B acute lymphoblastic leukemia with t(14;19)(q32;p13.1) involving IGH/EPOR: a clinically aggressive subset of disease

Jaso, Jesse Manuel; Yin, C. Cameron; Lu, Victoria; Zhao, Ming; Abruzzo, Lynne V.; You, M. James; Yang, Ya‐Ling; Luthra, Raja; Medeiros, L. Jeffrey; Lu, Gary

doi:10.1038/modpathol.2013.149

Cited by 10 publications

(7 citation statements)

References 17 publications

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“…Overall, the picture was consistent with a diagnosis of eosinophilia-associated myeloproliferative neoplasm with myelofibrosis MF-2, unclassified. Conventional cytogenetic analysis, performed according to the protocols used in our clinical cytogenetics laboratory as previously described,(6) confirmed the abnormal karyotype in 20/20 metaphases (Supplementary Figure 1A). Fluorescence in-situ hybridization (FISH) analyses for BCR-ABL or rearrangements of PDGFRA or PDGFRB were negative.…”

Section: Letter To the Editormentioning

confidence: 60%

ETV6–FLT3 fusion gene-positive, eosinophilia-associated myeloproliferative neoplasm successfully treated with sorafenib and allogeneic stem cell transplant

et al. 2014

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Section: Letter To the Editormentioning

confidence: 60%

ETV6–FLT3 fusion gene-positive, eosinophilia-associated myeloproliferative neoplasm successfully treated with sorafenib and allogeneic stem cell transplant

et al. 2014

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“…They are more frequent in adolescents and confer a poor prognosis [136] (Table 3). Several partners of IGH in BCP-ALL have been identified, including inhibitor of DNA binding 4 (ID4) at 6p22 [137], EPOR at 19p13 [98,138,139], a member of the CCAAT/enhancer binding protein (CEBP) family (e.g. CEBPA, CEBPG, CEBPB, CEBPD, CEBPE) [140,141] , BCL2 [142], the LIM domain Homeobox 4 (LHX4) at 1q25, and rarely, Interleukin 3 (IL-3) at 5q31 [136].…”

Section: Igh-rearranged Allmentioning

confidence: 99%

Molecular basis and clinical significance of genetic aberrations in B-cell precursor acute lymphoblastic leukemia

Ghazavi

Lammens

Roy

et al. 2015

Experimental Hematology

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“…Through genetic lesions, cytokine receptor chains that are normally expressed on myeloid, erythroid, or megakaryocytic lineages become aberrantly expressed on transformed B cells. Examples of oncogenic activation of non‐B lymphoid cytokine receptors include: (i) translocation of the erythropoietin receptor gene (EPOR) to the immunoglobulin heavy chain locus ( IGH‐EPOR ) ; (ii) in‐frame fusions of EBF1‐PDGFRB (platelet‐derived growth factor receptor, beta polypeptide) ; (iii) in‐frame fusions of ATF7IP‐PDGFRB ; and (iv) activating mutation in FLT3, including D835Y and, less frequent than in acute myeloid leukemia, in‐frame ITD (internal tandem duplication) within the FLT3 juxtamembrane domain .…”

Section: Oncogenic Mimicry Of Cytokine Receptor Signaling In Pre‐b Allmentioning

confidence: 99%

Mechanisms of pre‐B‐cell receptor checkpoint control and its oncogenic subversion in acute lymphoblastic leukemia

Buchner

Swaminathan

Chen

et al. 2014

Immunological Reviews

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Pre-B cells within the bone marrow represent the normal counterpart for most acute lymphoblastic leukemia (ALL). During normal early B-cell development, survival and proliferation signals are dominated by cytokines, particularly interleukin-7 (IL-7) for murine developing B cells. With expression of a functional pre-B-cell receptor (BCR), cytokine signaling is attenuated and the tonic/autonomous pre-BCR signaling pathway provides proliferation as well as differentiation signals. In this review, we first describe checkpoint mechanisms during normal B-cell development and then discuss how genetic lesions in these pathways function as oncogenic mimicries and allow transformed pre-B cells to bypass checkpoint control. We focus on cytokine receptor signaling that is mimicked by activating lesions in receptor subunits or downstream mediators as well as aberrant activation of non-B lymphoid cytokine receptors. Furthermore, we describe the molecular switch from cytokine receptor to pre-BCR signaling, how this pathway is of particular importance for certain ALL subtypes, and how pre-BCR signaling is engaged by genetic lesions, such as BCR-ABL1. We discuss the transcriptional control mechanisms downstream of both cytokine- and pre-BCR signaling and how normal checkpoint control mechanisms are circumvented in pre-B ALL. Finally, we highlight new therapeutic concepts for targeted inhibition of oncogenic cytokine or pre-BCR signaling pathways.

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B acute lymphoblastic leukemia with t(14;19)(q32;p13.1) involving IGH/EPOR: a clinically aggressive subset of disease

Cited by 10 publications

References 17 publications

ETV6–FLT3 fusion gene-positive, eosinophilia-associated myeloproliferative neoplasm successfully treated with sorafenib and allogeneic stem cell transplant

ETV6–FLT3 fusion gene-positive, eosinophilia-associated myeloproliferative neoplasm successfully treated with sorafenib and allogeneic stem cell transplant

Molecular basis and clinical significance of genetic aberrations in B-cell precursor acute lymphoblastic leukemia

Mechanisms of pre‐B‐cell receptor checkpoint control and its oncogenic subversion in acute lymphoblastic leukemia

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