Anaplastic, plasmablastic, and plasmacytic plasmacytomas of mice : Relationships to human plasma cell neoplasms and late-stage differentiation of normal B cells

Chen-Feng QI; Jeff X ZHOU; Siegfried JANZ; Herbert C MORSE; CHANG HOON LEE; Zohreh NAGHASHFAR; SHAO XIANG; Alexander L KOVALCHUK; Torgny N FREDRICKSON; Janet W HARTLEY; Derry C ROOPENIAN; Wendy F DAVIDSON

doi:10.1158/0008-5472.CAN-06-1561

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Anaplastic, plasmablastic, and plasmacytic plasmacytomas of mice : Relationships to human plasma cell neoplasms and late-stage differentiation of normal B cells

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Anaplastic, plasmablastic, and plasmacytic plasmacytomas of mice : Relationships to human plasma cell neoplasms and late-stage differentiation of normal B cells

Chen-Feng QI, Jeff X ZHOU, Siegfried JANZ, Herbert C MORSE, CHANG HOON LEE, Zohreh NAGHASHFAR, SHAO XIANG, Alexander L KOVALCHUK, Torgny N FREDRICKSON, Janet W HARTLEY, …

Cancer research (Chicago, Ill.), Vol.67(6), pp.2439-2447

2007

DOI: 10.1158/0008-5472.CAN-06-1561

PMID: 17363561

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Abstract

We have compared histologic features and gene expression profiles of newly identified plasmacytomas from NFS.V(+) congenic mice with plasmacytomas of IL6 transgenic, Fasl mutant, and SJL-beta2M(-/-) mice. NFS.V(+) tumors comprised an overlapping morphologic spectrum of high-grade/anaplastic, intermediate-grade/plasmablastic, and low-grade/plasmacytic cases with similarities to subsets of human multiple myeloma and plasmacytoma. Microarray and immunohistochemical analyses of genes expressed by the most prevalent tumors, plasmablastic plasmacytomas, showed them to be most closely related to immunoblastic lymphomas, less so to plasmacytomas of Fasl mutant and SJL mice, and least to plasmacytic plasmacytomas of IL6 transgenic mice. Plasmablastic tumors seemed to develop in an inflammatory environment associated with gene signatures of T cells, natural killer cells, and macrophages not seen with plasmacytic plasmacytomas. Plasmablastic plasmacytomas from NFS.V(+) and SJL-beta2M(-/-) mice did not have structural alterations in Myc or T(12;15) translocations and did not express Myc at high levels, regular features of transgenic and pristane-induced plasmacytomas. These findings imply that, as for human multiple myeloma, Myc-independent routes of transformation contribute to the pathogenesis of these tumors. These findings suggest that plasma cell neoplasms of mice and humans exhibit similar degrees of complexity. Mouse plasmacytomas, previously considered to be homogeneous, may thus be as diverse as their human counterparts with respect to oncogenic mechanisms of plasma cell transformation. Selecting specific types of mouse plasmacytomas that relate most closely to subtypes of human multiple myeloma may provide new opportunities for preclinical testing of drugs for treatment of the human disease.

Antineoplastic Agents

Tumors

Hematologic and hematopoietic diseases

Pharmacology. Drug treatments

Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis

Biological and medical sciences

Medical sciences

Details

Title: Subtitle: Anaplastic, plasmablastic, and plasmacytic plasmacytomas of mice : Relationships to human plasma cell neoplasms and late-stage differentiation of normal B cells
Creators: Chen-Feng QI - Laboratory of Immunopathology, National Institute of Allergy and Infectious Diseases, National Cancer Institute, NIH, Rockville, Maryland, United States
Jeff X ZHOU - Laboratory of Immunopathology, National Institute of Allergy and Infectious Diseases, National Cancer Institute, NIH, Rockville, Maryland, United States
Siegfried JANZ - laboratory of Genetics, National Cancer Institute, NIH, Rockville, Maryland, United States
Herbert C MORSE - Laboratory of Immunopathology, National Institute of Allergy and Infectious Diseases, National Cancer Institute, NIH, Rockville, Maryland, United States
CHANG HOON LEE - Laboratory of Immunopathology, National Institute of Allergy and Infectious Diseases, National Cancer Institute, NIH, Rockville, Maryland, United States
Zohreh NAGHASHFAR - Laboratory of Immunopathology, National Institute of Allergy and Infectious Diseases, National Cancer Institute, NIH, Rockville, Maryland, United States
SHAO XIANG - Laboratory of Immunopathology, National Institute of Allergy and Infectious Diseases, National Cancer Institute, NIH, Rockville, Maryland, United States
Alexander L KOVALCHUK - laboratory of Genetics, National Cancer Institute, NIH, Rockville, Maryland, United States
Torgny N FREDRICKSON - Laboratory of Immunopathology, National Institute of Allergy and Infectious Diseases, National Cancer Institute, NIH, Rockville, Maryland, United States
Janet W HARTLEY - Laboratory of Immunopathology, National Institute of Allergy and Infectious Diseases, National Cancer Institute, NIH, Rockville, Maryland, United States
Derry C ROOPENIAN - Jackson Laboratory, Bar Harbor, Maine, United States
Wendy F DAVIDSON - University of Maryland School of Medicine, Department of Microbiology and Immunology, Baltimore, Maryland, United States
Resource Type: Journal article
Publication Details: Cancer research (Chicago, Ill.), Vol.67(6), pp.2439-2447
Publisher: American Association for Cancer Research
DOI: 10.1158/0008-5472.CAN-06-1561
PMID: 17363561
ISSN: 0008-5472
eISSN: 1538-7445
Language: English
Date published: 2007
Academic Unit: Pathology
Record Identifier: 9984083896902771

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