Updated Metaanalysis Finds That Interferon-α Improves Progression-Free and Overall Survival in Low-Grade Non-Hodgkin's Lymphoma When Administered with Chemotherapy That Contains Anthracyclines or Mitoxantrone

Gibson, Angelia D.; Cheson, Bruce D.; Link, Brian K.; Oken, Martin M.

doi:10.1016/s1526-9655(11)70253-6

Cited by 4 publications

(2 citation statements)

References 12 publications

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“…4 With regard to its role as an anticancer compound, a documented activity for IFN (mainly evaluated for IFN-␣) as single therapy or combined with other treatment modalities has been demonstrated in hematologic diseases, such as hairy cell leukemia, chronic myeloid leukemia (CML) and other meyloproliferative disorders, 5 myeloma, 6 and B and T cell lymphomas. 7,8 A number of solid tumors have also proven to be responsive to IFN, including melanoma, 9 renal cell carcinoma, 10 and midgut carcinoids. 11 Premalignant virally induced neoplasms, such as human papillomavirus (HPV)-related papillomas are responsive to IFN.…”

Section: Type I Interferons Asmentioning

confidence: 99%

Alternative Signaling Pathways Regulating Type I Interferon-Induced Apoptosis

Pokrovskaja

Panaretakis

Grandér

2005

Journal of Interferon & Cytokine Research

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Type I interferons (IFNs) are pleiotropic cytokines that exert multiple effects on normal and tumor cells. These effects are supposedly mediated through the stimulation of several signal transduction pathways by type I IFNs. These include the well-studied canonical Jak-Stat pathway, largely responsible for the antiviral and growth-inhibitory activities of IFNs, as well as the phosphatidylinositol 3-kinase (PI3K) and mitogen-activated protein kinase (MAPK) pathways, whose importance in IFN-induced biologic outcomes has not been precisely established. One of the effects of type I IFNs on tumor cells is the induction of programmed cell death, apoptosis, which has been studied extensively over the last decade and has been suggested to be an important effector mechanism for IFN's antitumor effects in the treatment of cancer. The aim of this review is to summarize and discuss the recent data in the field of type I IFN-induced apoptosis, with special emphasis on the molecular mechanisms of apoptosis and on the role of alternative noncanonical signaling pathways stimulated by type I IFNs in this process.

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Section: Type I Interferons Asmentioning

confidence: 99%

Alternative Signaling Pathways Regulating Type I Interferon-Induced Apoptosis

Pokrovskaja

Panaretakis

Grandér

2005

Journal of Interferon & Cytokine Research

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“…First identified for their potent antiviral activities in the 1950s, type I interferons (α/β) have become recognized for their anti-tumor activities in both animal models as well as in clinical studies against solid and hematologic malignancies 24–28. Documented activity as an anticancer compound as single therapy or as a combined modality with other treatments has been shown in a variety of hematologic diseases including hairy cell leukemia, chronic myeloid leukemia (CML), myeloma, and B and T cell lymphomas 29–32. A number of solid tumors have also been found to be responsive to IFN, including melanoma, renal cell carcinoma, and midgut cardinoids 33, 34.…”

Section: Introductionmentioning

confidence: 99%

AAV-mediated Local Delivery of Interferon-β for the Treatment of Retinoblastoma in Preclinical Models

et al. 2009

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Interferon-β (IFN-β has been found to have anti-tumor properties against a variety of malignancies through different mechanisms. However, clinical trials involving systemic administration of IFN-β have been hampered by secondary toxicity and the short half-life of IFN-β in the circulation. In order to circumvent these limitations we have developed an adeno-associated viral (AAV) vector gene therapy approach to deliver IFN-β to tumors. In this study, we tested the efficacy of AAV mediated local delivery of IFN-β for the treatment of retinoblastoma in preclinical models. Retinoblastoma is an ideal candidate for gene-therapy based anti-cancer treatment because target cell transduction and, therefore, IFN-β delivery can be contained within the ocular environment, thereby minimizing systemic toxicity. We report here that retinoblastoma cell lines exhibit pleiotropic responses to IFN-β consistent with previous studies on a variety of tumor cell lines. Intravitreal injection of AAV-IFN-β resulted in efficient retinal infection and sustained IFN-β production in the eye with minimal systemic exposure. Vector spread outside of the eye was not detected. Using our orthotopic xenograft model of retinoblastoma we found that intravitreal injection of AAV-IFN-β had a potent anti-tumor effect in vivo. These data suggest that AAV mediated delivery of IFN-β may provide a complementary approach to systemic chemotherapy which is the standard of care for retinoblastoma around the world.

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