Preliminary observations on new lymphoblast strains (EB4, EB5) from Burkitt tumours in a British and a Ugandan patient.

Epstein, M. A.; Barr, Y M; Achong, B. G.

doi:10.1038/bjc.1966.58

Cited by 33 publications

(5 citation statements)

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“…A number of cell lines from patients with Burkitt's lymphoma have been established successfully and are maintained in cell culture. These cultured cells can be used to investigate a wide spectrum of biological features that can be correlated with clinical characteristics of Burkitt's lymphoma (Epstein et al, 1966;Klein et al, 1974;Miyoshi et al, 1977;. Growth kinetics and chromosome analyses of three tissue culture lines of Burkitt's lymphoma cells (Cooper et al, 1966b) revealed that these cells have a cell cycle time of approximately 20 hr, with an S period of 12 hr, and that cell death is high and occurs at random during the cell cycle.…”

Section: Discussionmentioning

confidence: 99%

“…The growth kinetics of Burkitt's lymphoma cells in culture provide baseline information to establish the quantitative relationship between the proliferation and regression of tumor cells and the levels of biological markers produced by the cells. The kinetics of Burkitt's lymphoma cells grown in cell culture have been investigated (Cooper, Hughes & Topping, 1966b;Cooper, Frank & Wright, 1966a;Epstein, Barr & Achong, 1966). The relative distribution of the cell population in each stage of the cell cycle in Burkitt's tumor biopsies was investigated by quantitative cytochemical and autoradiographic methods (Cooper el al., 1966a).…”

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confidence: 99%

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Analysis of the Proliferation Kinetics of Burkitt's Lymphoma Cells

et al. 1980

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The in vitro proliferation kinetics of a cell line derived from a patient with American Burkitt's lymphoma were investigated at three different growth phases: lag (day 1), exponential (day 3) and plateau (day 5). The growth curve, labeling and mitotic indices, percentage labeled mitosis (PLM) curves and DNA content distributions were determined. The data obtained have been analysed by the previously developed discrete‐time kinetic (DTK) model by which a time course of DNA distributions during a 10‐day growth period was characterized in terms of other cell kinetic parameters. The mean cell cycle times, initially estimated from PLM curves on days 1, 3 and 5, were further analysed by the DTK model of DNA distributions and subsequently the mean cell cycle times with respect to DNA distributions during the entire growth period were determined. The doubling times were 39·6, 31·2 and 67·2 hr, respectively, at days 1, 3 and 5. The mean cell cycle time increased from 23·0 to 37·7 hr from day 3 to day 5 mainly due to an elongation of the G1 and G2 phases. A slight increase in the cell loss rate from 0·0077 to 0·0081 fraction/hr was accompanied by a decrease in the cell production rate from 0·0299 to 0·0184 fraction/hr. This calculated cell loss rate correlated significantly with the number of dead cells determined by trypan blue exclusion. Analysis of the number of dead cells in relation to the cell cycle stage revealed that a majority of cell death occurred in G1 (r= 0·908; P < 0·0001). There was a good correlation between the in vitro proliferation kinetics at plateau phase of this Burkitt's lymphoma derived cell line and the in vivo proliferation kinetics of African Burkitt's lymphoma (Iversen et al., 1974), suggesting the potential utility of information obtained by in vitro kinetic studies.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Analysis of the Proliferation Kinetics of Burkitt's Lymphoma Cells

et al. 1980

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“…Long-term and presumably permanent lines of human lymphoid cells have been obtained from bone marrow (Benyesh-Melnick at al., 1963), lymph nodes (Trujillo et al, 1966(Trujillo et al, , 1967Ponten, 1967;Sinkovics et al, 1967), Burkitt tumors and peripheral blood (Brooke and Osgood, 1959;Pulvertaft, 1964;Epstein et al, , 1966Stewart et al, 1965;Foley et a/., 1965; Rabson et a/., 1966; Fahey et a/., 1966; Tanigaki et a/., 1966; Armstrong, 1966;Moore etal., 1967;Clarkson etal., 1967). The chain of events with three distinct phases is characteristic only of bone marrow and lymph node cell.…”

Section: Discussionmentioning

confidence: 99%

Development of immunocytes and immunoglobulin production in long‐term cultures from normal and malignant human lymph nodes

Nilsson

Pontén

Philipson

1968

Intl Journal of Cancer

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Fifteen human lymph nodes have been grown in vitro. Cells from seven of the nodes eventually developed into apparently permanent lines dominated by cells resembling lymphoblasts. When the results are combined with a previously published series (Pontén, 1967) no difference is found between the frequency at which the phenomenon occurs in lymph nodes obtained from patients without known malignancy (group L), from nodes draining carcinomas (group C), or from malignant lymphomas (group M). It is concluded that the spontaneous establishment of permanent lymphoid cell lines is a characteristic of human lymphoid tissue in general and that no relationship to malignant lymphoma has been proved. A random fibroblastoid growth, apparently unrelated to the appearance of a secondary lymphoid cell production phase, was observed in eight cases, seven of which belonged to group M or C. Five of seven lines were tested repeatedly for globulin production by immunoelectrophoresis and immunoprecipitation combined with autoradiography. Four lines produced immunoglobulins of the IgG type; the fifth, obtained from a tuberculous node, synthesized IgA. Each cell line produced only one detectable molecular species, suggesting a monoclonal origin of the immunoglobulins. The light chains were exclusively of the kappa type, whereas the heavy chains differed with respect to their subgroup specificity.

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“…[25], K562 from a chronic myeloid leukemia [26], and BJAB [27] and EB4 [28] from EB virus genome-negative "Burkitt-like" lymphomas of B cell type. All such lines were uniformly negative in EBNA tests.…”

Section: Tg Cell Depletion Of Effector Cell Preparationsmentioning

confidence: 99%

Cytotoxic T cell recognition of Epstein‐Barr virus‐infected B cells. I. Specificity and HLA restriction of effector cells reactivated in vitro

et al. 1981

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The experiments show that the phenomenon of regression, seen exclusively in Epstein-Barr (EB) virus-infected cultures of mononuclear cells from EB virus antibody-positive donors, is mediated by cytotoxic T cells reactivated in vitro and specifically recognizing an EB virus-induced lymphocyte-detected membrane antigen LYDMA. Thus, effector T cells from regressing cultures kill autologous EB virus-transformed cells but not autologous pokeweed mitogen-stimulates lymphoblasts nor any of a range of EB virus genome-negative human hemopoietic cell lines (K562, HSB2, BJAB, EB4) particularly sensitive to nonspecific natural killer-like activities. Moreover, these reactivated effector cells exhibit classical HLA restriction of target cell recognition; in a survey of 14 effector cell donors, preferential lysis of the autologous virus-transformed line was a consistent feature, while the relative degree of lysis of allogeneic lines was in general directly related to the number of HLA-A and B antigens shared between effector and target cells. The pattern of reactivity shown by effector T cell preparations from any one donor was strikingly reproducible, and the results from a number of donors revealed differences between particular HLA-A and B antigens with respect to the level of EB virus-specific killing which was associated with sharing through these determinants.

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Preliminary observations on new lymphoblast strains (EB4, EB5) from Burkitt tumours in a British and a Ugandan patient.

Cited by 33 publications

References 13 publications

Analysis of the Proliferation Kinetics of Burkitt's Lymphoma Cells

Analysis of the Proliferation Kinetics of Burkitt's Lymphoma Cells

Development of immunocytes and immunoglobulin production in long‐term cultures from normal and malignant human lymph nodes

Cytotoxic T cell recognition of Epstein‐Barr virus‐infected B cells. I. Specificity and HLA restriction of effector cells reactivated in vitro

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