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Biomedical subjects

D W Golde

Publications and source records attributed to D W Golde.

At least 19 recordsLinked to original sources
PubMed1979

Helper and suppressor t-lymphocyte leukemia in ataxia telangiectasia.

We investigated the nature of the lymphoid leukemia that developed in one of two siblings with ataxia telangiectasia. The leukemic cells were shown to be T lymphocytes. Furthermore, the neoplastic cells carried a characteristic 14q+ chromosome tandem translocation. This chromosome abnormality had been identified 11 years earlier among the patient's "normal" lymphocytes. The patient's neoplastic T lymphocytes in vitro provided helper and suppressor T-lymphocyte activity equivalent to that of normal T lymphocytes. Some neoplastic T lymphocytes bore a receptor for the Fc portion of IgM (45 per cent Tmu) whereas other carried receptors for the Fc portion of IgG (10 per cent Tgamma). All the Tmu and Tgamma lymphocytes possessed the chromosome 14 abnormality. These data suggest that neoplastic transformation occurred in an uncommitted T lymphocyte that was capable of further differentiation into the distinct pathways for help and suppression, in a lymphoid analogy of chronic myelogenous leukemia.

Ataxia Telangiectasia↗
PubMed1979

Cellular interactions in haematopoiesis.

In vitro culture of haematopoietic cells has provided some surprising insights into critical interactions of blood-forming cells. Subpopulations of lymphoid cells have been shown to produce colony-stimulating activity, to interact with macrophages, and to have important effects on the very early stages of erythropoiesis. Macrophages have multiple influences on the proliferation and differentiation of other haematopoietic cells.

Animals↗
PubMed1979

Transformation of DBA/2 mouse fetal liver cells infected in vitro by the anemic strain of Friend leukemia virus.

Fetal liver cells of DBA/2 mice were infected with the anemic strain of Friend leukemia virus (FLV-A), which has no spleen focus-forming virus (SFFV) activity. The infected cells were grown in medium with or without erythropoietin. Transformed lines were isolated only from the infected cultures that had been treated with erythropoietin at the time of their initiation. The properties of three permanent cell lines in serial passage for over 2 years are described. Each has an aneuploid karyotype. Only the immature hematopoietic cells of the first line have metacentric chromosomes. They grow in suspension, as do the erythroleukemic lines derived from leukemic spleens of FLV-infected mice, and clone on agar. They produce tumors resembling reticulum cell sarcomas upon subcutaneous inoculation into syngeneic hosts. Stimulation of differentiation induced after treatment with dimethyl sulfoxide identifies the cells of the first line as being erythroid in origin. The two other lines are adherent and epithelioid in appearance. These lines may have originated from the nonhematopoietic cells present in fetal liver. No tumors were produced after the subcutaneous inoculation of 10(6) cells. All three lines synthesize virus. The virus is attenuated for leukemogenicity and has no SFFV activity. The transforming event appears to be specific, because fetal liver cells from C57BL/6 mice, which are resistant to the induction of leukemia by FLV, were not affected by the virus. Malignant transformation of erythroid cells by FLV-A in vitro confirms the in vivo findings that SFFV may not be a necessary prerequisite for the induction of erythroleukemia in susceptible hosts.

Anemia↗
PubMed1979

Detection of glucocorticoid receptors on Friend erythroleukemia cells.

The inhibition of dimethyl sulfoxide-induced differentiation of Friend erythroleukemia cells by steroids led us to examine these cells for the presence of glucocorticoid receptors. Direct assessement of dexamethasone binding revealed high-affinity dexamethasone receptors on the untreated cells. The specific binding of [3H]dexamethasone was dose dependent. At a concentration of 10(-8) M, almost all binding sites were occupied. The mean number of binding sites per cell in two separate experiments was 8045 and 7191, respectively, and the Kd varied between 3.38 and 3.49 x 10(-9) M. Dimethyl sulfoxide treatment led to a decrease in the number of dexamethasone binding sites on the cells induced to differentiate. After 5 days of treatment, the mean number of sites per cell was reduced to 1216 and 896 in two experiments, with a Kd of 5 x 10(-9) M. Dexamethasone treatment resulted in a moderate decrease in the efficiency of colony formation within 72 hr after the cells were plated in methylcellulose. The mechanism of this inhibitory effect is unknown. However, it was also dose dependent and could be abrogated by appropriate concentrations of progesterone or 11-deoxycortisone. These results suggest that the steroid effects on growth and differentiation of the erythroleukemia cells may be mediated via glucocorticoid receptors.

Animals↗
PubMed1979

5-fluorocytosine: inhibition of hematopoiesis in vitro and reversal of inhibition by uracil.

The in vitro effect of 5-fluorocytosine on human and murine hematopoiesis was studied by means of soft-gel assays for erythroid and myeloid colony-forming cells. The drug consistently inhibited colony formation by granulocyte-monocyte and erythroid precursor cells. Clear effects were observable at concentrations of 5-fluorocytosine of 5 x 10(-5) M (6.5 micrograms/ml), and concentrations of 5 x 10(-4) M (65 micrograms/ml) caused approximately 90% inhibition of cloning of bone marrow myeloid colony-forming cells from mice and normal humans. Greater concentrations of 5-fluorocytosine were required to inhibit erythroid progenitors than to inhibit myeloid precursors. Uracil competitively reversed the toxicity of 5-fluorocytosine. Our data strongly suggest that the hematopoietic toxicity of 5-5-fluorocytosine is mediated through cellular metabolism of the drug. The reversal of mammalian, but not of fungal, cytotoxic effects of 5-fluorocytosine by uracil may have important clinical applications.

Animals↗
PubMed1979

Splenic irradiation in myelofibrosis: effect on circulating myeloid progenitor cells.

We have investigated the mechanism of splenic irradiation-induced granulocytopenia in two patients with myelofibrosis and marked splenomegaly. Serial assays were performed for circulating granulocyte-monocyte progenitors capable of colony formation in vitro (CFU-C). For comparison, similar studies were performed on two patients receiving whole brain irradiation for glioma. Splenic irradiation caused a significant decrease in circulating CFU-C in the myelofibrosis patients. There was no decrease in circulating CFU-C in the brain-irradiated patients. No radiation-induced humoral inhibitor of granulopoiesis and no increased CFU-C radiosensitivity could be demonstrated in the myelofibrosis patients. These observations, taken together with previous data on splenic blood flow and pooling, suggest that the major mechanism of irradiation-induced granulocytopenia in myelofibrosis is destruction of proliferating precursor cells in the splenic tissue and sinusoids.

Aged↗
PubMed1979

Human myeloma cells and their strong stimulating capacity in 'one-way' mixed lymphocyte reaction: a comparative study with leukaemic B lymphoid cells.

Cultured human myeloma cells (ARH-77, RPMI-8226 and U-266), like leukaemic B lymphoid cells, consistently exerted a strong stimulating capacity on allogeneic lymphocytes in the 'one-way' mixed lymphocyte reaction. An optimal stimulation was seen when a 1:1 ratio or 1:2 ratio of responding cell:stimulating cells of each cell line was utilized. The stimulating capacity of ARH-77 or RPMI-8226 cells was significantly diminished when a 1:4 ratio of responding cells:stimulating cells was utilized. Fresh bone marrow cells containing more than 80% plasma cells from a patient with multiple myeloma, on the other hand, failed to exert the stimulating capacity on two occasions. The striking difference between cultured myeloma cells and fresh plasma cells is that the Ia-like antigen is present on cultured myeloma cells, and this antigen is absent on fresh plasma cells. The relationship between the Ia-like antigen and the stimulating capacity in 'one-way' mixed lymphocyte reaction is discussed.

Antigens, Neoplasm↗
PubMed1979

Controlling the production of blood cells.

The development since 1966 of a technology for growing stem cells in vitro has provided new insights into the controls of blood cell production. Hematopoietic hormones have been purified and important cellular interactions in hematopoiesis have been defined.

Anemia, Aplastic↗
PubMed1979

Neutrophil migration-inhibition activity produced by a unique T lymphoblast cell line.

Fifteen lymphoblast cell lines, including B cell, T cell, Null cell, and myeloblast cells, were examined for the production of human neutrophil migration-inhibition activity. Only one T lymphoblast cell line established from a patient with hairy cell leukemia produced a neutrophil migration-inhibition factor spontaneously and after stimulation with Con A and PHA.

B-Lymphocytes↗
PubMed1978

Bone marrow origin of hepatic macrophages (Kupffer cells) in humans.

Hepatic macrophages (Kupffer cells) from two male recipients of bone marrow transplants from females were studied for fluorescent Y body staining and sex chromatin (Barr body). After the transplant, macrophages had the sex karyotype of the donor, indicating that human hepatic macrophages originate in bone marrow.

Adolescent↗
PubMed1978

Acute myelogenous leukemia: a human cell line responsive to colony-stimulating activity.

A permanent human cell line that maintains the granulocytic characteristics of acute myelogenous leukemia cells has been established. The cells of this line form myeloid colonies in soft gel culture in the presence of human colony-stimulating activity. The cell line may be useful for studying human acute myelogenous leukemia and the mechanism of response to colony-stimulating activity.

Cell Division↗