Genomic Characterization of Bladder Cancer Cell Lines using CGH Arrays
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE30754 | GEO | 2013/06/28
SECONDARY ACCESSION(S): PRJNA144129
REPOSITORIES: GEO
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Project description:Genomic rearrangements involving different chromosome translocation in bladder cancer cell lines and in primary tumor samples DNA extracted from 3 Bladder Cancer Cell lines (SW1710, JON, RT-4), and 1 bladder cancer (372C) in T3 Tumor stage and Grade 3 primary sample, were processed, Cy5 labeled and hybridized on Agilent CGH Arrays. As control DNA we used Cy3 labeled probes prepared starting from a pool of female DNA obtained mixing the DNA extracted from 20 healthy donors.
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Project description: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 first aberration characteristic for cHL and provide evidence that JAK2 rearrangements occur in a minority of cHL cases. Given the proven oncogenic potential of this novel fusion, our studies provide new insights into the pathogenesis of cHL and indicate that in at least some cases, constitutive activation of the JAK-STAT pathway is caused by JAK2 rearrangements. The finding that SEC31A-JAK2 responds to JAK inhibitors indicates that patients with cHL and JAK2 rearrangements may benefit from targeted therapies. Genomic profiling of primary and secondary transplanted mice expressing SEC31A-JAK2 with myeloid hyperplasia and T-lymphoblastic lymphoma Individual sample against a normal control
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Project description: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 first aberration characteristic for cHL and provide evidence that JAK2 rearrangements occur in a minority of cHL cases. Given the proven oncogenic potential of this novel fusion, our studies provide new insights into the pathogenesis of cHL and indicate that in at least some cases, constitutive activation of the JAK-STAT pathway is caused by JAK2 rearrangements. The finding that SEC31A-JAK2 responds to JAK inhibitors indicates that patients with cHL and JAK2 rearrangements may benefit from targeted therapies.
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