Cancer Research Translational Cancer Medicine 2008: Cancer Clinical Trials and Personalized Medicine  Susan G. Komen for the Cure-AACR Outstanding Investigator Award for Breast Cancer Research
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

[Cancer Research 49, 6989-6996, December 15, 1989]
© 1989 American Association for Cancer Research

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Petrini, M.
Right arrow Articles by Peschle, C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Petrini, M.
Right arrow Articles by Peschle, C.

Constitutive Expression and Abnormal Glycosylation of Transferrin Receptor in Acute T-Cell Leukemia1

M. Petrini, E. Pelosi-Testa, N. M. Sposi, G. Mastroberardino, A. Camagna, L. Bottero, F. Mavilio, U. Testa2 and C. Peschle2

Department of Hematology-Oncology, Istituto Superiore di Sanita, Viale Regina Elena, 299 [M. P., E. P-T., N. M. S., L. B., F. M., U. T., C. P.], Istituto Patologia Medica (V), University "La Sapienza" [G. M.], and the Clinica Medica II, University "La Sapienza" [A. C.] 00161 Rome, Italy

The expression of transferrin receptors (TrfRs) was investigated in acute T-cell leukemia (T-ALL) blasts at the molecular, biochemical, immunological, and functional level. TrFRs, although not detected on quiescent T-cells from normal adults, are constitutively expressed at high level on the blasts from all T-ALL patients and bind normally to transferrin. Their number is modulated by the intracellular iron level, but is independent of exogenous interleukin 2. They also exhibit immunological and biochemical abnormalities, in that: (a) they react preferentially with monoclonal antibodies (MAb) that recognize ligand-binding domains of TrfR (42/6 and 43/31), as compared to MAbs (B3/25, OKT9) that interact with the nonligand binding domains; (b) they have a reduced molecular weight, as compared to TrfR on normal thymocytes and activated T-lymphocytes: this phenomenon is apparently related to a defective glycosylation. It is noteworthy that expression of TrfR was not observed in a large series of other types of acute leukemias, i.e., pre-B, B, and myeloid leukemias, excluding erythroleukemias.

The constitutive, high level expression of TrfRs on T-ALL blasts may play a key role in the stepwise progression of this malignancy and particularly provide a proliferative advantage to T-ALL blasts as compared to normal T-lymphocytes. Furthermore, indirect evidence suggests that the glycosylation defect of TrfR on T-ALL blasts contributes to their tumorigenic capacity.

1 This study was supported by grants from CNR, "Progetto Finalizzato Oncologia" to C. P. (No. 87.01568.44) and the "Programma Italia-USA sulla Terapia dei Tumori," Ministry of Health, Rome, Italy.

2 To whom reprint requests should be addressed, at Department of Hematology-Oncology, Viale Regina Elena 299, 00161 Rome, Italy.

Received 4/18/89. Revised 9/11/89. Accepted 9/19/89.







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.