T-Cell Lymphoblastic Lymphoma With Eosinophilia Associated With Subsequent Myeloid Malignancy

Abruzzo, Lynne V.; Jaffe, ES; Cotelingam, James D.; Whang‐Peng, J.; Duca, V. Del; Medeiros, L. Jeffrey

doi:10.1097/00000478-199203000-00003

Cited by 107 publications

(49 citation statements)

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“…42 Patients with FGFR1 rearrangements, however, may initially have T-or B-lymphoblastic leukemia/lymphoma associated with prominent tissue eosinophilia that may later evolve to a myeloid neoplasm with eosinophilia. 42,43 Rare cases associated with PDGFRA rearrangements have also been reported to initially have a lymphoblastic neoplasm. 44 Therefore, although it might seem less confusing to categorize cases with rearranged PDGFRA, PDGFRB, or FGFR1 and eosinophilia as CEL within the MPN category, this would ignore cases with PDGRB rearrangements that have CMML as well as cases with rearrangements of FGFR1 and PDGFRA that may have a lymphoid component.…”

Section: Myeloproliferative Neoplasms and Myeloid Neoplasms Associatementioning

confidence: 99%

The 2008 revision of the World Health Organization (WHO) classification of myeloid neoplasms and acute leukemia: rationale and important changes

Vardiman

Thiele

Arber

et al. 2009

Blood

3,905

3,157

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1 That classification reflected a paradigm shift from previous schemes in that, for the first time, genetic information was incorporated with morphologic, cytochemical, immunophenotypic, and clinical information into diagnostic algorithms for the myeloid neoplasms. The 2001WHO classification was prefaced with a comment predicting that future revisions would be necessary because of rapidly emerging genetic and biologic information. Recently, a revised classification has been published as part of the 4th edition of the WHO monograph series. 2 The aim of the revision was to incorporate new scientific and clinical information to refine diagnostic criteria for previously described neoplasms and to introduce newly recognized disease entities. Our purpose in this communication is to highlight major changes in the revised WHO classification of myeloid neoplasms and acute leukemia and to provide the rationale for those changes.

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Section: Myeloproliferative Neoplasms and Myeloid Neoplasms Associatementioning

confidence: 99%

The 2008 revision of the World Health Organization (WHO) classification of myeloid neoplasms and acute leukemia: rationale and important changes

Vardiman

Thiele

Arber

et al. 2009

Blood

3,905

3,157

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“…2 Hepatosplenomegaly is common in SCLL patients, and, except for some cases with B-cell acute lymphoblastic lymphoma, 3 most patients exhibit T-lymphoblastic lymphoma. The clinical course for SCLL is aggressive, with rapid transformation to acute myeloid leukemia (AML) and lymphoblastic lymphoma of common T-cell origin.…”

Section: Introductionmentioning

confidence: 99%

Constitutive Notch pathway activation in murine ZMYM2-FGFR1–induced T-cell lymphomas associated with atypical myeloproliferative disease

Ren

Cowell

2011

Blood

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The ZMYM2-FGFR1 (formerly known as ZNF198-FGFR1) fusion kinase induces stem cell leukemia-lymphoma syndrome (SCLL), a hematologic malignancy characterized by rapid transformation to acute myeloid leukemia and T-lymphoblastic lymphoma. In the present study, we demonstrate frequent, constitutive activation of Notch1 and its downstream target genes in T-cell lymphomas that arose in a murine model of ZMYM2-FGFR1 SCLL. Notch up-regulation was also demonstrated in human SCLL-and FGFR1OP2- IntroductionStem cell leukemia-lymphoma syndrome (SCLL) 1 is an atypical myeloproliferative disease-associated lymphoma. 2 Hepatosplenomegaly is common in SCLL patients, and, except for some cases with B-cell acute lymphoblastic lymphoma, 3 most patients exhibit T-lymphoblastic lymphoma. The clinical course for SCLL is aggressive, with rapid transformation to acute myeloid leukemia (AML) and lymphoblastic lymphoma of common T-cell origin. [3][4][5] Conventional chemotherapy is often not effective, 3 making early allogeneic transplantation the only treatment. 6 The characteristic 8;13 reciprocal chromosome translocation 7 results in a chimeric protein consistently involving the fibroblast growth factor receptor-1 (FGFR1). 5 To date, ϳ 10 different gene partners have been shown to fuse to FGFR1, including ZMYM2, 4,7 CEP110, 8 and FGFR1OP, 9 among other more rare combinations. 10 In all cases, the fusion partner provides a dimerization domain for constitutive activation of FGFR1. ZMYM2-FGFR1 is the most common translocation, in which the zinc-finger-containing N-terminal part of ZMYM2 enables dimerization of FGFR1. 4 The FGFR1 rearrangement can be found in both myeloid and lymphoid cells in SCLL patients, suggesting a multipotent hematopoietic progenitor cell origin. Constitutive activation and mislocalization of the FGFR1 kinase leads to abnormal phosphorylation of downstream proteins such as PLC␥, PI3K, and various members of the STAT family of transcription factors. [11][12][13] We described previously a mouse model of ZMYM2-FGFR1 SCLL that closely resembles the clinical characteristics of patients with the ZMYM2-FGFR1 translocation, having a distinct myeloproliferative disorder and severe T-lymphoblastic leukemia. The constitutive and ligand-independent activation of the FGFR1 signal transduction pathway is believed to be essential for disease pathogenesis. [13][14] Evidence of tumor oligoclonality and normal differentiation of thymocytes in these animals, however, indicates that additional genetic alterations are required for disease development and progression. Array comparative genomic hybridization demonstrated Tcra and Tcrd gene deletion in leukemic cells in these animals. Lymphomas were CD4 ϩ /CD8 ϩ double-positive (DP), representing an arrest in the late stages of T-cell development, because rearrangement of Tcra is critical for these final maturation stages. However, because Tcra-null mice do not develop T-cell lymphoma, [15][16] it is clear that deletion of Tcra in itself is also not sufficient to induce T-lymphoblastic ly...

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“…IL-5 is a major soluble factor for mediating eosinophilia, and the production of IL-5 by T-cell lymphoma cells has been reported previously [1,5,9]. Quantifying the expression of such cytokines at the mRNA or protein level could clarify the cause of the eosinophilia, but it could not be examined in the present case.…”

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confidence: 88%

“…, Yasuhito FUJINO 1) *, Jun UGAI 1) , Yuko GOTO-KOSHINO 1) , Tetsuya IDE 2) , Masashi TAKAHASHI 1) , Koichi OHNO 1) , Kazuyuki UCHIDA 2) , Hiroyuki NAKAYAMA 2) and Hajime TSUJIMOTO 1) Eosinophilia can occur in dogs with non-neoplastic diseases such as allergy, parasitism, pulmonary eosinophilic infiltration and eosiniphilic gastroenteritis [6]. In addition, neoplasia-associated eosinophilia in dogs has been reported in the case of both hematopoietic and nonhematopoietic tumors, including anaplastic mammary carcinoma [7], oral fibrosarcoma [3] and rectal adenomatous polyps [14].…”

mentioning

confidence: 99%

Eosinophilia and Eosinophilic Infiltration into Splenic B-Cell High-Grade Lymphoma in a Dog

Tomiyasu

Fujino

Ugai

et al. 2010

The Journal of Veterinary Medical Science

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ABSTRACT. A 13-year-old mixed-breed dog showing ascites, anorexia and anemia was found to have leukocytosis with marked eosinophilia, splenomegaly and hepatomegaly. The dog died 4 days after initial presentation and was diagnosed with splenic high-grade Bcell lymphoma at necropsy. Remarkable infiltrations of eosinophils were observed in spleen and liver tissues. The eosinophilia and infiltration of eosinophils into the lesions could have been associated with B-cell lymphoma because causes other than lymphoma were excluded. This is the first report of eosinophilia and eosinophilic infiltrations into neoplastic lesions in a dog with high-grade B-cell lymphoma.KEY WORDS: B-cell centroblastic lymphoma, canine, hypereosinophilia, infiltration of eosinophils.

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T-Cell Lymphoblastic Lymphoma With Eosinophilia Associated With Subsequent Myeloid Malignancy

Cited by 107 publications

References 0 publications

The 2008 revision of the World Health Organization (WHO) classification of myeloid neoplasms and acute leukemia: rationale and important changes

The 2008 revision of the World Health Organization (WHO) classification of myeloid neoplasms and acute leukemia: rationale and important changes

Constitutive Notch pathway activation in murine ZMYM2-FGFR1–induced T-cell lymphomas associated with atypical myeloproliferative disease

Eosinophilia and Eosinophilic Infiltration into Splenic B-Cell High-Grade Lymphoma in a Dog

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