Tumour Necrosis Factor as an Autocrine Tumour Growth Factor for Chronic B-Cell Malignancies

Cordingley, F. T.; Hoffbrand, A. V.; Heslop, Helen E.; Turner, Martin; Bianchi, Andrea; Reittie, J. E.; Vyakarnam, Annapurna; Meager, Anthony; Brenner, Malcolm K.

doi:10.1016/s0140-6736(88)91782-5

Cited by 266 publications

(109 citation statements)

References 17 publications

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“…Similar findings have been previously reported for TNF-␣. 13 In contrast to TNF-␣ secretion, LT mRNA expression appears to be observed in every single case examined and its spontaneous production appears to be rather low. This suggests that LT may act in an autocrine fashion in B-CLL cells.…”

Section: Discussionmentioning

confidence: 89%

Lymphotoxin-α is an autocrine growth factor for chronic lymphocytic leukemia B cells

1998

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Section: Discussionmentioning

confidence: 89%

Lymphotoxin-α is an autocrine growth factor for chronic lymphocytic leukemia B cells

1998

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“…Both in small and larger DS-carcino- growth factor for chronic B-cell malignancies (Cordingley et al, 1988 (Sugarman et al, 1985;Creasey et al, 1987), action of activated host cells (Shau, 1988), a modulation of tumourspecific immunity (Talmadge et al, 1988) (Tracey et al, 1986). The flow reduction observed after single administration of high TNF doses can be caused by both systemic and tumour-specific mechanisms.…”

Section: Resultsmentioning

confidence: 99%

In vivo targets of recombinant human tumour necrosis factor-α: blood flow, oxygen consumption and growth of isotransplanted rat tumours

Kallinowski

Schaefer²,

Tyler³

et al. 1989

Br J Cancer

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“…Such studies will need to account for the dependence of MAPK activation on both Src and PKC. In addition, it will be necessary to differentiate between signals induced by autocrine cytokines already known to be produced by HCs (Cordingley et al, 1988;Chen et al, 1999;Gruber et al, 1999;Harris et al, 2000; Aziz KA, Till KJ, Chen HJ, Slupsky JR, Cawley JC and Zuzel M, submitted) and those attributable to primary transformation of signalling component(s).…”

Section: Discussionmentioning

confidence: 99%

Regulation of hairy-cell survival through constitutive activation of mitogen-activated protein kinase pathways

et al. 2003

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The hairy cells (HCs) of hairy-cell leukemia are intrinsically activated mature clonal B cells. The aims of this study were to gain further insights into the nature of this activation and to assess its importance for the prolonged HC survival in this chronic disease. We show that HCs contain phosphorylated/activated p38 MAPK, JNK and ERK1/ERK2 (ERK1/2). PKC inhibitors increased the activation of p38 and JNK, but reduced the phosphorylation of ERK1/2. Moreover, PKC inhibition resulted in cell death; cell death was also observed when the activation of ERK1/2 in HCs was abrogated with an inhibitor of MEK1/2 activation. In addition to PKC, active Src kinase was also shown to be involved in the maintenance of Raf-independent ERK activation in HCs. During cell culture on a nonadherent surface, ERK phosphorylation was sustained, while phosphorylation of p38 and JNK decreased. This decrease was not observed in HCs cultured on vitronectin (VN), indicating that p38/ JNK activation is probably a consequence of in vivo HC interaction with VN present in abundance in the red pulp of the spleen. Taken together, these results suggest that active p38/JNK make HCs susceptible to apoptosis, but the cells are effectively rescued by ERK activation involving constitutively active PKC and Src. These findings are relevant for the understanding of the prolonged cell survival of HCs and their selective sensitivity to some chemotherapeutic agents.

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Tumour Necrosis Factor as an Autocrine Tumour Growth Factor for Chronic B-Cell Malignancies

Cited by 266 publications

References 17 publications

Lymphotoxin-α is an autocrine growth factor for chronic lymphocytic leukemia B cells

Lymphotoxin-α is an autocrine growth factor for chronic lymphocytic leukemia B cells

In vivo targets of recombinant human tumour necrosis factor-α: blood flow, oxygen consumption and growth of isotransplanted rat tumours

Regulation of hairy-cell survival through constitutive activation of mitogen-activated protein kinase pathways

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