Eruptive keratoacanthoma and squamous cell carcinoma complicating imiquimod therapy: Response to oral acitretin

Foxton, Glen; Delaney, Tom

doi:10.1111/j.1440-0960.2010.00676.x

Cited by 12 publications

(14 citation statements)

References 33 publications

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“…Virtually every form of skin therapy that causes inflammation directly or indirectly has been reported as responsible for development of KAs. Examples are cryotherapy, [54][55][56] imiquimod, [57][58][59][60] ingenol mebutate (unpublished observation), PDT, 61 UVB, 4 laser treatment, 62 cosmetic peel 63 and photothermolysis. 64 Similar reports of SCCs as a response to external trauma, stress or short-lived inflammatory reactions, etc.…”

Section: Reactive Kasmentioning

confidence: 99%

Squamous cell carcinoma and keratoacanthomas are biologically distinct and can be diagnosed by light microscopy: a review

et al. 2016

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Keratoacanthomas (KAs) are self-limiting squamoproliferative lesions usually seen on sun damaged skin. These tumours are in many ways enigmatic, and the relation between KAs and squamous cell carcinoma is still a contested topic. In this review the biology and histology of KAs will be discussed, and based on morphology, clinical outcome and recent genetic analysis of the tumour types, we conclude that KAs and SCCs are two distinct biological entities which can usually be distinguished by conventional microscopy. The sentinel observation of rapid and frequent appearance of KAs after BRAF treatment of malignant melanoma patients has paved the way for a more general understanding of the pathogenesis leading to the appearance of KAs in patients with inflammation in the skin. In BRAF treated patients, the KAs are a consequence of paradoxical activation of the MAP kinase pathway. Similarly, any external trauma or pharmaceutical interventions resulting in inflammation in the skin will activate the MAP kinase pathway. Such inflammation-mediated MAP kinase activation in the skin will result in the development of KAs through the same pathway as demonstrated for BRAF treated patients. It is characteristic that skin tumours following short acting inflammatory stimulation of severely sun damaged skin develop almost exclusively into KAs, whereas it is exceedingly rare that such inflammatory conditions lead to formation of SCCs. The understanding that inflammatory reactions in sun-damaged skin may activate pathways specifically leading to the formation of KAs may spare the patient the discomfort and disfigurement of needless overtreatment.

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Section: Reactive Kasmentioning

confidence: 99%

Squamous cell carcinoma and keratoacanthomas are biologically distinct and can be diagnosed by light microscopy: a review

et al. 2016

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“…However, further studies are required to confirm efficacy and assess the appropriate application frequency and treatment duration. In addition, eruptive KAs complicating imiquimod therapy has been reported, though this may have just been a coincidence …”

Section: Off‐label Uses Of Imiquimod In Cutaneous Disordersmentioning

confidence: 99%

Imiquimod in dermatology: an overview

2016

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Imiquimod is an immune response modifier commercially available as a 3.75 and 5% cream. Topical imiquimod stimulates the innate and adaptive immune responses and induces cytokine production. This allows its use for the treatment of a wide variety of benign and malignant skin conditions due to its potential antiviral, antitumor, and immunoregulatory effects. Currently, topical imiquimod is US Food and Drug Administration (FDA)-approved for the treatment of anogenital warts, actinic keratosis, and superficial basal cell carcinomas. However, it has also shown a beneficial effect in the treatment of many other skin disorders. In this review, we describe existing evidence on the mechanism of action of topical imiquimod, its FDA-approved indications, off-label uses, and side effects.

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“…Further etiological factors are immune‐compromised or immune‐suppressed patients , skin trauma when pretreated with chemicals , carbondioxide ablation therapy, likely by induction of a wound healing response , and most importantly, genetic predisposition in multiple KA of Ferguson Smith type . Drugs as Imiquimod and BRAF‐inhibitors induce KA as a side effect . Contradictory results were published on the implication of human papilloma viruses (HPV) .…”

Section: Etiologymentioning

confidence: 99%

“…It leads to upregulation of pro‐inflammatory cytokines due to activation of the NFkB pathway. Recently, there is a growing evidence of Imiquimod induced KA as a secondary effect of the treatment .…”

Section: Molecular Pathways Contributing To Scc and Ka Formationmentioning

confidence: 99%

Keratoacanthoma: a distinct entity?

Gleich

Chiticariu

Huber

et al. 2015

Experimental Dermatology

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Keratoacanthoma (KA) are common but exceptional benign tumors, often appearing on sun-exposed areas of light skinned people and showing spontaneous resolution. The goal of this study was to review existing literature, to point out the etiological complexity of KA biology and to answer the controversial debate if or not KA is a distinct entity or a variant of squamous cell carcinoma (SCC). Relying on recent results, we highlight that KA is an individual lesion with a unique molecular signature caused by alterations in the TGFb signalling pathway. These recent findings will help to understand the nature of KA and to develop new reliable diagnostic tools, simplifying the discrimination of the histologically similar KA and SCC.

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Eruptive keratoacanthoma and squamous cell carcinoma complicating imiquimod therapy: Response to oral acitretin

Cited by 12 publications

References 33 publications

Squamous cell carcinoma and keratoacanthomas are biologically distinct and can be diagnosed by light microscopy: a review

Squamous cell carcinoma and keratoacanthomas are biologically distinct and can be diagnosed by light microscopy: a review

Imiquimod in dermatology: an overview

Keratoacanthoma: a distinct entity?

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