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Recently, we detected a new fusion transcript  LMO3-BORCS5  in a patient with Ewing sarcoma within a cohort of relapsed pediatric cancers . LMO3-BORCS5  was as highly expressed as the characteristic fusion oncogene  EWS/FLI1 . However, the expression level of  LMO3-BORCS5  at diagnosis was very low. Sanger sequencing depicted two  LMO3-BORCS5  variants leading to loss of the functional domain LIM2 in  LMO3  gene, and disruption of  BORCS5 . In vitro studies showed that  LMO3-BORCS5  (i) increases proliferation, (ii) decreases expression of apoptosis-related genes and treatment sensitivity, and (iii) downregulates genes involved in differentiation and upregulates proliferative and extracellular matrix-related pathways. Remarkably, in vivo  LMO3-BORCS5  demonstrated its high oncogenic potential by inducing tumors in mouse fibroblastic NIH-3T3 cell line. Moreover,  BORCS5  probably acts, in vivo, as a tumor-suppressor gene. In conclusion, functional studies of fusion oncogenes at relapse are of great importance to define mechanisms involved in tumor progression and resistance to conventional treatments.

Newly identified LMO3-BORCS5 fusion oncogene in Ewing sarcoma at relapse is a driver of tumor progression