P53 protein expression in human leukemia and lymphoma cells.
The purpose of this study was to determine the value of p53 protein overexpression in human leukemia and lymphoma cells. We examined PB and/or BM samples on a series of 111 patients with immunophenotypically defined hematological malignancies at diagnosis, in remission and in relapsed disease comparing to 20 control samples of healthy individuals. p53 protein has been studied by flow cytometry using three monoclonal antibodies specific for epitopes on N-terminus (Bp53-12, DO-1) and central region (DO-11) of p53 protein. Our findigs showed, that p53 expression may contribute to phenotype of leukemic cells and that overexpression of this protein is often associated with progression of disease. All samples of early B-ALL patients and samples of patients with immunophenotypically defined T- cell disorders examined at diagnosis of disease were p53 positive. Eleven of 19 patient samples from AML at diagnosis showed also increased expression of p53 protein. The cells of all patients who responded to therapy with complete immunophenotypically defined remission were p53 negative. Relapsed T-, B- ALL and AML develop p53 alteration. We reported positive p53 expression in cells of patients with advanced stages of CLL in comparison to them with initial stage of disease at examination. As well as in the group of B- cell lymphomas only samples of patients with generalized FCC lymphoma at diagnosis were p53 positive. We detected p53 positive cells in immunologically defined myeloid blast crisis of CML opposite to p53 negativity in chronic phase of disease. The finding of p53 positive BM cells without immunophenotypic blast markers in two of followed cases documented the contributing value of p53 detection in their characterization. On the basis of above findings we conclude, that cytofluorometric determination of p53 expression may contribute to the better definition of leukemic phenotype. Loss of the normal p53 function may be important in the genesis of some leukemias. Elucidation of the mechanisms of p53 inactivation needs some more study.
Koníková
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Cancer Research Institute, Slovak Academy of Sciences, Bratislava, Slovak Republic. exonneo@savba.sk
Kusenda
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D000208:Acute Disease; D000911:Antibodies, Monoclonal / Q000276:immunology; D001854:Bone Marrow Cells / Q000473:pathology; D005434:Flow Cytometry; D006801:Humans; D016130:Immunophenotyping; D007938:Leukemia / Q000097:blood / Q000175:diagnosis / Q000378:metabolism*; D015448:Leukemia, B-Cell / Q000175:diagnosis / Q000378:metabolism; D007943:Leukemia, Hairy Cell / Q000175:diagnosis / Q000378:metabolism; D015451:Leukemia, Lymphocytic, Chronic, B-Cell / Q000175:diagnosis / Q000378:metabolism; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000175:diagnosis / Q000378:metabolism; D007951:Leukemia, Myeloid / Q000175:diagnosis / Q000378:metabolism; D015458:Leukemia, T-Cell / Q000175:diagnosis / Q000378:metabolism; D016393:Lymphoma, B-Cell / Q000097:blood / Q000175:diagnosis / Q000378:metabolism*; D009364:Neoplasm Recurrence, Local; D010265:Paraproteinemias / Q000175:diagnosis / Q000378:metabolism; D014407:Tumor Cells, Cultured; D016159:Tumor Suppressor Protein p53 / Q000276:immunology / Q000378:metabolism*
D000911:Antibodies, Monoclonal; D016159:Tumor Suppressor Protein p53