t(1;19) without detectable  E2A  rearrangements in two t(14; 18)‐positive lymphoma/leukemia cases | Zendy

Wlodarska Iwona | Zendy; Stul Michel | Zendy; De WolfPeeters Chris | Zendy; Verhoef Gregor | Zendy; Mecucci Cristina | Zendy; Cassiman JeanJacques | Zendy; Van Den Berghe Herman | Zendy

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t(1;19) without detectable E2A rearrangements in two t(14; 18)‐positive lymphoma/leukemia cases

Author(s) -

Wlodarska Iwona,

Stul Michel,

De WolfPeeters Chris,

Verhoef Gregor,

Mecucci Cristina,

Cassiman JeanJacques,

Van Den Berghe Herman

Publication year - 1994

Publication title -

genes, chromosomes and cancer

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.754

H-Index - 119

eISSN - 1098-2264

pISSN - 1045-2257

DOI - 10.1002/gcc.2870100304

Subject(s) - chromosomal translocation , leukemia , lymphoma , karyotype , cancer research , fusion gene , biology , follicular lymphoma , pathogenesis , gene , bcl10 , gene rearrangement , childhood leukemia , chromosome , genetics , immunology , lymphoblastic leukemia

Translocation t(1;19)(q23;p13) plays a crucial role in the pathogenesis of childhood pre‐B cell leukemia and results in the formation of a fusion gene E2A‐PBXI that encodes a hybrid transcription factor with oncogenic potential. Here we describe two cases, one follicular lymphoma and one acute lymphoblastic leukemia/lymphoma, characterized by a complex karyotype including t(14;18), t(8;14), as well as t(1;19). Molecular studies in both cases failed to show rearrangements of the E2A gene. These results suggest that the t(1;19) found as a secondary chromosome change in t(14;18)‐positive lymphoma/leukemia might be a molecular variant of the t(1;19) that is typical of childhood pre‐B cell leukemia. Genes Chromosom Cancer 10:171–176 (1994). © 1994 Wiley‐Liss, Inc.

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