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. doi: 10.21873/anticanres.14632.


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.

Keywords: Pediatric; RNA sequencing; TYRO3 gene; acute myeloid leukemia; chromosome translocation.

Publication types

  • Case Reports

MeSH terms

  • Base Sequence
  • Child
  • Chromosomes, Human, Pair 10 / genetics*
  • Chromosomes, Human, Pair 15 / genetics*
  • Humans
  • Leukemia, Myeloid, Acute / genetics*
  • Male
  • Receptor Protein-Tyrosine Kinases / genetics*
  • Translocation, Genetic*


  • Receptor Protein-Tyrosine Kinases
  • TYRO3 protein, human