Morphological spectrum of cyclin D1‐positive mantle cell lymphoma: Study of 168 cases

Yatabe, Yasushi; Suzuki, Ritsuro; Matsuno, Yoshihiro; Tobinai, Kensei; Ichinohazama, Ryo; Tamaru, Jun Ichi; Mizoguchi, Yoshikazu; Hashimoto, Yuko; Yamaguchi, Motoko; Kojima, Masaru; Uike, Naokuni; Okamoto, Masanori; Isoda, Kentaro; Ichimura, Koichi; Morishima, Yasuo; Seto, Masao; Suchi, Taizan; Nakamura, Shigeo

doi:10.1046/j.1440-1827.2001.01277.x

Cited by 39 publications

(44 citation statements)

References 66 publications

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“…Fresh human fetal bones of 17 to 19 gestation wk were provided by Advanced Bioscience Resources. N-Ndiethyl-8,8-dipropyl-2-azaspiro [4,5] decane-2-propanamine (atiprimod), provided by Callisto Pharmaceuticals, was dissolved in PBS and injected i.p. to MCL-bearing mice at a dose of 50 mg/kg/d for 6 consecutive d.…”

Section: Methodsmentioning

confidence: 99%

“…It is characterized by overexpression of cyclin D1 with a t (11;14) chromosomal translocation. Accurate diagnosis of MCL is based on morphology, immunophenotype (CD5 + , CD19 + , CD20 + , CD10 -, CD23 F , IgM + , and IgD + ), and detection of either the characteristic chromosomal translocation t (11;14) or overexpression of cyclin D1 (4,5). Most MCL patients present with advanced stage disease, and up to 90% have involvement of the bone marrow, spleen, and/or gastrointestinal tract.…”

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confidence: 99%

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A Severe Combined Immunodeficient–hu In vivo Mouse Model of Human Primary Mantle Cell Lymphoma

Wang¹,

Zhang²,

Han

et al. 2008

Clinical Cancer Research

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Purpose: To establish a severe combined immunodeficient (SCID)-hu in vivo mouse model of human primary mantle cell lymphoma (MCL) for the study of the biology and novel therapy of human MCL. Experimental Design: Primary MCL cells were isolated from spleen, lymph node, bone marrow aspirates, or peripheral blood of six different patients and injected respectively into human bone chips, which had been s.c. implanted in SCID-hu. Circulating human h 2 -microglobulin in mouse serum was used to monitor the engraftment and growth of patient's MCL cells. H&E staining and immunohistochemical staining with anti-human CD20 and cyclin D1 antibodies were used to confirm the tumor growth and migration. Results: Increasing levels of circulating human h 2 -microglobulin in mouse serum indicated that the patient's MCL cells were engrafted successfully into human bone chip of SCID-hu mice. The engraftment and growth of patient's MCL cells were dependent on human bone marrow microenvironment. Immunohistochemical staining with anti-human CD20 and cyclin D1 antibodies confirmed that patient's MCL cells were able to not only survive and propagate in the bone marrow microenvironment of the human fetal bone chips, but also similar to the human disease, migrate to lymph nodes, spleen, bone marrow, and gastrointestinal tract of host mice.Treatment of MCL-bearing SCID-hu mice with atiprimod, a novel antitumor compound against the protection of bone marrow stromal cells, induced tumor regression. Conclusion: This is the first human primary MCL animal model that should be useful for the biological and therapeutic research on MCL.

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Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

A Severe Combined Immunodeficient–hu In vivo Mouse Model of Human Primary Mantle Cell Lymphoma

Wang¹,

Zhang²,

Han

et al. 2008

Clinical Cancer Research

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“…14 MCL responds to similar agents used effectively for MM. For example, the chemotherapy regimens CHOP (cyclophosphamide, doxorubicin, vincristine, and prednisone) and hyperCVAD (cyclophosphamide, vincristine, doxorubicin, decadron, cytarabine, and methotrexate) are effective in B-cell NHL, especially in MCL, 15 but their slight modifications are also effective in MM.…”

Section: Introductionmentioning

confidence: 99%

Atiprimod inhibits the growth of mantle cell lymphoma in vitro and in vivo and induces apoptosis via activating the mitochondrial pathways

Wang

Zhang

Han

et al. 2007

Blood

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Atiprimod is a novel cationic amphiphilic compound and has been shown to exert antimyeloma effects both in vitro and in mouse experiments. This study was undertaken to evaluate the therapeutic efficacy of atiprimod on mantle cell lymphoma (MCL) and elucidate the mechanism by which it induces cell apoptosis. IntroductionMantle cell lymphoma (MCL) represents approximately 8% of all non-Hodgkin lymphomas (NHLs). It has the worst prognosis among all B-cell-derived malignancies with median survival of 3 to 4 years. [1][2][3] Although MCL has been treated with chemotherapy, radiotherapy, hematopoietic stem cell transplantation, molecular targeted therapy, and combination therapy of these treatments, no standard treatment approach has been established thus far. Novel therapeutic agents are needed in clinical trials. [4][5][6][7][8]5] decane-2-propanamine), a novel cationic amphiphilic compound, has been studied for its anticancer properties in malignancies. [9][10][11] Recent reports have suggested that atiprimod exhibits antiproliferative and antiangiogenic activities, induces apoptosis via activation of caspases-3 and -8, and inhibits phosphorylation of Akt and STAT3 in multiple myeloma (MM). 10,12 In addition, atiprimod exhibits in vivo antimyeloma effects in xenograft severe combined immunodeficient (SCID) mouse models. 10,13 These results provide a framework for clinical trials of atiprimod in MM.MCL has distinct biologic, morphologic, and immunophenotypic features in NHL. 14 MCL responds to similar agents used effectively for MM. For example, the chemotherapy regimens CHOP (cyclophosphamide, doxorubicin, vincristine, and prednisone) and hyperCVAD (cyclophosphamide, vincristine, doxorubicin, decadron, cytarabine, and methotrexate) are effective in B-cell NHL, especially in MCL, 15 but their slight modifications are also effective in MM. [16][17][18][19] Bortezomib, a potent and specific proteasome inhibitor that was U. S. Food and Drug Administration-approved for relapsed MM, was also proven to be effective in MCL. 20 Thalidomide is active in MM, and thalidomide in combination with rituximab induces impressive antitumor activity in relapsed/ refractory MCL patients. 21 Revlimid, an immunomodulatory drug that produces durable clinical responses in patients with relapsed and refractory MM, 22 also is showing activity in clinical trials for treatment of NHL. Thus, we hypothesize that MCL and MM share certain biologic mechanisms in responding to various compound therapies. Atiprimod, which exhibits significant antitumor ability against MM cells by growth inhibition and apoptosis, 10 may also prove effective in MCL. In this study, we demonstrate that atiprimod not only inhibited growth and induced apoptosis of MCL cell lines SP53, MINO, Grant 519, Jeko-1, and freshly isolated patient-derived primary MCL cells in vitro, but it was also therapeutic against established human MCL in xenograft SCID mouse models. Of importance, atiprimod exhibited lower cytotoxicity against normal T cells. Furthermore, we attempted to eluc...

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“…Although follicular colonization is frequently seen in marginal zone lymphoma, this phenomenon may also be seen in other B-cell lymphomas, including follicular lymphoma [28][29][30][31] and mantle cell lymphoma. 32 In the 2009 Society for Hematopathology/European Association of Hematopathology workshop, cases of putative lymphoplasmacytic lymphoma with follicular colonization were accepted as bona fide lymphoplasmacytic lymphoma by some, but not all, members of the expert review panel. 4 The presence of MYD88 L265P mutations in such cases, as observed in this study, also suggests that such cases may represent bona fide lymphoplasmacytic lymphoma.…”

Section: F Hamadeh Et Almentioning

confidence: 99%

MYD88 L265P mutation analysis helps define nodal lymphoplasmacytic lymphoma

et al. 2015

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The diagnosis of lymphoplasmacytic lymphoma is often challenging, especially in extramedullary tissues where the differential diagnosis includes nodal marginal zone lymphoma, splenic marginal zone lymphoma, or other small B-cell neoplasms with plasmacytic differentiation. The MYD88 L265P mutation has been recently identified in 490% of bone-marrow-based lymphoplasmacytic lymphoma, but the incidence of this abnormality and corresponding morphologic correlates in nodal lymphoplasmacytic lymphoma have not been established. We analyzed 87 cases of extramedullary lymphoplasmacytic lymphoma, splenic marginal zone lymphoma, unclassifiable splenic B-cell lymphomas, nodal marginal zone lymphoma with plasmacytic differentiation, and chronic lymphocytic leukemia/small lymphocytic lymphoma with plasmacytic differentiation for MYD88 L265P. Eighteen cases (21%) were positive, including 9/9 (100%) lymphoplasmacytic lymphomas with classic histologic features, 5/12 (42%) cases that met 2008 WHO criteria for lymphoplasmacytic lymphoma but with atypical morphologic features, 3/15 (20%) cases initially considered nodal marginal zone lymphoma with plasmacytic differentiation, and 1/6 (17%) unclassifiable splenic B-cell lymphomas. The presence of MYD88 L265P was associated with IgM paraprotein (Po0.001) and a trend for bone marrow involvement (P ¼ 0.09). Each of 44 splenectomy-defined splenic marginal zone lymphomas (19 with plasmacytic differentiation) and the chronic lymphocytic leukemia/small lymphocytic lymphoma with plasmacytic differentiation were negative for the mutation. Morphologic re-review with knowledge of MYD88 mutation status and all available clinical features suggested all MYD88 mutated cases were consistent with lymphoplasmacytic lymphoma (either classic or variant histology), except for one case which remained most consistent with nodal marginal zone lymphoma with plasmacytic differentiation. These results demonstrate the importance of MYD88 mutational analysis in better defining lymphoplasmacytic lymphoma as a relatively monomorphic small B-cell lymphoma with plasmacytic differentiation that may show total nodal architectural effacement and follicular colonization. Cases previously considered lymphoplasmacytic lymphoma that are more polymorphous and are often associated with histiocytes should no longer be included in the lymphoplasmacytic lymphoma category. Clinicopathologic review suggests that although MYD88 mutated non-lymphoplasmacytic lymphoma small B-cell neoplasms exist, they are very uncommon.

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Morphological spectrum of cyclin D1‐positive mantle cell lymphoma: Study of 168 cases

Cited by 39 publications

References 66 publications

A Severe Combined Immunodeficient–hu In vivo Mouse Model of Human Primary Mantle Cell Lymphoma

A Severe Combined Immunodeficient–hu In vivo Mouse Model of Human Primary Mantle Cell Lymphoma

Atiprimod inhibits the growth of mantle cell lymphoma in vitro and in vivo and induces apoptosis via activating the mitochondrial pathways

MYD88 L265P mutation analysis helps define nodal lymphoplasmacytic lymphoma

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