ABSTRACT
Basal cell carcinoma (BCC) is the most common cancer worldwide. While most BCC cases respond to surgical management, complex BCC often presents treatment challenges for patients unsuitable for, or refractory to, surgery and radiotherapy-limiting treatment options. Hedgehog pathway inhibitors (HHI) have emerged as an important treatment option for patients with complex BCC-providing a durable treatment modality and improved clinical outcomes. We present a case series of 10 patients with complex BCC treated with sonidegib, an oral HHI, at a dose of 200 mg once daily for a mean duration of 6 months and a mean follow-up of 7 months. Of these patients, sonidegib monotherapy was curative in eight cases. Of the remaining two patients, treatment with sonidegib arrested tumor progression and decreased tumor size to a point where surgical removal was straightforward. The positive treatment response we observed supports use of sonidegib as an effective treatment option for patients with complex BCC.
Subject(s)
Antineoplastic Agents , Carcinoma, Basal Cell , Skin Neoplasms , Antineoplastic Agents/adverse effects , Biphenyl Compounds , Carcinoma, Basal Cell/pathology , Hedgehog Proteins/therapeutic use , Humans , Pyridines/adverse effects , Skin Neoplasms/pathologyABSTRACT
Basal cell carcinoma (BCC) is the most common cancer globally, with the incidence increasing worldwide by approximately 1% annually. While most cases of BCC can be treated surgically, advanced BCC often poses treatment challenges for patients unsuitable for, or refractory to, radiotherapy and surgery. Since the majority of cases of BCC demonstrate Hedgehog signaling hyperactivation, Hedgehog pathway inhibitors provide durable treatment options and improved clinical outcomes for patients with advanced BCC. One of the most common adverse events seen in patients taking Hedgehog inhibitors includes muscle spasms, which are hypothesized to occur because of calcium influx into the muscle cells. Here we present a case series of patients with muscle spasms during treatment with sonidegib and propose an alternate etiology related to increased actin expression.
