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S M Hsu

Publications and source records attributed to S M Hsu.

At least 73 records · Page 4Linked to original sources
PubMed1992

Correlation of c-fos/c-jun expression with histiocytic differentiation in Hodgkin's Reed-Sternberg cells. Examination in HDLM-1 subclones with spontaneous differentiation.

The c-fos proto-oncogene, which is the normal homolog of the transforming gene carried by murine osteogenic sarcoma viruses, interacts with the protein product of another proto-oncogene, c-jun, to form a heterodimer that can recognize and bind to a specific sequence of nucleotides in the DNA. The expression of c-fos and c-jun is linked to the proliferation of certain cells and the differentiation of others, including those of monomyelocyte lineage. The authors used two cultured Hodgkin's Reed-Sternberg (H-RS) cell lines, KM-H2 and HDLM-1, and their single-cell clones to study the correlation of c-fos/c-jun expression with cell differentiation in H-RS cells. Within 48 hours after induction with phorbol ester (TPA), both parent lines exhibited markedly increased expression of c-fos/c-jun. The expression returned to the preinduction level after 96 hours, however, and the cells retained their differentiated status. The transitory increase in c-fos/c-jun expression suggests that binding of these proteins to a specific promoter in the nucleus triggers a cascade of events that result in cell differentiation. Expression of these proteins may not be required for the cells to maintain their differentiation. The authors selected three groups of sublines of HDLM-1 cells based on their degree of spontaneous cytologic differentiation. The first group, without obvious differentiation, showed a c-fos/c-jun expression pattern similar to that of the parent line. The second group, with moderate differentiation, had a high degree of expression, which decreased on treatment with TPA. The third group, which had morphologic features resembling those of histiocytes, expressed minimal amounts of c-fos/c-jun, irrespective of TPA treatment. These findings provide further evidence that c-fos/c-jun expression is related to differentiation of H-RS cells, and that these proteins are not byproducts of TPA induction. Expression of c-fos/c-jun also was noted in a subpopulation of H-RS cells in tissues; and this expression also was enhanced when these cells were treated with TPA in culture. These findings indicate that H-RS cells can differentiate to become mature-appearing cells in tissues.

Adult↗
PubMed1991

Differentiation-associated expression of prostaglandin H and thromboxane A synthases in monocytoid leukemia cell lines.

To elucidate the differentiation-associated expression of enzymes catalyzing arachidonic acid metabolism, we measured arachidonate metabolites by reverse-phase high pressure liquid chromatography in monocytoid leukemia (ML-1, THP-1, and U937) and myeloid leukemia (KG-1) cell lines. Undifferentiated ML-1 or THP-1 cells produced trace amounts of eicosanoids via the cyclooxygenase (COX) and lipoxygenase (LOX) pathways. Upon differentiation induced by phorbol ester (phorbol 12-myristate 13-acetate [PMA]), metabolites via the COX pathway were increased by 100-fold in ML-1 and THP-1 cells, while the LOX products remained barely detectable. All the COX metabolites were elevated, but thromboxane A2 (TXA2) formation was threefold higher in ML-1 cells than in THP-1 cells. Similar time-related increases in COX metabolites were observed in THP-1 cells induced to differentiate with retinoic acid. Undifferentiated U937 cells were capable of generating a much higher quantity of COX products than ML-1 or THP-1 cells, but, upon PMA-induced differentiation, COX products were increased by only two-fold to threefold over the undifferentiated cells and the total COX products in differentiated U937 cells were only one-seventh of those produced by differentiated ML-1 or THP-1 cells. KG-1 cells had an entirely different metabolic profile. They produced a large quantity of a metabolite coeluted with prostaglandin D2, and PMA had no effect on inducing changes in arachidonic acid (AA) metabolism. Increased COX metabolite formation in differentiated THP-1 and ML-1 cells was due to an enhanced level of prostaglandin H synthase enzyme mass, as measured by Western blot analysis. The TXA synthase activity was also increased by approximately 100-fold in PMA-induced ML-1 cells and 10-fold in THP-1 cells. These findings indicate that increased expression of prostaglandin H and TXA synthase enzymes is a feature of differentiated monocytoid leukemia cell lines.

Arachidonic Acid↗
PubMed1991

Two cell lines with epithelial cell-like characteristics established from malignant fibrous histiocytomas.

Two malignant fibrous histiocytoma (MFH) cell lines were established: one from a storiform-pleomorph subtype and the other from a myxoid one (codes, MFH-3 and MFH-4). Light microscopic examination revealed large rounded cells, growing mostly separately, in both cell lines. Their ultrastructure was different in various aspects. The MFH-3 cells showed abundant lysosomal activity, a well-developed Golgi apparatus, and a few desmosome-like cell contacts. The MFH-4 cells had a well-developed rough endoplasmic reticulum, delicate bundles of tonofilaments, the formation of pseudoacini, and the presence of small completely developed desmosomes. Based on immunostaining and immunoblotting assays of cultured cells, both cell lines expressed immunoreactivity for vimentin; cytokeratins 7, 8, and 18; desmin; and laminin, but they lacked reactivity for cytokeratins 10 and 19, neurofilament, alpha-smooth muscle actin, S-100 protein, collagen type IV, carcinoembryonic antigen, and antigens specific for macrophages. Fibronectin and, to a variable extent, glial fibrillary acid protein and epithelial membrane antigen (EMA) were detectable in MFH-3 cells only. Furthermore, a 60-kilodalton band was present in both cell lines which was reactive for cytokeratins 8 and 18. The MFH-3 cells had the capacity to grow as xenografts with a carcinoma-like pattern. The cells retained their immunoreactivity for vimentin and cytokeratin 8 and showed the presence of desmosomes. Several of these immunophenotypic features also were noticed in established sarcoma cell lines and in short-term cultures of fibroblasts, smooth muscle cells, and endothelial cells. However, experimental data on the two MFH cell lines show that the MFH cell line may express some immunophenotypic and ultrastructural features considered to be specific for epithelial cells. The MFH cells may originate from multipotential mesenchymal cells with a capacity to differentiate to fibroblast-like cells, and less frequently, to epithelial cells, smooth muscle cells, and Schwannian cells. Such a differentiation became evident when these cells were adapted to culture conditions or grew in nude mice.

Aged↗
PubMed1991

Lymphomas of true histiocytic origin. Expression of different phenotypes in so-called true histiocytic lymphoma and malignant histiocytosis.

The authors determined the phenotypes of neoplastic cells in true histiocytic lymphoma and malignant histiocytosis by using a large panel of monoclonal antibodies and enzyme histochemistry procedures. Although the phenotypes overlapped slightly, the authors noted a distinct pattern in these tumors. The tumor cells of malignant histiocytosis generally expressed the monocyte markers CD11b, CD11c, CD14, and CD45, especially after induction with phorbol ester. In contrast, the tumor cells of true histiocytic lymphoma exhibited a marker expression very similar to that of Reed-Sternberg cells in Hodgkin's disease. These cells expressed markers CD30, 2H9, and 1A2, but rarely expressed CD11b, CD11c, CD14, or CD45. Regardless of their cytologic features, the tumor cells from both types of histiocytic lymphoma exhibited diffuse nonspecific esterase and acid phosphatase activities, and they expressed histiocyte markers CD15, CD68, LN5, 1E9, and M387 to varying degrees. The tumor cells from both lymphomas did not exhibit T- or B-cell markers, T-cell receptor or immunoglobulin gene rearrangements, or gene translation products, even when they were induced with phorbol ester. The phenotypic expression in these two histiocytic malignancies suggests that they are derived from different types of histiocytes, or from histiocytes in different stages of maturation or differentiation, or from histiocytes that have distinct mechanisms of tumorigenic transformation. The expression of circulating monocyte markers in malignant histiocytosis suggests that this tumor originates in monocytes or free histiocytes, whereas the phenotype of true histiocytic lymphoma is compatible with an origin in fixed histiocytes, which generally are devoid of the monocyte markers CD11b and CD14.

Adolescent↗
PubMed1991

Expression of macrophage colony-stimulating factor (M-CSF) in two Hodgkin's Reed-Sternberg (H-RS) cell lines, HDLM-1 and KM-H2, and in H-RS cells in tissues.

The authors studied the production of macrophage colony-stimulating factor (M-CSF) and the expression of its receptor (c-fms) in two Hodgkin's Reed-Sternberg (H-RS) cell lines, HDLM-1 and KM-H2 and in H-RS cells in tissues. We found that both types of H-RS cell can produce M-CSF, as was confirmed by the presence of M-CSF mRNA and protein in the cells and by the presence of macrophage colony-stimulating activity in conditioned medium. M-CSF was also expressed by H-RS cells in lymph nodes from patients with Hodgkin's disease. In cultures, KM-H2 cells appeared to produce a lesser amount of M-CSF than did HDLM-1 cells, as indicated by weaker staining with anti-M-CSF in the former cells. In KM-H2 cells, most of the M-CSF was located in the cytoplasm, and in HDLM-1 cells, in the Golgi apparatus and/or on the cell membrane. The two types of cultured H-RS cell either did not express c-fms at all, or expressed it only extremely weakly, perhaps because of the loss of dependence on specific growth factors during culture. The production of M-CSF by H-RS cells may contribute to the clinical and pathologic changes seen in patients with Hodgkin's disease, such as the increased abundance of histiocytes in tissues infiltrated by H-RS cells. Alternatively, the expression of both M-CSF and c-fms could confer a growth advantage to some H-RS cells in an autocrine fashion.

Animals↗
PubMed1990

Antitumor effects of ricin A chain immunotoxins prepared from intact antibodies and Fab' fragments on solid human Hodgkin's disease tumors in mice.

Three monoclonal antibodies which strongly bind to Hodgkin and Reed-Sternberg cells and two corresponding Fab' fragments were linked to deglycosylated ricin A chain (dg A) to evaluate their potential as immunotoxins for the treatment of Hodgkin's disease. Two of the antibodies, Ber-H2 and HRS-3, were shown to bind to the same epitope on the CD30 antigen, whereas the third antibody, IRac, bound to a different antigen. None of the antibodies significantly cross-reacted with normal human tissues as judged by indirect immunofluorescence and immunoperoxidase analyses on frozen sections from 28 normal tissues. All three antibodies formed potent and specific immunotoxins. They inhibited protein synthesis of the L540 Hodgkin's disease cell line in vitro by 50% at concentrations of 1 x 10(-11) M for IRac.dgA, 9 x 10(-11) M for HRS-3.dgA, and 2 x 10(-10) M for Ber-H2.dgA. HRS-3 Fab' and IRac Fab' immunotoxins were 7.8- and 60-fold less cytotoxic, respectively, than their intact counterparts in vitro. In vivo, a single i.v. injection of a dose of Ber-H2.dgA, HRS-3.dgA, or IRac.dgA corresponding to 40% of the LD50 induced lasting complete remissions in 38, 44, and 50%, respectively, of mice with solid s.c. L540 tumors of 60 to 80 mm3 size (0.5-cm diameter). At equivalent dosage (40% of the LD50), the HRS-3 Fab'.dgA and the IRac Fab'.dgA both induced lasting complete remissions in 25% of the mice, although the HRS-3 Fab'.dgA was significantly superior to IRac Fab'.dgA at retarding tumor growth in the remaining animals. The effectiveness of the immunotoxins depended on the size of the tumor at the time of injection, since IRac.dgA treatment induced complete remissions in 100% of mice with small tumors (10 to 20 mm3, approximately 0.3 cm in diameter) but only 13% of mice with larger tumors of 400 to 600 mm3 (approximately 1 cm in diameter). Tumors which regrew after IRac.dgA treatment mainly consisted of antigen-deficient mutants having reduced sensitivity to IRac.dgA but normal sensitivity to HRS-3.dgA. It is concluded that HRS-3.dgA, HRS-3 Fab'.dgA, and IRac.dgA are candidates for the treatment of Hodgkin's disease in humans.

Animals↗
PubMed1990

Identification of an Mr 70,000 antigen associated with Reed-Sternberg cells and interdigitating reticulum cells.

We obtained a monoclonal antibody that has restricted reactivity with tumor cells [Hodgkin's mononuclear cells and Reed-Sternberg (H-RS) cells] in Hodgkin's disease by immunizing mice with 12-O-tetradecanoyl phorbol-13-acetate-induced H-RS cells. The antibody, anti-IRac, reacted with H-RS cells in 8 of 20 patients who had Hodgkin's disease, as well as with interdigitating reticulum cells in dermatopathic lymph nodes and with cells of three H-RS cell lines, HDLM-1, L428, and KM-H2. The antigen IRac is a protein of molecular weight 70,000 which we found to have the following properties. (a) After 12-O-tetradecanoyl phorbol-13-acetate induction, the expression of IRac was decreased slightly in HDLM and L428 cells but increased in KM-H2. This is in contrast to a rapid decrease in the expression of two other H-RS-cell-associated antigens, CD30 and 2H9, in all 12-O-tetradecanoyl phorbol-13-acetate-treated H-RS cells. Thus, IRac may be associated with H-RS cells at advanced stages of differentiation, and its expression may not be attributable solely to cellular proliferation. (b) IRac was detected rarely in normal or in antigen- or mitogen-activated lymphocytes but was observed frequently in virus-transformed B- or T-lymphocytes. These findings were similar to those with CD30 and 2H9, indicating that the expression of all three of these antigens is probably under a similar regulatory control. (c) IRac was absent from cells in most non-Hodgkin's lymphomas; its expression could not be modulated by treatment of cells with anti-IRac. We conclude that use of IRac could facilitate the diagnosis of Hodgkin's disease and that it may be suitable for immunotherapy or immunoimaging. The expression of IRac in both H-RS cells and interdigitating reticulum cells, along with earlier evidence, indicates that H-RS cells have antigenic and functional similarities to interdigitating reticulum cells or to cells of interdigitating reticulum cell/histiocyte lineage.

Animals↗
PubMed1990

Immunohistochemistry.

The use of the ABC technique, in which an avidin-biotin interaction is used for immunohistochemical studies, is a simple and straightforward procedure. All required reagents are commercially available. The main advantages of this technique are its sensitivity, specificity, and flexibility. It is crucial for the success of this staining procedure that the antibodies, the type of tissues, and the fixatives that are used be selected properly. The method can easily be adapted for electron microscopy, flow cytometry, in situ hybridization, Western blotting, and ELISA.

Animals↗
PubMed1990

Characterization of a porcine CD1-specific mAb that distinguishes CD4/CD8 double-positive thymic from peripheral T lymphocytes.

Porcine peripheral T-cells bear CD4 and CD8 cell surface antigens that distinguish helper from cytotoxic T-cells. In distinction from what has been found in other species, a large percentage of peripheral T-cells simultaneously express both CD4 and CD8. Monoclonal antibody 76-7-4 was found to stain all cortical and 7 +/- 3% of medullary thymocytes, Ia+ epidermal cells (i.e. Langerhans cells), no peripheral T-cells and 50% of peripheral B-cells. The antigen detected appears analogous to human CD1. All cortical thymocytes were also stained with CD4 and CD8 mAb. Since 76-7-4 did not stain peripheral T-cells, we conclude that CD4/CD8 dual-expressing peripheral T-cells are not simply immature thymic emigrants.

Animals↗
PubMed1990

Localization and growth hormone (GH)-releasing activity of rat testicular GH-releasing hormone-like peptide.

The testis contains many peptides originally described as originating in the central nervous system. The physiological function of these factors in the testis is generally unknown. We previously reported that the rat testis contains both a peptide with GH-releasing hormone-like immunoactivity (tGHRH-LI) and a mRNA species that cross-hybridizes with a hypothalamic cDNA for rat GHRH (rGHRH). The current study was designed to further characterize tGHRH-LI by determining its location within rat testis, and to evaluate whether tGHRH-LI and hypothalamic GHRH share similar biological and electrophoretic properties. Partially purified tGHRH is capable of stimulating GH secretion from cultured anterior pituitary cells in a dose-dependent manner. Testicular GHRH and rGHRH have different HPLC retention times and significantly different electrophoretic properties by Western gel analysis. The estimated size of tGHRH-LI is approximately 3.7 times that of synthetic rGHRH. Using immunohistochemistry, tGHRH-LI is localized to mature sperm forms in rat testis. We conclude that rat tGHRH-LI and rGHRH share some structural and functional properties and are probably related peptides. However, the difference in electrophoretic mobility and HPLC retention time indicates that they are not identical. The presence of tGHRH-LI in rat sperm, within the confines of the blood-testis barrier, which is generally impermeable to peptides, leads us to speculate that tGHRH serves a paracrine or autocrine role in testicular physiology.

Animals↗
PubMed1990

Lack of effect of colony-stimulating factors, interleukins, interferons, and tumor necrosis factor on the growth and differentiation of cultured Reed-Sternberg cells. Comparison with effects of phorbol ester and retinoic acid.

The neoplastic Hodgkin's Reed-Sternberg (H-RS) cells in Hodgkin's disease are surrounded in vivo by abundant reactive cells, the function of which may be attributed in part to their elaboration of various cytokines. Thus, a study of the interaction of H-RS cells with exogenous cytokines may provide information as to the mechanism of the clinical and histopathologic changes observed in Hodgkin's disease. This study examined the effect of various cytokines, and of phorbol ester (TPA) and retinoic acid, on the differentiation and proliferation of cultured H-RS cells (cell lines HDLM-1 and KM-H2). In addition, it was determined whether these cells were able to secrete cytokines after being treated with exogenous cytokines. The cytokines used included various types of interleukins (1, 2, and 3), colony-stimulating factors (GM, G, and M), interferons (alpha, beta, and gamma), and tumor necrosis factor (alpha). It was found that these cytokines, used alone or in combination, were not effective in modulating the proliferation and differentiation of cells, or the production of cytokines, in cultured H-RS cells. In contrast, this study revealed that retinoic acid can potentiate TPA-induced growth inhibition in cultured H-RS cells. Retinoic acid, when used alone, exhibited a minimal effect on cell differentiation. No synergistic effects of cytokines and retinoic acid on H-RS cells were observed. The failure of cultured H-RS cells to respond to exogenous cytokines suggests that, during the course of neoplastic transformation, of progression of disease, or of establishment of the cells in culture, H-RS cells lose their dependence on cytokines, although they retain the capacity to produce various cytokines.

Aged↗
PubMed1990

Expression of p55 (Tac) interleukin-2 receptor (IL-2R), but not p75 IL-2R, in cultured H-RS cells and H-RS cells in tissues.

The authors studied the secretion of interleukin-2 (IL-2), the expression of interleukin-2 receptors (IL-2R; p55/Tac and p75), and the response to exogenous IL-2 by cultured Hodgkin's Reed-Sternberg cells (cell lines HDLM-1, HDLM-1d, and KM-H2) and T cells (H9, HuT78, HuT102, MOLT-4, and MT-2). All of these cells did not produce IL-2 or produced it in undetectable amounts, and their growth was not affected by the addition of anti-IL-2 or anti-IL-2R antibodies. This indicates that H-RS cells in long-term culture, as well as T cells, can grow independently of IL-2. The three H-RS cell lines, as well as two of the T-cell lines (HuT102 and MT-2), expressed Tac, whereas the other three T-cell lines were Tac negative. Expression of p75 was noted in the two Tac-positive T-cell lines, but not in cultured H-RS cells. The expression of Tac and p75 in HuT102 and MT-2 cells correlated well with their capacity to proliferate on treatment with exogenous IL-2. On IL-2 treatment, nucleic-acid uptake in Tac/p75-positive T cells increased approximately four- to sixfold, whereas the Tac/p75-negative T cells did not show increased proliferation. Unlike the T cells, the Tac-positive H-RS cells did not respond to IL-2. The lack of a proliferative response to IL-2 appears to be related to the absence of p75 in H-RS cells. A similar pattern (Tac positivity and p75 negativity) was noted in H-RS cells in lymph nodes involved by Hodgkin's disease. Thus the exogenous IL-2 released by surrounding T lymphocytes may not cause the proliferative activity of H-RS cells because of the lack of high-affinity IL-2 receptors in the latter cells. In contrast to H-RS cells in culture, H-RS cells in tissues were stained by a specific anti-IL-2 monoclonal antibody. This indicates that the expression of IL-2 or an IL-2-like substance by H-RS cells in tissues may be responsible, in part, for the great increase in the number of reactive T lymphocytes in tissues involved by Hodgkin's disease.

Blotting, Northern↗
PubMed1990

Lymphocyte functional antigens stabilize agglutination between Reed-Sternberg cells and T cells, but are not responsible for homotypic binding of Hodgkin's Reed-Sternberg cells.

The neoplastic (Hodgkin's Reed-Sternberg [H-RS]) cells in Hodgkin's disease (HD) are known for their unique capacity to form rosettes with unprimed T cells. Recently, a family of leukocyte-adherence molecules (LFA-1 and LFA-2) has been identified on T lymphocytes. The molecules bind to intercellular-adhesion molecules (ICAMs) and to LFA-3, respectively, which are associated with antigen-presenting cells. In this study, the authors examined whether these molecules are responsible for the homotypic and heterotypic agglutination that occurs in the cultured H-RS cells HDLM-1, HDLM-1d, and KM-H2. Despite their similar expressions of LFA-3 and ICAM-1, the different H-RS cells tested showed different growth patterns in culture. HDLM-1 cells grew singly, whereas HDLM-1d and KM-H2 cells grew in clumps. The HDLM-1 cells formed clumps when mixed with peripheral-blood T lymphocytes, cells of two lymphoblastic T-cell lines (MOLT-3 and MOLT-4), and cells of two monocyte lines (ML-1 and U-937). The addition of anti-LFA and ICAM-1 antibodies to cultures did not result in disassembly of the homotypic clusters of HDLM-1d or KM-H2 cells and it did not cause any significant changes in the size of heterotypic clusters or in the timing of cluster formation of HDLM-1 cells with other types of cells. In all studies, the cell clusters formed during homotypic and heterotypic aggregation were disassembled only minimally by cell shearing with pipetting. The disaggregation by pipetting was slightly more prominent in the presence of antibodies than was that of control cultures. However, in no case did the use of monoclonal antibodies (MAbs) and cell shearing cause complete disaggregation of homotypic and heterotypic clusters. The result seems to suggest that binding between H-RS cells and T cells and between H-RS cells and monocytes is not mediated primarily by LFAs and ICAMs, but that the binding may be strengthened in the presence of these molecules.

Adult↗
PubMed1990

Cultured Reed-Sternberg cells HDLM-1 and KM-H2 can be induced to become histiocytelike cells. H-RS cells are not derived from lymphocytes.

Two Hodgkin's Reed-Sternberg cell (H-RS) lines, HDLM-1 and KM-H2, have phenotypes and functional properties very similar to those of H-RS cells in tissues. These two types of cells were induced to differentiate with a combination of phorbol ester, retinoic acid, and extracellular matrix. The induced cells displayed the morphology of histiocytes or histiocytelike cells, with a small, round or oval, eccentric nucleus and abundant cytoplasm. In ultrastructural studies, many cytoplasmic projections and rugae were observed. These induced cells exhibited abundant cytoplasmic lysosomal enzymes, such as esterase, acid phosphatase, alpha 1-antitrypsin, or lysozyme. The histiocytic nature of these induced cells was further confirmed by the increased expression of many monocyte/histiocyte markers, including CD11b, CD11c, CD13, CD14, CD15, CD33, CD68, Mac387, and 1E9. In functional tests, the induced cells were shown to produce interleukin-1, tumor necrosis factor, macrophage colony-stimulating factor, and/or prostaglandin E2. Phagocytosis was detected in less than 5% to 10% of the cells when Candida albicans was added to cultures. The results strongly suggest that H-RS cells are related to cells of histiocyte lineage.

Adult↗
PubMed1990

Trial of intralesional interferon alfa in the treatment of alopecia areata.

Eleven patients with alopecia areata, ranging from patchy disease to alopecia universalis, were treated with intralesional interferon alfa-2 on a selected area of alopecia. Follow-up at 3 months revealed local terminal hair growth in one patient. At 12 months, variable disease activity was seen. Regional lymphadenopathy, a new finding with interferon, was seen in four patients during the treatment. Immunohistochemical studies showed some changes in the inflammatory infiltrates and in HLA-DR expression that may be related to the interferon or to the dynamics of the inflammatory infiltrate in alopecia areata. Interferon, at the dosage and treatment schedule used in our trial, had no significant effect on alopecia areata.

Adult↗
PubMed1989

Coexistence of myelodysplastic syndrome and untreated chronic lymphocytic leukemia with development of acute myeloid leukemia immediately after treatment of chronic lymphocytic leukemia.

A 72-year-old man originally seen for anemia and thrombocytopenia was determined to have chronic lymphocytic leukemia (CLL). Bone marrow examination at the time of CLL diagnosis revealed a small but significant population of atypical blasts. Cytogenetic analysis of the bone marrow aspirate disclosed chromosomal abnormalities (-7, +8) suggestive of a myelodysplastic syndrome. Shortly after treatment of the CLL, there was proliferation of the previously noted blast population, which cytochemical studies demonstrated to be of the myeloid series thus indicating acute myeloid leukemia superimposed on CLL. This report presents microscopic, cytogenetic, immunophenotypic, and cytochemical evidence to document the evolution of acute myeloid leukemia in the bone marrow of a patient with CLL after one course of chemotherapy.

Aged↗