Differential effects of BCL-2 on survival and proliferation of human B-lymphoma cells following γ-irradiation

Milner, Andrew; Grand, Roger J. A.; Vaughan, Andrew T M; Armitage, Richard J.; Gregory, Christopher D.

doi:10.1038/sj.onc.1201355

Cited by 26 publications

(28 citation statements)

References 25 publications

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“…13,47 This phenotype was confirmed here using established immuno-phenotyping methods. 13,47 Cells were used in early passage (550) only. Stable Bcl-2 transfectants were obtained as described.…”

Section: Cellssupporting

confidence: 52%

“…7,47 L3055 cells have been previously classified as group I and are also Bcl-2-negative. 13,47 This phenotype was confirmed here using established immuno-phenotyping methods. 13,47 Cells were used in early passage (550) only.…”

Section: Cellsmentioning

confidence: 99%

“…47 Although the group I BL surface phenotype (CD10 + CD23 7 CD39 7 CD77 + ) ± that of the freshly isolated biopsy cells ± was originally described for EBV-positive BL, it can also be applied to EBV-negative cells. 7,47 L3055 cells have been previously classified as group I and are also Bcl-2-negative. 13,47 This phenotype was confirmed here using established immuno-phenotyping methods.…”

Section: Cellsmentioning

confidence: 99%

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Micro-environmental factors in the survival of human B-lymphoma cells

2000

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Burkitt lymphoma (BL) cells retain a high inherent propensity to undergo apoptosis indicating that net growth of the tumour population in vivo is likely to be influenced profoundly by its micro-environment. Here we investigate micro-environmental factors that affect BL-cell survival in vitro. We show that survival, and consequently net production, of tumour cells is enhanced by autocrine factors and, to a greater extent, by paracrine factors provided by relevant stromal elements of the tumour (fibroblasts and follicular dendritic cells) and by macrophages. Promotion of BL-cell survival by paracrine elements was mediated by cell/cell contact and by short-range soluble factor(s). IL-4, IL-10 and TNF-a promoted, whereas TGF-b1 inhibited, tumour-cell production. Macrophages engaged in phagocytosis of apoptotic BL cells were less effective than untreated macrophages in supporting net expansion of BL populations. These results suggest that the net production of tumour cells in BL is supported by multiple micro-environmental factors that modulate apoptosis. Cell Death and Differentiation (2000) 7, 59 ± 69.

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Section: Cellssupporting

confidence: 52%

Section: Cellsmentioning

confidence: 99%

Section: Cellsmentioning

confidence: 99%

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Micro-environmental factors in the survival of human B-lymphoma cells

2000

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“…In the case of Burkitt's lymphoma cell lines, PI3K plays a critical role in cell survival. An essential feature of BL-cells is the myc translocation, which drives apoptosis in BL-cells (Milner et al, 1993). PI3K has been shown to suppress c-myc induced apoptosis (Kaumann-Zeh et al, 1997) and a more recent study suggests that PI3K can provide a survival signal for murine B-lymphocytes expressing high levels of c-myc (Carey and Scott, 2001).…”

Section: Discussionmentioning

confidence: 99%

Phosphatidylinositol 3-kinase is essential for the proliferation of lymphoblastoid cells

et al. 2002

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“…Cell death by c-Myc in the Rat1 system was subsequently shown to be associated with the activation of certain Jun kinases (Jnks) and caspase-3 (Kagaya et al, 1997;Yu et al, 1997;Kangas et al, 1998), which is crucial to produce the associated chromatin collapse and nucleosomal DNA degradation. c-Myc is also responsible for cell death in Burkitt's lymphoma cells and EBVimmortalized B cells deprived of autocrine factors (Milner et al, 1993;Cherney et al, 1994). Lastly, epithelial cells have also been shown to be susceptible to apoptosis by c-Myc (Sakamuro et al, 1995).…”

Section: C-myc Induces Apoptosismentioning

confidence: 99%