Nonmalignant cutaneous findings associated with vemurafenib use in patients with metastatic melanoma

Boyd, Kevin P.; Vincent, Bethaney; Andea, Aleodor A.; Conry, Robert M.; Hughey, Lauren C.

doi:10.1016/j.jaad.2012.06.045

Cited by 46 publications

(39 citation statements)

References 22 publications

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“…If necessary, strong potent local steroids can be associated, as well as topical lidocaine for its analgetic effect. 17,18 In our series three patients (16%) presented a hand-foot skin reaction after 4-6 weeks. They experienced benefit from an exfoliative ointment with salicylic acid and a potent local steroid.…”

Section: Discussionmentioning

confidence: 53%

Cutaneous adverse effects of BRAF inhibitors in metastatic malignant melanoma, a prospective study in 20 patients.

Vanneste

Wolter

Stas

et al. 2014

Acad Dermatol Venereol

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Section: Discussionmentioning

confidence: 53%

Cutaneous adverse effects of BRAF inhibitors in metastatic malignant melanoma, a prospective study in 20 patients.

Vanneste

Wolter

Stas

et al. 2014

Acad Dermatol Venereol

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“…Thus, patients are spared long durations of BRAFi toxicity and expense compared with the approach of continuous BRAFi until melanoma progression. Vemurafenib toxicities include hyperkeratotic rash, photosensitivity, arthralgias, headache, weakness, fatigue, uveitis, decreased creatinine clearance, QT-interval prolongation, and risk for second malignancies, most notably, well-differentiated squamous cell skin cancers and second primary melanomas [14]. With a median of 5.8 months of BRAFi, our patients experienced significant toxicities and were pleased to undergo consolidative radiation with subsequent observation.…”

Section: Discussionmentioning

confidence: 89%

Induction vemurafenib followed by consolidative radiation therapy for surgically incurable melanoma

Seeley¹,

Santos²,

Conry

2015

Melanoma Research

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Approximately half of melanomas are driven by a point mutation in the BRAF kinase gene, targetable with vemurafenib. However, the chief limitation of continuous BRAF inhibition is that the majority of patients develop resistance within 8 months, including those with surgically unresectable stage III melanoma. Researchers retrospectively reviewed medical records of all patients at our institution with surgically incurable BRAF V600E mutated stage III or limited stage IV melanoma treated with induction vemurafenib, stopped electively during ongoing response, followed by consolidative radiation therapy with or without intervening surgery to debulk nodal metastases. In our six-patient cohort, the median duration of vemurafenib was 5.8 months and the median radiation dose was 57 Gy using conventional fractionation. This algorithm produced 100% locoregional control at 29+ months following radiation and a median progression-free survival of 32.5+ months. Three of six patients remained progression free, and three relapsed in a single organ and achieved ongoing complete response to subsequent therapy. Outcomes greatly exceeding those reported with either BRAF inhibition or radiation alone suggest unanticipated synergies with this therapeutic sequence for both in-field and distant melanoma control, which may be mediated by radiosensitization and immune activation, respectively. In patients with surgically incurable melanoma encompassed within a radiation field, induction vemurafenib and consolidative radiation therapy, rather than continuing vemurafenib until progression, also limit the duration of vemurafenib toxicity and preserve sensitivity to future BRAF inhibition.

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“…In these diseases, vemurafenib was also responsible for squamoproliferative eruptions such as keratosis pilaris lesions with a decrease in skin manifestations after dose reduction. This supposed dose-dependent effect and the ability to restart vemurafenib suggest that theses eruptions would rather be secondary to a dysregulation of signaling pathway than to a hypersensitivity response [2,9]. …”

Section: Review and Discussionmentioning

confidence: 99%

“…Indeed the chest biopsy on which ESS was described also revealed follicular infundibular hyperkeratosis, another well-characterized lesion induced by vemurafenib [9]. Considering the clinical presentation, a possible alternative or coexisting diagnosis could be milia, which have also been reported secondary to vemurafenib [15,16].…”

Section: Review and Discussionmentioning

confidence: 99%

Vemurafenib-Induced Eccrine Squamous Syringometaplasia

Lescoat

Droitcourt²,

Stock³

et al. 2013

Dermatology

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We report herein a patient treated with vemurafenib for a stage IV melanoma who developed an eruption related to eccrine squamous syringometaplasia (ESS). This entity is a well-described side effect of cytostatic therapies used for malignant neoplasia and is clinically characterized by a symmetric cutaneous eruption composed of papules and vesicles preferentially located on fold and intertriginous areas. It is histologically defined by a squamous metaplasia of eccrine ductal epithelium. ESS represents another skin eruption to be added to the list of cutaneous adverse events associated with vemurafenib, a selective BRAF inhibitor used to treat patients with metastatic melanoma harboring the V600E mutation. The discussion focuses on the pathogenesis of ESS secondary to vemurafenib and on alternative diagnoses.

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Nonmalignant cutaneous findings associated with vemurafenib use in patients with metastatic melanoma

Cited by 46 publications

References 22 publications

Cutaneous adverse effects of BRAF inhibitors in metastatic malignant melanoma, a prospective study in 20 patients.

Cutaneous adverse effects of BRAF inhibitors in metastatic malignant melanoma, a prospective study in 20 patients.

Induction vemurafenib followed by consolidative radiation therapy for surgically incurable melanoma

Vemurafenib-Induced Eccrine Squamous Syringometaplasia

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