Dorit Gurfel

Generation of a monoclonal anti-GP70 antibody and characterization of its reactivity with various human cell lines and cells from leukemia-lymphoma patients

Monoclonal anti GP-70 antibodies (BI) were generated in mice and used for screening of various malignant and non-malignant cell lines. The reactivity of these monoclonal antibodies was compared with that obtained with the polyclonal anti GP-70 antibody described in earlier studies [1-3]. The results indicated complete similarity in reactivity of both of the antibodies used. Furthermore, the reactivity of BI antibodies with cell samples obtained from a variety of leukemia and lymphoma patients and with peripheral blood samples from healthy blood donors was also very similar to the pattern of specificity described in earlier reports for the polyclonal preparation. From these studies we conclude that the monoclonal antibodies can substitute the polyclonal anti GP-70 antibodies in the diagnosis and subtyping of B-type leukemias and lymphomas.

Surface Morphology of Leukemic Cells as seen by Scanning Electron Microscopy

During the past few years scanning electron microscopy (SEM) has been used to study the surface morphology of leukemic cells [1–7]. Despite some overlap of surface features and controversy relating to the recognition of B- and T-lymphocytes [2, 3, 7–9] it has become evident that it is frequently possible to distinguish lymphoid and nonlymphoid cells on the basis of their surface architecture using SEM [ 1, 3, 10]. Initial controversies relating to lymphocyte surface morphology have been settled and attributed in part to faulty preparatory techniques [8] and to unnecessary comparisons of lymphocytes concentrated from different sources [11].

Involvement of HLA Antigens, Interleukin 2 Receptor and B-Cell Growth Factor in Interferon Action in Hairy Cell Leukemia

Little is known about the mechanism(s) by which alpha-interferon (aIFN), when used as a biotherapeutic agent, suppresses the malignant cells and restores the normal phenotype of cells in patients with hairy cell leukemia (HCL). In previous studies using scanning electron microscopy (SEM) we found that alFN induced unique membrane alterations in target hairy cells in vitro. In addition, aIFN was shown to enhance the expression of HLA class II antigens on HCL cells, to induce the production of new proteins in such cells, and to lower the high levels of soluble IL-2 receptors in the serum of HCL patients. In the light of these results, and the fact that restoration of natural killer cell activity occurs in aIFN-treated patients well after the hematologic profile begins to improve, our studies have focused on the hypothesis that IFNs act directly on the target malignant cells, leading to the elimination of these cells either by inhibiting the proliferation of the malignant cells and/or triggering changes in the differentiation status of the malignant cells that lead to suppression (cytoconversion) of the malignant phenotype. We review the current hypotheses regarding alFN action on leukemic cells, with special reference to its potential antagonism with BCGF.

Blastic Transformation of Chronic Granulocytic Leukemia and other Myeloproliferative Disorders

Myeloproliferative disorders such as polycythemia vera (PV) and agnogenic myeloid metaplasia (AMM) with myelofibrosis (MF) progress to acute leukemia in about 30% of cases [1–3]. However, careful cytochemical, surface marker, and ultra-structural studies have not been performed in all these cases [4].

Immuno-Scanning Electron Microscopy of Human Leukemic Cells

During recent years normal, leukemic, and transformed leukocytes have been studied by means of scanning electron microscopy (SEM) [1–3]. Under the SEM different cell types display relatively consistent surface features and despite some overlap, cell types can be recognized on the basis of their surface topography. While SEM is useful in confirming the diagnosis of the cell type in lymphoid and nonlymphoid leukemias, it does not appear to contribute much in unclassified or undifferentiated leukemia or in the distinction of subtypes of acute lymphoblastic leukemia (ALL) [3,4].