contact about access to these data

Dataset ID Description Technology Samples
EGAD00001008994 Illumina HiSeq 2500 6
EGAD00001008995 Illumina HiSeq 2500 6
EGAD00001008996 unspecified 6
EGAD00001008997 unspecified 6