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Biomedical subjects

Z Estrov

Publications and source records attributed to Z Estrov.

At least 163 records · Page 9Linked to original sources
PubMed1986

Clinical and in vitro antiproliferative properties of recombinant DNA-derived human interferon-alpha 2.

The properties of the recombinant DNA-derived human leukocyte interferon, HuIFN alpha 2, were studied in patients with advanced leukemia or lymphoma. In vitro, HuIFN alpha 2 induced an increased activity of 2-5A synthetase in leukemic and in control cells indicating cellular responsiveness to IFN. HuIFN alpha 2 also produced a dose-responsive decline in marrow leukemia blast progenitor colony growth, and in normal hematopoietic colony formation in vitro, confirming its antiproliferative effect. A course of intravenous therapy given to a lymphoma patient produced a modest decline in peripheral white blood cell (WBC) and neutrophil counts; higher, more frequent doses in a second patient induced a profound drop in WBC's, neutrophils, and platelets. When the leukemia patients were given an intravenous course of HuIFN alpha 2 as a sole agent, blast cytoreduction was seen in peripheral blood in three patients, and in marrow of one patient with acute myeloblastic leukemia (AML). Elevated 2-5A synthetase levels could be detected after therapy. No modulation of leukemic cell markers was seen after in vitro or in vivo treatment with HuIFN alpha 2, implying that the cytoreduction was not linked to blast cell differentiation. These studies suggest that this subtype of recombinant DNA-derived IFN has antileukemic properties, and indicates the possibilities for IFN as an adjunctive form of therapy in leukemia.

2',5'-Oligoadenylate Synthetase↗
PubMed1986

Secretory piece and IgA deficiency in a patient with Waldenstrom's macroglobulinemia.

A case of a patient suffering from Waldenstrom's macroglobulinemia who developed diarrhea and mild steatorrhea is described. Laboratory studies revealed low serum IgA, intestinal secretory IgA deficiency, and small intestine bacterial overgrowth as demonstrated by the C14-cholylglycine breath test. These findings suggest that selective IgA deficiency and secretory component deficiency may be contributing factors in the development of diarrhea in Waldenstrom's macroglobulinemia.

Aged↗
PubMed1986

Induction of differentiation in HL-60 promyelocytic cells: a comparative study in two sublines.

Two variants of HL-60 promyelocytic leukemia cells (HSC, OCI) that were indistinguishable by morphology, cell surface markers, DNA histograms, and by their inability to reduce nitroblue tetrazolium, were induced to differentiate by retinoic acid (RA), 12-O-tetradecanoyl-phorbol-13-acetate (TPA), and by phytohemagglutinin-leucocyte conditioned medium (PHA-LCM). Only OCI cells were induced to differentiate to mature granulocytes by TPA. Both cell lines expressed, however, the monocytic associated cell surface antigen detected by MO1 monoclonal antibody in response to TPA. MO1 expression was detected as early as 32 hours after initiation of differentiation by TPA, whereas partial morphologic changes were apparent only after 72 hours. Induction of differentiation by retinoic acid led to a significant inhibition of colony formation in HSC variant (from 1522 +/- 60 to 523 +/- 20/10(4) cells plated) and in the OCI variant (from 628 +/- 20 to 185 +/- 33 colonies/10(4) cells plated). The addition of PHA-LCM further inhibited colony growth of both RA-induced cell lines (155 +/- 7/10(4) cells plated in HSC, and 59 +/- 4 in OCI). PHA-LCM by itself reduced HL-60 colony numbers in a dose-related manner, and also increased the expression of MO1 on noninduced HSC and OCI cells. These observations suggest that differentiation of HL-60 cells is not necessarily accompanied by concomitant change in morphology, cell surface characteristics, and proliferation potentials, and may be dependent on different degrees of cellular commitment. They also suggest a role for growth factors in the induction to maturation of leukemic cells.

Antibodies, Monoclonal↗
PubMed1986

Characterization of malignant peripheral blood cells of juvenile chronic myelogenous leukemia.

Characterization studies were performed on the malignant peripheral blood cells from three patients with juvenile chronic myelogenous leukemia (JCML) by allowing the cells to increase numerically in liquid cultures. JCML cells proliferated rapidly and excessively in the absence of an added humoral growth factor, whereas control peripheral blood cells declined in number when cultured under identical conditions. Clonality of JCML cells was proven by cytogenetic analysis of the proliferating population. JCML cells were exclusively of monocytic lineage as determined by morphology, staining characteristics, and monoclonal antibody identification of cell-specific surface antigens, but cytochemical and functional studies identified aberrant properties indicating defective differentiation. Striking differences from control cells in ultrastructure and topography were also observed by transmission and scanning electron microscopy. These data provide new information on the cellular origin of JCML and form the basis for further study of leukemic cell biology in this disease.

Child, Preschool↗
PubMed1986

Juvenile chronic myelogenous leukemia: characterization of the disease using cell cultures.

To characterize juvenile chronic myelogenous leukemia (JCML), the proliferative properties of bone marrow (BM) and peripheral blood (PB) cells from nine patients were studied using assays for CFU-C and CFU-GEMM and liquid cultures. All specimens showed two reproducible abnormalities: impaired growth of normal hematopoietic progenitors and excessive proliferation of monocyte-macrophage colonies in the absence of exogenous colony-stimulating activity (CSA). Cytogenetic studies in one patient indicated that the CFU-C were malignant because BM cells at diagnosis and monocyte-macrophage colonies showed an abnormal karyotype, whereas PB lymphocytes did not. In contrast to JCML, PB from six adults with Philadelphia (Ph1) chromosome-positive chronic myelogenous leukemia (Ph1 + CML) yielded CSA-dependent CFU-C colonies which were composed of granulocytes, macrophages, or both, as well as exuberant growth of BFU-E colonies. Co-cultures of JCML BM adherent or nonadherent cells with normal BM resulted in suppression of normal hematopoietic colony formation. Supernatant from JCML adherent cells in liquid culture or plasma from newly diagnosed untreated JCML patients also suppressed control BM colony growth in a dose-dependent manner. These findings confirm that JCML is a malignant disorder of monocytic lineage and suggest that the mechanism of hematopoietic failure in JCML is mediated by an inhibitory monokine secreted by malignant JCML cells.

Bone Marrow Cells↗
PubMed1986

The regulatory role of interleukin 2-responsive T lymphocytes on early and mature erythroid progenitor proliferation.

To analyze the role of T lymphocytes in human erythropoiesis, we evaluated the effect of recombinant interleukin 2 (IL 2) on marrow CFU-E and BFU-E colony formation in vitro. IL 2 resulted in an increase in CFU-E and BFU-E colony numbers in a dose-dependent manner. This increase could be prevented by anti-Tac, a monoclonal antibody to the IL 2 receptor. Moreover, anti-Tac on its own resulted in an overall decrease in colony numbers. Depletion of marrow adherent cells did not alter the effect of either IL 2 or anti-Tac on colony growth. Following the removal of marrow T lymphocytes, CFU-E and BFU-E colony formation proceeded normally; however, the effects of IL 2 and anti-Tac were markedly diminished. Readdition of T lymphocytes to the cultures restored the IL 2 effect. Although T lymphocytes were not themselves essential for in vitro erythropoiesis, our studies suggest that IL 2 and IL 2-responsive T cells can regulate both early and mature stages of erythroid differentiation.

Animals↗
PubMed1985

High incidence of acute myeloid leukemia in SJL/J mice after X-irradiation and corticosteroids.

SJL/J mice which developed a high incidence of spontaneous reticulum cell neoplasms, developed a low rate incidence (20-25%) of myeloid leukemia (ML) after X-irradiation. The possible effect of adrenal steroid imbalance to radiation-induced ML in SJL/J mice was tested. Intact and thymectomized animals were exposed to a single dose of 300 r whole body irradiation and treated with either hydrocortisone acetate, prednisone, metyrapone and adrenocorticotropin as coleukemogenic agents. Hydrocortisone and prednisone exerted a marked coleukemogenic effect, increasing the ML incidence to a similar rate of about 50-70%, at a mean latent period of 300 days. Prominent leukemic infiltration were observed in the bone marrow, spleen, lymph nodes and liver of the leukemic animals. Results of cytological and histological studies, including cytochemistry and ultrastructure, were all consistent with the diagnosis of acute myeloid leukemia (AML). Since AML is the type of human secondary leukemia which appears increasingly in patients treated with alkylating drugs and/or irradiation and corticosteroids for Hodgkin's disease or other neoplastic diseases, the experimental model of AML induced in SJL/J mice could be used for elucidation of mechanisms of leukemogenesis in secondary leukemia.

Adrenal Cortex Hormones↗
PubMed1985

Growth inhibitory effect of gene-cloned interferons on human myeloblast colonies.

The effect on marrow myeloblast colony formation in blood from nine patients with acute myeloid leukemia was studied by using three recombinant-DNA-derived human leukocyte interferons (IFN alpha 2, IFN alpha-A, and IFN alpha-C). In preliminary experiments, a brief exposure of leukemic marrow cells to IFN alpha resulted in a sharp increase in the IFN-induced enzyme 2-5A synthetase, indicating the expression of IFN cell receptors as well as the ability of leukemia cells to respond metabolically. Dose-response studies showed a dose-dependent suppression of myeloblast colony formation in all experiments using concentrations of 10(2)-10(5) U/ml of the three IFN subtypes. In self-renewal assays derived from the primary cultures that initially contained IFN alpha 2, a "carryover" antiproliferative effect was observed with a dose-dependent decline in secondary growth. In comparison studies of IFN alpha-A and IFN alpha-C, the suppressive effect on primary myeloblast growth was much more pronounced with IFN alpha-C at concentrations of 10(3) U/ml and higher; in self-renewal assays, the antiproliferative effect of IFN alpha-C on secondary growth was no longer observed, whereas that of IFN alpha-A persisted. These three subtypes of gene-cloned IFN have antileukemic properties in vitro, with differences in degree of suppression of primary myeloblast growth and of self-renewal.

2',5'-Oligoadenylate Synthetase↗
PubMed1984

Candidemia and sternal Candida albicans osteomyelitis in a patient with chronic lymphatic leukemia.

Sternal osteomyelitis caused by Candida albicans without previous surgery or trauma occurred in a patient with chronic lymphatic leukemia and recurrent skin cancer. The osteomyelitic process healed without antifungal treatment. Three weeks later, following a radical neck dissection, candidemia, without recurrence of the osteomyelitis, was diagnosed and treated successfully with intravenous amphotericin B and 5-fluorocytosin. The presentation of Candida osteomyelitis as a manifestation of disseminated candidiasis in immunocompromised hosts is discussed and the relevant literature is briefly reviewed.

Bone Marrow↗
PubMed1984

Hypo-osmolal syndrome due to prolonged nausea.

Hyponatremia and hypo-osmolality developed in a 70-year-old patient. It was probably mediated by hypersecretion of antidiuretic hormone, which, in turn, was due to prolonged nausea and vomiting. Severe esophagitis was the cause of the nausea. The patient was not given large amounts of fluids intravenously, and it is likely that she continued to drink for nondipsetic reasons. In view of her medical history of neurosyphilis, the possibility of a disturbance in the mechanism of thirst regulation is discussed, but remains unproved.

Aged↗
PubMed1983

Enhancement of hemopoietic stem cell proliferation by prostaglandin inhibitory drugs.

The in vivo effect of several prostaglandin inhibitory drugs on the hemopoietic stem cell was studied in SJL/J mice. Repeated intramuscular administration of Indomethacin increased the total number of bone marrow (BM) and spleen pluripotent hemopoietic stem cells (CFUS). The number of spleen colonies in lethally-irradiated normal BM recipients, which had been treated with Indomethacin, Aspirin or Flufenamic acid (all prostaglandin inhibitory drugs), was significantly greater than controls' spleen colonies. After exposure of SJL/J mice to different amounts of irradiation, more endogenous spleen colonies and a greater splenic weight were found among mice which had been treated with Indomethacin in comparison to PBS-treated mice. According to our results, treatment with prostaglandin inhibitory drugs stimulates murine hemopoietic stem cell proliferation and enhances stem cell recovery following irradiation.

Acetaminophen↗