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[Cancer Research 39, 1534-1538, May 1, 1979]
© 1979 American Association for Cancer Research

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Correlation of Tumor Cell Kinetic Studies with Surface Marker Results in Childhood Non-Hodgkin's Lymphoma1

Sharon B. Murphy2, Susan L. Melvin and Alvin M. Mauer

St. Jude Children's Research Hospital, Memphis, Tennessee 38101

Tumor cell kinetic observations were made in 40 children with advanced stage, diffuse types of non-Hodgkin's lymphomas (NHL's) in order to characterize the patterns of proliferation present and explain the diversity of clinical behavior exhibited by childhood lymphoproliferative neoplasms. The in vitro [3H]thymidine autoradiographic labeling index (LI) percentage was determined on samples of blood, marrow, effusions, cerebrospinal fluid, and solid tumors. Blasts from 33 of the 40 children also had T- and B-cell surface markers determined. Extensive variability in the LI percentage of tumor cells was related to surface markers, individual patient differences, sample source, and stage of disease progression. The median LI of marrow blasts in the leukemic phase of NHL was 42% (range, 13 to 60%; n = 17). This is significantly higher (p < 0.005) than childhood acute lymphoblastic leukemia cases studied, either at diagnosis or relapse. Study of surface markers from marrow blasts in NHL and acute lymphoblastic leukemia revealed a hierarchical relationship in proliferative activity: B-cells > T-cells > non-T and non-B. The greater LI of B-cell NHL was also shown for samples of cerebrospinal fluid (median, 30%) and for pleural fluid blasts, particularly at relapse (median, 39.5%). We conclude that the intrinsic state of neoplastic lymphoid cell differentiation (B, T, or "null") conditions the growth fraction of lymphoid neoplasia. Conceivably, the clinical and kinetic behavior of childhood lymphoproliferative disease reflects the patterns of growth characteristic of their normal lymphocyte counterparts. Eleven children had tumor cells sampled simultaneously from more than one site, and the results typically differed markedly. Local environmental or systemic factors apparently regulate tumor growth as well.

1 Supported by NIH Grants CA 08480, CA 21765, and CA 15956 and by American Lebanese Syrian Associated Charities. The data were presented in part at the 68th Annual Meeting of the American Association for Cancer Research, Inc. (19).

2 To whom requests for reprints should be addressed, at St. Jude Children's Research Hospital, 332 N. Lauderdale, P.O. Box 318, Memphis, Tenn. 38101.

Received 10/ 2/78. Accepted 1/24/79.







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 © 1979 by the American Association for Cancer Research.