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Malignant diseases of the skin
Published in Rashmi Sarkar, Anupam Das, Sumit Sethi, Concise Dermatology, 2021
Anupam Das, Yasmeen Jabeen Bhat
Investigations: The keratoacanthoma is diagnosed on clinical grounds. On histopathology, keratoacanthoma has a characteristic, symmetrical, cup-shaped, or flask-shaped structure with epidermis extending over the sides of the crater. There is a minor degree of epidermal dysplasia and little evidence of tissue invasion.
Skin cancer
Published in Peter Hoskin, Peter Ostler, Clinical Oncology, 2020
This includes: KeratoacanthomaSolar keratosisBowen disease
Malignant disease of the skin
Published in Ronald Marks, Richard Motley, Common Skin Diseases, 2019
It usually appears within a week or two on light-exposed skin as a solitary crateriform nodule (Fig. 15.7). It then gradually enlarges for a few weeks and stays at that size for a variable period before finally remitting after several months. The keratoacanthoma is diagnosed on clinical grounds, however occasionally true squamous cell carcinomas may also arise rapidly and be indistinguishable. The histopathological features are often identical to squamous cell carcinoma and rarely will the histopathologist positively report lesions as keratoacanthomas. Untreated these lesions may often reach 2–3 cm in diameter and become offensive due to necrotic infected tissue. Although spontaneous resolution may occur this does not happen for many months – and frequently leaves an unsightly scar. For these reasons therapeutic intervention is usually indicated.
Update on BRAF and MEK inhibition for treatment of melanoma in metastatic, unresectable, and adjuvant settings
Published in Expert Opinion on Drug Safety, 2019
Kristy Kummerow Broman, Lesly A Dossett, James Sun, Zeynep Eroglu, Jonathan S Zager
In the phase II study (n = 132), the most common AE were grade 1 or 2 arthralgia, rash, photosensitivity, fatigue, and alopecia [33]. One patient experienced retinal-vein occlusion and three developed transient palsies of the seventh cranial nerve but were able to resume vemurafenib after resolution. One patient died due to rapidly progressive melanoma and acute renal failure, possibly related to the study drug. Dose reduction was required in 45% (59/132) of patients and dose interruption was required in 85 patients (64%). Cutaneous SCC were diagnosed in 26% (n = 34) of patients, at a median of 8 weeks (range 2–36 weeks) from the first dose. The early development of these lesions suggested a role for underlying damage from chronic sun exposure. The majority of the lesions (39/43) were keratoacanthoma type with only four representing invasive cutaneous SCC and there were no cases of mucosal SCC or metastatic cutaneous SCC. There were also eight cases of basal cell carcinoma [33].
BRAF in the cross-hairs
Published in Expert Review of Hematology, 2019
Mark B. Geyer, Omar Abdel-Wahab, Martin S. Tallman
Cutaneous toxicities are observed in the vast majority of patients with advanced BRAF V600E-mutant melanoma treated with single-agent vemurafenib [56]. While pruritic maculopapular rash, hyperkeratosis, and hand-foot syndrome are common and generally manageable with topical corticosteroids, exfoliants, oral antihistamines and other supportive measures, and while photosensitivity is typically manageable with sun protection strategies, approximately 20–25% of patients develop keratoacanthoma or cutaneous SCC, generally managed with surgical excision or destructive therapy. Of some note, HRAS mutations are frequently observed in cutaneous SCC lesions arising on vemurafenib therapy [57]. As described in section 2.2, vemurafenib may paradoxically increase signaling through the MAPK pathway in this setting, particularly in the presence of co-existing activating mutations in RAS. Progression of chronic myelomonocytic leukemia (CMML) bearing an activating mutation in NRAS has also been observed in a patient with BRAF mutant melanoma treated with vemurafenib, providing further clinical evidence BRAF inhibitor monotherapy can accelerate RAS-driven malignancies [58].
Supportive Oncodermatology: Addressing dermatologic adverse events associated with oncologic therapies
Published in Oncology Issues, 2018
Epidermal neoplasms are adverse skin reactions frequently associated with BRAF gene inhibitor therapy (vemurafenib, dabrafenib) used to treat metastatic melanoma. The characteristic keratinocyte proliferation found in all BRAF inhibitor-induced skin toxicities drives the formation of lesions such as squamous cell carcinoma, keratoacanthoma, and verrucous keratosis.52 The mechanism behind BRAFI-induced squamous cell carcinoma is unknown, yet biochemical studies have shown that RAF blockade in wild-type BRAF cells, particularly in the presence of oncogenic RAS mutations caused by sun damage to keratinocytes, can lead to paradoxical mitogen-activated protein kinase (MAPK) pathway activation via dimerization of RAF isomers.53-55 To support this theory, studies have shown a high prevalence of RAS gene mutations in cutaneous squamous cell carcinomas developing in patients treated with RAF inhibitors (see photo on page 72).55 Therefore, the RAF inhibitor-driven activation of MAPK may unmask the oncogenic events in keratinocytes harboring preexisting RAS mutations caused by sun damage.55