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[Cancer Research 49, 665-671, February 1, 1989]
© 1989 American Association for Cancer Research

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Progression of Transplanted SJL/J Lymphomas Attributed to a Single Aggressive H-2Ds-negative Lymphoma1

Lynne Sopchak, Steven R. King, Dorothy A. Miller, Nashwa Gabra, Gerald R. Thrush and Stephen P. Lerman2

Wayne State University School of Medicine, Departments of Immunology and Microbiology [L. S., S. R. K., G. R. T., S. P. L.], Pathology [D. A. M.], and Molecular Biology and Genetics [D. A. M., N. G.], Detroit, Michigan 48201

Spontaneously arising, H-2Ds-positive SJL/J lymphomas have been reported to become irreversibly more aggressive and H-2Ds-negative upon successive transplantation in syngeneic mice. In an effort to determine whether this process was one of tumor progression, we sought to: (a) establish whether a clonal relationship exists between readily transplantable aggressive SJL/J lymphomas and their respective indolent predecessors; and (b) identify genetic events critical to the process of acquisition of increased malignancy. Examination of putatively distinct, aggressive, H-2Ds-negative lymphomas, including the long term transplantable line RCS5, revealed them to have the same heavy and light immunoglobulin chain gene rearrangement patterns, a characteristic karyotype marked by nine chromosomal abnormalities, and approximately ten newly acquired ecotropic murine leukemia proviruses at similar genomic sites. Independent, spontaneously arising H-2Ds-positive lymphomas, in early transplant, were found to be genetically distinct from the respective more malignant H-2Ds-negative tumors to which they gave rise during successive transplantation. The data are interpreted as indicating that the aggressive H-2Ds-negative tumors in this study originated from a common source, most likely the RCS5 tumor, rather than through progression of separate spontaneously arising SJL/J lymphomas. It cannot be concluded which of the multiple genetic abnormalities of the H-2Ds-negative tumors were critical to their highly malignant phenotype. However, chromosomal abnormalities and newly acquired murine leukemia proviruses are discussed as to the roles they might play in SJL/J lymphomas.

1 Supported by USPHS Grant CA-38663, March of Dimes Grant 1-950, and grants from the Center for Molecular Biology of Wayne State University and the Childrens Leukemia Foundation of Michigan. The Wayne State University Department of Immunology and Microbiology Flow Cytometry Facility (Funded by BRS-Shared Instrumentation Grant 1-S10-RR020806) is supported by the Comprehensive Cancer Center of Metropolitan Detroit (CA-22453) and the Center for Molecular Biology of Wayne State University.

2 To whom requests for reprints should be addressed, at Wayne State University School of Medicine, Department of Immunology and Microbiology, 550 East Canfield, Detroit, MI 48201.

Received 7/18/88. Revised 10/20/88. Accepted 10/24/88.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Cell Growth & Differentiation
Copyright © 1989 by the American Association for Cancer Research.