Activation of Epstein–Barr virus latent genes protects human B cells from death by apoptosis

Gregory, Christopher D.; Dive, Caroline; Henderson, Scott; Smith, Christopher A.; Williams, Gwyn T.; Gordon, John; Rickinson, Alan B.

doi:10.1038/349612a0

Cited by 479 publications

(277 citation statements)

References 19 publications

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“…Morphological features of apoptosis were identified after staining cells with acridine orange (AO, 5 pgml, Molecular Probes Inc., Eugene, OR) and examining stained cells using fluorescence microscopy as previously described Field inversion gel electrophoresis (FIGE). To examine cleavage of DNA to 5Okbp fragments FIGE was performed essentially as described by Oberhammer et al (24).…”

Section: Cell Culture and Exposure To Anticancer Agentsmentioning

confidence: 99%

Further characterisation of the in situ terminal deoxynucleotidyl transferase (TdT) assay for the flow cytometric analysis of apoptosis in drug resistant and drug sensitive leukaemic cells

et al. 1995

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Apoptosis, originally defined by specific morphological changes, is characterised biochemically by non-random cleavage of DNA. Depending on cell type, this DNA cleavage proceeds from 300 and 5Okbp fragments prior to, concomitantly with, or in the absence of l80bp integer fragmentation. Incorporation into fragmented DNA of biotin-labelled nucleotides by terminal deoxynucleotidyl transferase (TdT) has recently become a standard flow cytometric assay for the idenacation and quantitation of apoptosis. Nucleotide incorportion is visualized using avidin-tagged fluorescein isothiocyanate (FITC) (Gorczyca et al.: Cancer Res 53:1945-1951; Jonker et al.: Cytometry (Suppl13)Abstr 99A, 1993). Here, we charaderise this assay further in three different haemopoietic cell lines. Drug-induced DNA damage is not i d e n a e d by the TdT assay unless it is coupled to the apoptotic response.This was demonstrated using cells in which activation of the oncogenic Abelson-encoded protein tyrosine kinase suppressed drug-induced apoptosis, but did not inhibit drug-induced DNA damage (by melphalan, hydroxyurea, or etoposide). Furthermore, the TdT assay identifies DNA fragments formed during apoptosis induced by etoposide and N-methylformamide in HL60 and MOLT-4 cells, including those high molecular weight DNA fragments formed in MOLT-4 cells which were not further cleaved to 180-2OObp integer fragments. Our results support the use of flow cytometry and the TdT assay to reliably measure apoptotic cells in heterogeneous cell samples. 0 1995 Wiley-Liss, Inc.Key terms: Apoptosis, drug resistance, Abelson tyrosine kinase; DNA damage, non-random DNA fragmentation, TdT assay Apoptosis is now widely recognised as the predominant mode of cell death induced by anticancer agents in sensitive tumour cells (25). An increasing body of evidence demonstrates that apoptotic cell death is actively regulated ( 17,52,54); several proteins suppress apoptosis downstream of drug-induced DNA damage including Bcl-2 (20,38,51), Bcr-Abl (37), and the virally encoded proteins, adenovirus E1B (14) and v-Abl(7). The tumour suppressor gene pS3 is thought to sense DNA strand breaks and to either block cell cycle progression and/or induce apoptotic cell death (8,32,35,36,39). Being an active process, the apoptotic pathway presents opportunities for therapeutic intervention; understanding the molecular mechanisms underlying the induction, and perhaps more importantly, the suppression of apoptosis in tumour cells is now a major thrust of much cancer research.The accurate measurement of apoptosis is problematic; apoptosis in vitro is generally rapid and asynchronous with final non-specific degradation of apoptotic cells (secondary necrosis). The most commonly used, the most certain, and the most laborious method for identification and quantitation of apoptosis is examination of the characteristic changes in nuclear morphology of apoptotic cells by microscopy. However, over the past S years flow cytometric assays for apoptosis have been developed; these (to a large extent) o...

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Section: Cell Culture and Exposure To Anticancer Agentsmentioning

confidence: 99%

Further characterisation of the in situ terminal deoxynucleotidyl transferase (TdT) assay for the flow cytometric analysis of apoptosis in drug resistant and drug sensitive leukaemic cells

et al. 1995

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“…26, 29). Its product, the inner mitochondrial membrane protein Bcl-2, might thus be an itnportant anti-apoptosis protein (22,(28)(29)(30). hi humans, some nonlymphoid tissues also exhibit Bel-2 expression, and within these tissues Bel-2 is often topographically restricted to long-lived or proliferating cell populations (31).…”

Section: Biochemistry and Regulationmentioning

confidence: 99%

Patterns of cell death: the significance of apoptosis for dermatology

Paus

Rosenbach

Haas

et al. 1993

Experimental Dermatology

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Development, function, remodelling, and senescence of multicellular organisms depend on the coordinated occurrence of physiological, actively induced cell death in two major patterns: terminal differentiation and programmed cell death (apoptosis). Apoptosis is a highly selective form of “cell suicide” with characteristic morphological and biochemical features: chromatin condensation, formation of apoptotic bodies, and DNA fragmentation by activation of endonucleases. Here, we outline the current understanding of apoptosis and its subtypes, discuss their biological functions, and delineate why apoptosis is relevant to the skin and its diseases. We distinguish apoptosis from necrosis, and discuss the regulation of apoptosis by selected genes, hormones, growth factors and cytokines. The epidermis and the regressing hair follicle offer interesting models for studying the as yet ill‐understood biology of epithelial cell apoptosis. The selective manipulation of cell death programs may become part of the therapeutic arsenal of clinical dermatology.

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“…MO. USA) as described elsew here (Gregory et al 1991) and obserned by fluorescence microscopy. Cells designated as apoptotic wxere those that displaved the characteristic morphological features of apoptosis.…”

mentioning

confidence: 99%

5-Fluorouracil induces apoptosis in human colon cancer cell lines with modulation of Bcl-2 family proteins

Nita

Nagawa²,

Tominaga³

et al. 1998

Br J Cancer

144

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Summary Recently. apoptosis has been implicated as one of the end points of cells exposed to chemotherapeutic agents. The p53 and Bcl-2 family of proteins are involved in chemotherapy-induced apoptosis. but in a cell type-dependent manner. We sought to determine the roles played by the p53 and Bcl-2 family of proteins in 5-fluorouracil (5-FU)-induced apoptosis of human colon cancer cell lines. We first studied the p53 genetic and functional status, and then 5-FU, at inhibitory concentration of 50% (ICj)

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Activation of Epstein–Barr virus latent genes protects human B cells from death by apoptosis

Cited by 479 publications

References 19 publications

Further characterisation of the in situ terminal deoxynucleotidyl transferase (TdT) assay for the flow cytometric analysis of apoptosis in drug resistant and drug sensitive leukaemic cells

Further characterisation of the in situ terminal deoxynucleotidyl transferase (TdT) assay for the flow cytometric analysis of apoptosis in drug resistant and drug sensitive leukaemic cells

Patterns of cell death: the significance of apoptosis for dermatology

5-Fluorouracil induces apoptosis in human colon cancer cell lines with modulation of Bcl-2 family proteins

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