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A New Paper by Kickuchi, Keller and Colleagues on a completely new way of thinking about what Pax3:Foxo1a does. The paper is titled: Cell-Cycle Dependent Expression of a Translocation-Mediated Fusion Oncogene Mediates Checkpoint Adaptation in Rhabdomyosarcoma.

In alveolar rhabdomyosarcoma, 70-75% of tumors carry the Pax3:Foxo1a oncogene. This oncogene seems to account for a large difference in the response to chemotherapy and radation relative to rhabdomyosarcomas that do not carry this fusion gene. In a report just released in PLoS Genetics, Kickuchi, Keller and colleagues report that Pax3:Foxo1a levels fluctuate during tumor cell replication, and that a primary function of Pax3:Foxo1a seems to be “checkpoint adaptation” – the process of giving the cell permission to continue cell division despite damage from therapy… with the hopes that this damage can be later repaired, simply tolerated – or may offer an advantage to the tumor cell as a result of newly gained mutations/properties.

The paper is freely available online at: