Drug hypersensitivity syndrome in a patient receiving vismodegib

Lam, Thomas; Wolverton, Stephen E.; Davis, Carrie L.

doi:10.1016/j.jaad.2013.11.018

Cited by 11 publications

(3 citation statements)

References 4 publications

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“…Because this antifungal drug has a long record of clinical safety, it has excellent potential for use as a systemic agent for the chemoprevention of BCCs in NBCCS [ 34 , 35 ]. A major limitation of vismodegib is the frequent development of drug resistance as a result of acquired Smo mutations that reduce its SMO- binding affinity [ 32 , 57 , 84 ]. Since ITRA binds to SMO at a different site, its efficacy seems to be unaffected by these vismodegib-associated mutations [ 60 ].…”

Section: Discussionmentioning

confidence: 99%

Shh and p50/Bcl3 signaling crosstalk drives pathogenesis of BCCs in gorlin syndrome

et al. 2015

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Nevoid basal cell carcinoma syndrome (NBCCS) is a rare autosomal dominant disorder that is due, in large measure, to aberrant Shh signaling driven by mutations in the tumor suppressor gene Ptch1. Here, we describe the development of Ptch1+/−/SKH-1 mice as a novel model of this disease. These animals manifest many features of NBCCS, including developmental anomalies and are remarkably sensitive to both ultraviolet (UVB) and ionizing radiation that drive the development of multiple BCCs. Just as in patients with NBCCS, Ptch1+/−/SKH-1 also spontaneously develops BCCs and other neoplasms such as rhabdomyomas/rhabdomyosarcomas. Administration of smoothened inhibitors (vismodegib/itraconazole/cyclopamine) or non-steroidal anti-inflammatory drug (sulindac/sulfasalazine) each result in partial resolution of BCCs in these animals. However, combined administration of these agents inhibits the growth of UVB-induced BCCs by >90%. Employing small molecule- and decoy-peptide-based approaches we further affirm that complete remission of BCCs could only be achieved by combined inhibition of p50-NFκB/Bcl3 and Shh signaling. We posit that Ptch1+/−/SKH-1 mice are a novel and relevant animal model for NBCCS. Understanding mechanisms that govern genetic predisposition to BCCs should facilitate our ability to identify and treat NBCCS gene carriers, including those at risk for sporadic BCCs while accelerating development of novel therapeutic modalities for these patients.

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Section: Discussionmentioning

confidence: 99%

Shh and p50/Bcl3 signaling crosstalk drives pathogenesis of BCCs in gorlin syndrome

et al. 2015

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“…Drug rash with vismodegib has only rarely been reported (11), including a case of drug hypersensitivity without cutaneous eruption (12). In our case, vismodegib was continued despite the eruption.…”

Section: Q223 Microdeletion Syndrome With Multiple Basal Cell Carcimentioning

confidence: 57%

9q22.3 Microdeletion Syndrome with Multiple Basal Cell Carcinomas Treated with Vismodegib: Three Key Messages in One Patient

Kieny¹,

Kremer²,

Scheidecker³

et al. 2018

Acta Derm Venerol

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“…41,42). One report describes a 77-year-old woman being treated with vismodegib for numerous and recurrent BCCs who developed on-target side effects in addition to sudden onset of fevers, chills, myalgia, and fatigue 3 weeks after drug initiation (41). Treatment was discontinued, and laboratory testing revealed elevated liver function and hypereosinophilia.…”

Section: Hypersensitivity Reactionmentioning

confidence: 99%

Management of Cutaneous and Extracutaneous Side Effects of Smoothened Inhibitor Therapy for Advanced Basal Cell Carcinoma

Mohan

Chang

2015

Clinical Cancer Research

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Smoothened inhibitors represent the first class of targeted drugs approved for use in advanced and metastatic basal cell carcinoma. For many patients with limited treatment options, this drug class has led to significant clinical improvements, but is not without side effects. In this review, we outline the basic mechanism of smoothened inhibitors and the most commonly observed cutaneous and extracutaneous side effects. We also highlight possible mechanisms for these adverse events and current management strategies.

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Drug hypersensitivity syndrome in a patient receiving vismodegib

Cited by 11 publications

References 4 publications

Shh and p50/Bcl3 signaling crosstalk drives pathogenesis of BCCs in gorlin syndrome

Shh and p50/Bcl3 signaling crosstalk drives pathogenesis of BCCs in gorlin syndrome

9q22.3 Microdeletion Syndrome with Multiple Basal Cell Carcinomas Treated with Vismodegib: Three Key Messages in One Patient

Management of Cutaneous and Extracutaneous Side Effects of Smoothened Inhibitor Therapy for Advanced Basal Cell Carcinoma

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