Combination therapy with interferon alpha‐2b plus low‐dose interferon gamma in pretreated patients with Ph‐positive chronic myelogenous leukaemia

Wandl, U.; Kloke, O.; Nagel-Hiemke, M.; Möritz, Thomas; Becher, R.; Opalka, Bertram; Holtkamp, W.; Bartels, H.; Seeber, S.; Niederle, N.

doi:10.1111/j.1365-2141.1992.tb02984.x

Cited by 28 publications

(10 citation statements)

References 17 publications

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“…There are 4 reported cases of sarcoidosis with CML. Three patients had underlying sarcoidosis when diagnosed with CML [2][3][4]. In the fourth, both diseases were diagnosed simultaneously [5].…”

Section: Discussionmentioning

confidence: 99%

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Cutaneous sarcoidosis in a patient with philadelphia‐positive chronic myelogenous leukemia treated with interferon‐α

et al. 1998

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A patient with Philadelphia-positive (Ph+) chronic myelogenous leukemia (CML) was diagnosed with cutaneous sarcoidosis after treatment with interferon-alpha (IFN-␣). Following IFN-␣ dose reduction, the skin lesions disappeared. Few cases of sarcoidosis associated with IFN treatment have been reported, and only in one patient with preexisting CML. Our patient was unique in that (1) the sarcoidosis was induced by the IFN-␣ treatment alone, (2) it developed de novo, and (3) it was confined to the skin. Am. J. Hematol. 58:80-81, 1998.

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Section: Discussionmentioning

confidence: 99%

“…A variety of complications of IFN-␣ therapy have been reported [6], but there have been only 3 sarcoidosis cases [4,7,8]. IFN-␣ and IFN-␥ therapy exacerbated preexisting sarcoidosis in one CML patient [4]. Another hepatitis C patient developed cutaneous sarcoidosis during IFN-␣ treatment [8].…”

Section: Discussionmentioning

confidence: 99%

Cutaneous sarcoidosis in a patient with philadelphia‐positive chronic myelogenous leukemia treated with interferon‐α

et al. 1998

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“…Three patients had underlying sarcoidosis when diagnosed with CML [2][3][4]. Three patients had underlying sarcoidosis when diagnosed with CML [2][3][4].…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Cutaneous sarcoidosis in a patient with philadelphia-positive chronic myelogenous leukemia treated with interferon-α

et al. 1998

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A patient with Philadelphia-positive (Ph+) chronic myelogenous leukemia (CML) was diagnosed with cutaneous sarcoidosis after treatment with interferon-alpha (IFN-). Following IFN-dose reduction, the skin lesions disappeared. Few cases of sarcoidosis associated with IFN treatment have been reported, and only in one patient with pre-existing CML. Our patient was unique in that (1) the sarcoidosis was induced by the IFN-treatment alone, (2) it developed de novo, and (3) it was confined to the skin. Am. J. Hematol. 58:80-81, 1998.

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“…Development of symptoms of SLE has been reported, however, in patients with RA treated with recombinant IFNγ [139,140]. IFNγ has also been implicated in the pathogenesis of sarcoidosis, an autoimmune disease characterized by a Th1 dominant cytokine profile, with high levels of IL-12, IL-18, IFNγ, and IP-10, in the bronchoaleveolar lavage [141,142,143,144,145], it remains to be established whether treatment with recombinant IFNγ would induce or exacerbate underlying sarcoidosis as has been reported in patients treated with IFNα [121,122,123,124,125,126,127] and in patients treated with IFNα combined with IFNγ [146]. …”

Section: Interferon γmentioning

confidence: 99%

Safety, Tolerability, and Immunogenicity of Interferons

Tovey

Lallemand

2010

Pharmaceuticals

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Interferons (IFNs) are class II cytokines that are key components of the innate immune response to virus infection. Three IFN sub-families, type I, II, and III IFNs have been identified in man, Recombinant analogues of type I IFNs, in particular IFNα2 and IFNβ1, have found wide application for the treatment of chronic viral hepatitis and remitting relapsing multiple sclerosis respectively. Type II IFN, or IFN gamma, is used principally for the treatment of chronic granulomatous disease, while the recently discovered type III IFNs, also known as IFN lambda or IL-28/29, are currently being evaluated for the treatment of chronic viral hepatitis. IFNs are in general well tolerated and the most common adverse events observed with IFNα or IFNβ therapy are “flu-like” symptoms such as fever, headache, chills, and myalgia. Prolonged treatment is associated with more serious adverse events including leucopenia, thrombocytopenia, increased hepatic transaminases, and neuropsychiatric effects. Type I IFNs bind to high-affinity cell surface receptors, composed of two transmembrane polypeptides IFNAR1 and IFNAR2, resulting in activation of the Janus kinases Jak1 and Tyk2, phosphorylation and activation of the latent cytoplasmic signal transducers and activators of transcription (STAT1) and STAT2, formation of a transcription complex together with IRF9, and activation of a specific set of genes that encode the effector molecules responsible for mediating the biological activities of type I IFNs. Systemic administration of type I IFN results in activation of IFN receptors present on essentially all types of nucleated cells, including neurons and hematopoietic stem cells, in addition to target cells. This may well explain the wide spectrum of IFN associated toxicities. Recent reports suggest that certain polymorphisms in type I IFN signaling molecules are associated with IFN-induced neutropenia and thrombocytopenia in patients with chronic hepatitis C. IFNγ binds to a cell-surface receptor composed of two transmembrane polypeptides IFGR1 and IFGR2 resulting in activation of the Janus kinases Jak1 and Jak2, phosphorylation of STAT1, formation of STAT1 homodimers, and activation of a specific set of genes that encode the effector molecules responsible for mediating its biological activity. In common with type I IFNs, IFNγ receptors are ubiquitous and a number of the genes activated by IFNγ are also activated by type I IFNs that may well account for a spectrum of toxicities similar to that associated with type I IFNs including “flu-like” symptoms, neutropenia, thrombocytopenia, and increased hepatic transaminases. Although type III IFNs share the major components of the signal transduction pathway and activate a similar set of IFN-stimulated genes (ISGs) as type I IFNs, distribution of the IFNλ receptor is restricted to certain cell types suggesting that IFNλ therapy may be associated with a reduced spectrum of toxicities relative to type I or type II IFNs. Repeated administration of recombinant IFNs can cause in a break in immune to...

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Combination therapy with interferon alpha‐2b plus low‐dose interferon gamma in pretreated patients with Ph‐positive chronic myelogenous leukaemia

Cited by 28 publications

References 17 publications

Cutaneous sarcoidosis in a patient with philadelphia‐positive chronic myelogenous leukemia treated with interferon‐α

Cutaneous sarcoidosis in a patient with philadelphia‐positive chronic myelogenous leukemia treated with interferon‐α

Cutaneous sarcoidosis in a patient with philadelphia-positive chronic myelogenous leukemia treated with interferon-α

Safety, Tolerability, and Immunogenicity of Interferons

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