TYRO3 truncation resulting from a t(10;15)(p11;q15) chromosomal translocation in pediatric acute myeloid Leukemia

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Abstract

Background/Aim: Novel acquired chromosome aberrations in cancer may provide insights into pathogenetic mechanisms, be of diagnostic and/or prognostic significance and pave the way for new modes of therapeutic intervention. Here, we report a novel chromosome translocation and its molecular genetic consequences in a pediatric acute myeloid leukemia (AML) case. Materials and Methods: Cytogenetic, RNA sequencing, and molecular analyses were performed on the bone marrow cells of a child with AML. Results: The patient entered complete hematologic remission after treatment according to the NOPHO-AML 2004 protocol. A novel t(10;15)(p11;q15) translocation was found in leukemic cells at diagnosis resulting in a fusion of exon 13 of TYRO3 with a sequence from 10p11. The transcript codes for a putative TYRO3 protein lacking the tyrosine kinase domain. Conclusion: The t(10;15)(p11;q15) translocation in neoplastic bone marrow cells results in truncated TYRO3. Because the role of the truncated TYRO3 cannot be predicted functional studies are required.

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Brunetti, M., Zeller, B., Tierens, A., Heim, S., Micci, F., & Panagopoulos, I. (2020). TYRO3 truncation resulting from a t(10;15)(p11;q15) chromosomal translocation in pediatric acute myeloid Leukemia. Anticancer Research, 40(11), 6115–6121. https://doi.org/10.21873/anticanres.14632

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