Identification Of Leukemic Cells Research Articles

Expression of JL1 Is an Effective Adjunctive Marker of Leukemia Cutis

Specific differentiation of leukemia cutis (LC) from nonleukemic dermatoses is crucial to ensure proper treatment for the disease. Because of the exceptionally variable histologic features of LC and the frequent nonleukemic dermatoses in leukemia patients, identification of leukemic cells that infiltrate skin lesions is important. Here, we introduce JL1, a novel leukemia-associated surface antigen, which is not expressed in mature human tissue but in cortical thymocytes and small subpopulations of bone marrow hematopoietic precursors. To assess the expression pattern of JL1 in LC and compare it with other commonly used markers. Also, to evaluate the expression of JL1 in other cutaneous lesions that need differential diagnoses. Immunohistochemical staining with anti-JL1 and other commonly used markers for LC was performed on paraffin-embedded skin biopsies from 32 cases of LC with acute lymphoblastic leukemia/lymphoma and acute myelogenous leukemia. Immunohistochemical staining score was evaluated in each case according to the proportion of positive tumor cells found. JL1 staining was also done on 96 reactive or neoplastic cutaneous lesions. JL1 was detected in 7 of 11 acute lymphoblastic leukemia/lymphoma LC (63.6%) and 7 of 21 acute myelogenous leukemia LC (33.3%), with invariably high-staining scores. None of the other cutaneous lesions or normal tissues expressed JL1. The expression pattern of JL1 was not altered in 2 patients with follow-up biopsies. Our finding that JL1 is expressed exclusively and stably by leukemic cells suggests that it can be used as a useful adjunctive marker for initial diagnosis and follow-up biopsy of LC, particularly in cases of scarce infiltrates.

Identification of leukaemic cells in bone marrow and blood samples by a new cytofluorometric assay.

The expression of thymidine kinase--an enzyme of the DNA precursor pathway--is strictly regulated during the normal cellular cycle, but is much higher and permanently expressed in malignant growing cells. We used this fact to detect neoplastic cells in samples freshly taken from leukaemia patients and kept frozen in liquid nitrogen until analysis. Using a new cytofluorometric assay for thymidine kinase in single cells, we were able to identify leukaemic cells in a surplus of normal ones. Our results demonstrate the benefits of this assay for leukaemia diagnosis.

Cell surface antigen expression in human erythroid progenitors: erythroid and megakaryocytic markers.

This review summarizes the changes in cell surface antigen expression during proliferation and differentiation of human erythroid progenitors. The content is based on our experimental data obtained from complement-mediated cytotoxicity assays against hematopoietic progenitors and a combined technique of sequential micromanipulations of paired daughter cells derived from erythroid burst-forming units (BFU-E) and immunostaining with a panel of monoclonal antibodies, as well as from current information. BFU-E has CD34, CD41a (platelet glycoprotein[GP]IIb/IIIa) and CD41b(GPIIb) antigens. Paired daughter cells derived from BFU-E have CD41a, CD41b, CD71 (transferrin receptor) and HLA-DR antigens, but not CD34 or CD33 antigen. The CD36 antigen (thrombospondin receptor or GPIV) is first expressed on the cells after 5 days of culture, in agreement with the report that the anti-CD36 positive fraction contained a greater part of the erythroid colony-forming units (CFU-E). The blood group A antigen is first expressed on cells from aggregates derived from BFU-E after 5 days of culture. Glycophorin A is expressed on cell surface after 7 days of culture when proerythroblasts first appear. Hemoglobin alpha is expressed after 8 days of culture and coincides with the first appearance of basophilic erythroblasts. This review provides useful information on the identification of leukemic cells from poorly differentiated acute leukemias such as early erythroblastic leukemia and acute megakaryoblastic leukemia, and is useful in the understanding of the commitment and differentiation of erythroid and megakaryocytic progenitors in normal hematopoiesis.

Identification of leukemic cells in the cerebrospinal fluid from children with acute lymphoblastic leukemia: advances and dilemmas.

As more children survive acute lymphoblastic leukemia, new challenges face the pediatric oncologist. One is the need for early recognition of subclinical nonsymptomatic disease, or occult meningeal leukemia. By obtaining spinal fluid specimens, one can frequently monitor the central nervous system (CNS) for the presence of residual or recurrent leukemia. Methods for identifying small numbers of lymphoblasts in the spinal fluid have progressed from subjective descriptions of nucleated cells to assignment of objective methods for labeling the cells in question. These more sensitive methods of detection have challenged the "old" definitions of remission. The unequivocal identification of lymphoblasts in the spinal fluid of a child with less than 5 cells/mm3 of fluid is an example of such a dilemma. Does this finding herald overt CNS relapse or hematologic relapse? Does it warrant further, more aggressive treatment beyond giving standard prophylactic CNS therapy? It can be suggested that the finding of even a small number or proportion of leukemic cells in the spinal fluid in a child being given continuation/maintenance therapy has a high probability of being followed by an adverse event (relapse). If this is true, then the definition of CNS leukemia needs refinement and the methods for unequivocally identifying leukemic cells in a spinal fluid sample depend on techniques of cytologic examination beyond routine cytomorphology. Such laboratory methods are now available, but they require more clinical testing and standardization before their sensitivity and specificity in identifying leukemic cells is established.