Response of hairy cells to IFN-α involves induction of apoptosis through autocrine TNF-α and protection by adhesion

Baker, P.K.; Pettitt, Andrew R.; Slupsky, Joseph R.; Chen, Hai J.; Glenn, Mark A.; Zuzel, Mirko; Cawley, James F.

doi:10.1182/blood.v100.2.647

Cited by 53 publications

(34 citation statements)

References 38 publications

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“…We therefore suggest that circulating HCs have received signals for p38/JNK activation during their passage through spleen. This p38/JNK activation itself does not result in the induction of apoptosis, and our present and previous studies (Baker et al, 2002) suggest that this is because of the cytoprotective effect of ERK activated by PKC and possibly of other cosignals such as those that activate NFkB (Busuttil et al, 2002). This conclusion is supported by our demonstration that the cell death induced by MEK inhibition is accelerated when cells are cultured on VN to restore activation of p38.…”

Section: Discussionsupporting

confidence: 88%

“…Dead cells are PI permeable and lose their mitochondrial potential required for DiOC 6 , staining and are therefore PI bright, DiOC 6 dim. Cell survival was also measured by dual staining of the cells with ethidium bromide and acridine orange as described before (Baker et al, 2002).…”

Section: Cell Survivalmentioning

confidence: 99%

“…This activated state of HCs is not only reflected in the phenotype of the malignant cells, but also in their distinctive pattern of tissue invasion, in their prolonged survival and uniquely high sensitivity to interferon (aIFN) (Baker et al, 2002), nucleosides (Piro et al, 1990) and some therapeutic monoclonal antibodies (Kreitman et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

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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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Section: Discussionsupporting

confidence: 88%

Section: Cell Survivalmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

et al. 2003

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“…This is consistent with the reported results at most time points after PH (Columbano et al, 2005). Interferon-alpha 1 (IFNA1) can induce apoptosis of hair cells by inhibitors of apoptosis (IAP) (Baker et al, 2002). IFNA1 was downregulated 1, 4, and 12 h after PH, which indicates that it also inhibits cell apoptosis in liver tissue regeneration.…”

Section: Discussionsupporting

confidence: 91%

Expression profiles of the apoptosis signaling pathway mediated by death receptor and endoplasmic reticulum in rat liver regeneration

Xing

Zhu

et al. 2016

Genet. Mol. Res.

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ABSTRACT. The death receptor and endoplasmic reticulum (ER) are closely related to cell apoptosis, and it is worth studying whether the apoptosis pathways mediated by them are involved in liver regeneration. To understand the mechanism underlying death receptor-and ERmediated apoptosis during rat liver regeneration, we used the Rat Genome 230 2.0 Array to determine the changes in gene expression. We then searched the gene ontology (GO) and NCBI databases for genes associated with cell apoptosis mediated by the death receptor and ER. QIAGEN and KEGG databases were used for the related signaling pathways. We used the expression profile function to calculate the activity levels of the known apoptosis signaling pathways. The results of our study showed that the initial gene expression numbers in initiation, G0/G1 transition, cell proliferation, and redifferentiation and structural reconstruction phases were 32, 25, 44, and 29, respectively. This demonstrates that liver regeneration-related genes primarily start their expression in the initiation phase and work differently in each phase. By calculation and analysis using the gene synergy formula, it was suggested that the apoptosis signaling pathways [FAS, death receptor 3 (DR3), tumor necrosis factor receptor 1 (TNFR1), and ER] induced cell apoptosis in whole liver regeneration and anti-apoptosis pathways (DR3 and TNFR2) restrained apoptosis in the early phase of liver regeneration. In summary, these apoptosis pathways coordinated and regulated quality and quantity of the regenerating liver cells.

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“…66 However, IFN-a, a cytokine that is produced in response to viral infection, is the primary focus of the majority of melanoma clinical trials. 15,54 In addition to promoting apoptosis and inhibiting the growth of melanoma cells, 4,15,35,76 IFN-a stimulates the development of cytotoxic NK cells and CD8+ T cells.…”

Section: High-dose Il-2 and Interferonmentioning

confidence: 99%

Stereotactic radiosurgery and immunotherapy for metastatic spinal melanoma

Caruso¹,

Cohen-Inbar

Bilsky

et al. 2015

FOC

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The management of metastatic spinal melanoma involves maximizing local control, preventing recurrence, and minimizing treatment-associated toxicity and spinal cord damage. Additionally, therapeutic measures should promote mechanical stability, facilitate rehabilitation, and promote quality of life. These objectives prove difficult to achieve given melanoma's elusive nature, radioresistant and chemoresistant histology, vascular character, and tendency for rapid and early metastasis. Different therapeutic modalities exist for metastatic spinal melanoma treatment, including resection (definitive, debulking, or stabilization procedures), stereotactic radiosurgery, and immunotherapeutic techniques, but no single treatment modality has proven fully effective. The authors present a conceptual overview and critique of these techniques, assessing their effectiveness, separately and combined, in the treatment of metastatic spinal melanoma. They provide an up-to-date guide for multidisciplinary treatment strategies. Protocols that incorporate specific, goal-defined surgery, immunotherapy, and stereotactic radiosurgery would be beneficial in efforts to maximize local control and minimize toxicity.

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Response of hairy cells to IFN-α involves induction of apoptosis through autocrine TNF-α and protection by adhesion

Cited by 53 publications

References 38 publications

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

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

Expression profiles of the apoptosis signaling pathway mediated by death receptor and endoplasmic reticulum in rat liver regeneration

Stereotactic radiosurgery and immunotherapy for metastatic spinal melanoma

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