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 radiation relative to
rhabdomyosarcomas that do not carry this fusion gene.
In a report just
released in PLoS Genetics, Ken from our lab reports 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: http://www.plosgenetics.org/doi/pgen.1004107.
