Interferon and Malignant Disease - How Does it Work and Why Doesn't it Always?

Grandér, Dan; Einhorn, Stefan

doi:10.1080/028418698430548

Cited by 53 publications

(35 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…However, besides antiviral functions, IFNs also inhibit cell proliferation by inducing p21 and p202 expression and downregulating c-myc expression, inhibit caspases, and enhance antigen presentation by inducing MHC expression. Hence, it is not surprising that tumor cells present a truncated IFN pathway (Grander and Einhorn, 1998). In such tumor cells the function of VARNAs becomes dispensable and their deletion can confer oncotropism (Cascallo et al, 2003.…”

Section: A Current Model Backbonementioning

confidence: 98%

Cancer selective adenoviruses

Alemany

2007

Molecular Aspects of Medicine

View full text Add to dashboard Cite

Section: A Current Model Backbonementioning

confidence: 98%

Cancer selective adenoviruses

Alemany

2007

Molecular Aspects of Medicine

View full text Add to dashboard Cite

“…Multiple mechanisms contribute to the overall clinical outcome of IFN-α treatment of malignancies including direct antiproliferative actions on the tumor cells [7]and indirect mechanisms, such as inhibition of angiogenesis, induction of tumor mesenchyme and immunomodulation [8, 9]. In order to explore relevant mechanisms of IFN-α-dependent growth control in GEP NETs, we studied IFN-α effects on cell cycle progression and regulation of tumor angiogenesis.…”

Section: Introductionmentioning

confidence: 99%

Interferon-α: Regulatory Effects on Cell Cycle and Angiogenesis

Rosewicz¹,

Detjen²,

Scholz³

et al. 2004

Neuroendocrinology

View full text Add to dashboard Cite

In the current study, we investigated the effects of interferon-α (IFN-α) on proliferation and angiogenesis in neuroendocrine tumor disease. Using a panel of human neuroendocrine tumor cell lines, we confirmed functionally active IFN-α signaling by STAT activation and nuclear translocation as well as transactivation. IFN-α results in anchorage-dependent and -independent growth inhibition due to a delayed progression from S-phase to G2 phase of the cell cycle. This was due to substantial reduction in cellular cyclin B levels resulting in the inhibition of Cdc2 kinase activity. In parallel to growth inhibition, we observed a profound inhibition of VEGF gene transcription by IFN-α in human neuroendocrine tumor cells due to an Sp1/Sp3-dependent inhibition of VEGF promoter activity. Treatment of neuroendocrine tumors with IFN-α in nude mice resulted in growth inhibition and inhibition of angiogenesis. Furthermore, treatment of neuroendocrine tumor patients with IFN-α resulted in decreased VEGF expression as well as tumor angiogenesis in liver metastases. In summary, IFN-α acts via direct antiproliferative effects as well as inhibition of tumor angiogenesis mediated by suppression of VEGF gene expression in neuroendocrine tumor disease.

show abstract

“…IFN-α is frequently used as a supplementary therapeutic agent to eradicate micrometastatic deposits in patients with a high risk of systemic recurrence (Grander & Einhorn, 1998;Lens, 2006). Sartoris and colleagues found that MSCs expressing IFN-α could be efficiently delivered inside the tumor microenvironment of a mouse plasmacytoma model (Sartoris et al, 2011).…”

Section: Stem Cell -Cytokine Therapymentioning

confidence: 99%