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[Cancer Research 52, 4678-4681, September 1, 1992]
© 1992 American Association for Cancer Research

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Cytogenetic Characterization of B-Cell Lymphomas from Severe Combined Immunodeficiency Disease Mice Given Injections of Lymphocytes from Epstein-Barr Virus-positive Donors1

Maya Thangavelu, Leslee Snyder, John Anastasi, Michelle M. Le Beau, Marybeth Kirven, Gaston Picchio, Donald E. Mosier and Janet D. Rowley2

Section of Hematology/Oncology, Department of Medicine [M. T., L. S., M. M. L., J. D. R.] and Department of Pathology [J. A.], The University of Chicago, Chicago, Illinois 60637-1470, and Division of Immunology, Medical Biology Institute, La Jolia, California 92037 [M. K., G. P., D. E. M.]

We analyzed the karyotype of 27 B-cell lymphomas of human origin that developed in mice with severe combined immunodeficiency disease following the injection of peripheral blood leukocytes from Epstein-Barr virus-seropositive donors. Three tumors had clonal abnormalities detected with conventional techniques, 2 had trisomy 11, and 1 had a del(6)(q21q25). One other tumor had trisomy 11 detected with fluorescence in situ hybridization. Twelve tumors had a normal karyotype, 11 tumors had nonclonal abnormalities (which included trisomy 9 or 12 in 3 or 2 tumors, respectively), and one tumor had a karyotype of 92,XXXX(75%)/46,XX(25%) by conventional cytogenetic analysis. Trisomy for chromosomes, 9, 11, and 12 are recurring abnormalities that have been observed in lymphomas associated with an immunocompromised state. Clonal or nonclonal abnormalities were observed in 8 of 11 tumors derived from 3 donors whose peripheral lymphocytes induced a high incidence of tumors in mice with severe combined immunodeficiency disease compared with a clonal abnormality and 2 nonclonal abnormal cells in 2 of 5 tumors derived from 3 donors whose lymphocytes induced an intermediate to low incidence. These observations suggest an association between a higher incidence of karyotypically abnormal cells in lymphomas and the increased tumorigenic potential of the lymphocytes that induced these tumors.

1 This study was supported by NIH Grants CA 42557 (J. D. R.) and AI 24526, AI 22871, and AI 29182 (D. E. M.). M. M. L. is a Scholar of the Leukemia Society of America, and J. A. is a Fellow of the Leukemia Society of America.

2 To whom requests for reprints should be addressed, at Section of Hematology/Oncology, University of Chicago Medical Center, 5841 South Maryland Avenue, MC2115, Chicago, IL 60637-1470.

Received 2/ 4/92. Accepted 6/24/92.







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 Meeting Abstracts Online
Copyright © 1992 by the American Association for Cancer Research.