Successful management with interferon alpha-2a after prednisone therapy failure in an infant with a giant cavernous hemangioma

Castello, Manuel A.; G, Ragni; Antimi, A.; Ar, Todini; Patti, Gianluca; Lubrano, Riccardo; Clerico, A.; Calisti, Alessandro

doi:10.1002/(sici)1096-911x(199703)28:3<213::aid-mpo12>3.0.co;2-f

Cited by 15 publications

(9 citation statements)

References 15 publications

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“…To date, many factors known to promote or inhibit angiogenesis have been identified, including growth factors, cytokines and proteases [27]. Previous studies showed that IFN-α has anti-angiogenic properties in various tumors such as Kaposi's sarcomas [28], infantile hemangiomas [29] and some vascular-rich malignancies, melanoma, renal cell carcinoma and neuroendocrine tumors [30]. Therefore, we focused in the present study on the anti-angiogenic effects of the combination of IFN-α and 5-FU to determine the mechanism of action.…”

Section: Discussionmentioning

confidence: 99%

Combination of interferon-alpha and 5-fluorouracil inhibits endothelial cell growth directly and by regulation of angiogenic factors released by tumor cells

et al. 2009

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BackgroundThe combination therapy of interferon (IFN)-alpha and 5-fluorouracil (5-FU) improved the prognosis of the patients with hepatocellular carcinoma (HCC). To determine the molecular mechanisms of the anti-tumor and anti-angiogenic effects, we examined the direct anti-proliferative effects on human umbilical vein endothelial cells (HUVEC) and indirect effects by regulating secretion of angiogenic factors from HCC cells.MethodsThe direct effects on HUVEC were examined by TUNEL, Annexin-V assays and cell cycles analysis. For analysis of the indirect effects, the apoptosis induced by the conditioned medium from HCC cell treated by IFN-alpha/5-FU and expression of angiogenic factors was examined.ResultsIFN-alpha and 5-FU alone had anti-proliferative properties on HUVEC and their combination significantly inhibited the growth (compared with control, 5-FU or IFN alone). TUNEL and Annexin-V assays showed no apoptosis. Cell cycle analysis revealed that IFN-alpha and 5-FU delayed cell cycle progression in HUVEC with S-phase accumulation. The conditioned medium from HuH-7 cells after treatment with IFN/5-FU significantly inhibited HUVEC growth and induced apoptosis, and contained high levels of angiopoietin (Ang)-1 and low levels of vascular endothelial growth factor (VEGF) and Ang-2. Knockdown of Ang-1 in HuH-7 cells abrogated the anti-proliferative effects on HUVEC while knockdown of Ang-2 partially rescue the cells.ConclusionThese results suggested that IFN-alpha and 5-FU had direct growth inhibitory effects on endothelial cells, as well as anti-angiogenic effects through regulation of angiogenic factors released from HCC cells. Modulation of VEGF and Angs secretion by IFN-alpha and 5-FU may contribute to their anti-angiogenic and anti-tumor effects on HCC.

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Section: Discussionmentioning

confidence: 99%

Combination of interferon-alpha and 5-fluorouracil inhibits endothelial cell growth directly and by regulation of angiogenic factors released by tumor cells

et al. 2009

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“…IFN therapy has been clinically evaluated as the treatment of melanoma (136, 137), renal cell carcinoma (138, 139), myeloproliferative disorders (140, 141), lymphomas (142), neuroendocrine tumors (143) as well as vascular neoplasias including pulmonary hemangiomatosis (144), infantile hemangiomas (145), Kaposi’s sarcoma (146), and malignant hemangiopericytomas (147). …”

Section: Clinical Aspects Of Type I Ifn-mediated Polarization Of Neutmentioning

confidence: 99%

The Essential Role of Type I Interferons in Differentiation and Activation of Tumor-Associated Neutrophils

2016

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Type I interferons (IFNs) were first characterized in the process of viral interference. However, since then, IFNs are found to be involved in a wide range of biological processes. In the mouse, type I IFNs comprise a large family of cytokines. At least 12 IFN-α and one IFN-β can be found and they all signal through the same receptor (IFNAR). A hierarchy of expression has been established for type I IFNs, where IFN-β is induced first and it activates in a paracrine and autocrine fashion a cascade of other type I IFNs. Besides its importance in the induction of the IFN cascade, IFN-β is also constitutively expressed in low amounts under normal non-inflammatory conditions, thus facilitating “primed” state of the immune system. In the context of cancer, type I IFNs show strong antitumor function as they play a key role in mounting antitumor immune responses through the modulation of neutrophil differentiation, activation, and migration. Owing to their plasticity, neutrophils play diverse roles during cancer development and metastasis since they possess both tumor-promoting (N2) and tumor-limiting (N1) properties. Notably, the differentiation into antitumor phenotype is strongly supported by type I IFNs. It could also be shown that these cytokines are critical for the suppression of neutrophil migration into tumor and metastasis site by regulating chemokine receptors, e.g., CXCR2 on these cells and by influencing their longevity. Type I IFNs limit the life span of neutrophils by influencing both, the extrinsic as well as the intrinsic apoptosis pathways. Such antitumor neutrophils efficiently suppress the pro-angiogenic factors expression, e.g., vascular endothelial growth factor and matrix metallopeptidase 9. This in turn restricts tumor vascularization and growth. Thus, type I IFNs appear to be the part of the natural tumor surveillance mechanism. Here we provide an up to date review of how type I IFNs influence the pro- and antitumor properties of neutrophils. Understanding these mechanisms is particularly important from a therapeutic point of view.

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“…In cases associated with TAs, therapies directed at tumor destruction have been numerous and, unfortunately, associated with unpredictable results. Reported pharmacologic therapies, used either alone or in combination with other treatments, include corticosteroids, interferon‐alpha, vincristine, and cyclophosphamide . Procedural therapies have included surgical excision ± grafting, pulsed‐dye laser, radiation, arterial embolization, and pneumatic compression .…”

Section: Discussionmentioning

confidence: 99%

Kasabach–Merritt phenomenon in an adult man with a tufted angioma and cirrhosis responding to radiation, bevacizumab, and prednisone

et al. 2014

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To our knowledge, this represents the first report of KMP in an adult man associated with TA and challenges previous hypotheses arguing that KMP occurs only in children. We offer our own hypothesis concerning how, in extremely rare circumstances, this life-threatening consumptive coagulopathy may occur in adults. Electron beam radiation therapy in association with corticosteroids can be an effective treatment in these rare patients.

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Successful management with interferon alpha-2a after prednisone therapy failure in an infant with a giant cavernous hemangioma

Cited by 15 publications

References 15 publications

Combination of interferon-alpha and 5-fluorouracil inhibits endothelial cell growth directly and by regulation of angiogenic factors released by tumor cells

Combination of interferon-alpha and 5-fluorouracil inhibits endothelial cell growth directly and by regulation of angiogenic factors released by tumor cells

The Essential Role of Type I Interferons in Differentiation and Activation of Tumor-Associated Neutrophils

Kasabach–Merritt phenomenon in an adult man with a tufted angioma and cirrhosis responding to radiation, bevacizumab, and prednisone

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