Genomic profiling of neoplasms developed in SEC31A-JAK2 expressing mice

ABSTRACT: The genetics of classical Hodgkin lymphoma (cHL) is poorly understood. The finding of a JAK2-involving t(4;9)(q21;p24) in one case of cHL prompted us to characterize this translocation on a molecular level and to determine the prevalence of JAK2 rearrangements in cHL. We showed that the t(4;9)(q21;p24) leads to a novel SEC31A-JAK2 fusion. Screening of 131 cHL cases identified one additional case with SEC31A-JAK2 and two additional cases with rearrangements involving JAK2. We demonstrated that SEC31A-JAK2 is oncogenic in vitro and acts as a constitutively activated tyrosine kinase that is sensitive to JAK inhibitors. In vivo, SEC31A-JAK2 was found to induce a T-lymphoblastic lymphoma or myeloid hyperplasia in a murine bone marrow transplant model. Altogether, we identified SEC31A-JAK2 as a

ORGANISM(S): Mus musculus

SUBMITTER: Julio Finalet 

PROVIDER: E-GEOD-22404 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress