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TYRO3 Truncation Resulting From a t(10;15)(p11;q15) Chromosomal Translocation in Pediatric Acute Myeloid Leukemia.

Anticancer Res. 2020 Nov;40(11):6115-6121
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摘要


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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