Development of Aggressive Squamous Cell Carcinoma With Perineural Invasion During Ruxolitinib Treatment

Dunaway, Spencer; Yu, Yang; Neltner, Scott

doi:10.1097/00042728-900000000-98655

Cited by 4 publications

(6 citation statements)

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“…253 Studies have found an increased incidence of second primary malignancy (SPM) with ruxolitinib. [254][255][256][257] Analysis of 700 myelofibrosis patients found 15 basal cell carcinomas (BCCs) in 14 patients (2%), 29 SCCs in 24 patients (3%), and one melanoma, with cutaneous malignancies accounting for more than half (45 of 87) the SPMs found in 80 patients (11%). 258 Table 1 lists in detail the types of dermatologic toxicities associated with JAK inhibitors.…”

Section: Jak Inhibitorsmentioning

confidence: 99%

Diverse landscape of dermatologic toxicities from small‐molecule inhibitor cancer therapy

et al. 2021

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Background: Advances in molecular biology and genetics have contributed to breakthrough treatments directed at specific pathways associated with the development of cancer. Small-molecule inhibitors (Nibs) aimed at a variety of cellular pathways have been efficacious; however, they are associated with significant dermatologic toxicities. Methods: We conducted a comprehensive review of dermatologic toxicities associated with Nibs categorized into the following five groups: (a) mitogen-activated protein kinase; (b) growth factor/multi-tyrosine kinase; (c) cell division/DNA repair; (d) signaling associated with myeloproliferative neoplasms; and (e) other signaling pathways. Prospective phase I, II, or III clinical trials, retrospective literature reviews, systematic reviews/meta-analyses, and case reviews/reports were included for analysis.Results: Dermatologic toxicities reviewed were associated with every class of Nibs and ranged from mild to severe or life-threatening adverse skin reactions.Inflammatory reactions manifesting as maculopapular, papulopustular/acneiform, and eczematous lesions were frequent types of dermatologic toxicities seen with Nibs.Squamous cell carcinoma with keratoacanthoma-like features was associated with a subset of Nibs. Substantial overlap in dermatologic toxicities was found between Nibs.Conclusions: Dermatologic toxicities from Nibs are diverse and may overlap between classes of Nibs. Recognition of the various types of toxicities from Nibs is critical for patient care in the era of "oncodermatology/dermatopathology."

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Section: Jak Inhibitorsmentioning

confidence: 99%

Diverse landscape of dermatologic toxicities from small‐molecule inhibitor cancer therapy

et al. 2021

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“…1 Reported adverse events are varied, likely because of the ubiquitous nature of JAK signaling in normal physiology. 1,4,5 This case of LyP in a patient taking tofacitinib highlights the need for further investigation of these agents' relationship with lymphoproliferative disorders and immune-mediated adverse events.…”

Section: Discussionmentioning

confidence: 96%

“…2 Predisposition to infection, immunemediated adverse events, and development of aggressive keratinocyte carcinomas are well-documented side effects of these medications, although the etiologic mechanisms remain unclear. [3][4][5] Because these medications see increased usage, reports of less common reactions are appearing in the literature. We report the development of lymphomatoid papulosis (LyP) with ophthalmologic involvement in a patient receiving tofacitinib for refractory erythema elevatum diutinum (EED).…”

Section: Introductionmentioning

confidence: 99%

A Case of Tofacitinib-Induced Lymphomatoid Papulosis With Ocular Involvement

Knapp

Steele

Mengden-Koon

et al. 2022

The American Journal of Dermatopathology

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Janus kinase (JAK) inhibitors are being prescribed with increasing regularity in dermatology. We report on a patient who initiated treatment with tofacitinib for refractory erythema elevatum diutinum and subsequently developed a novel cutaneous outbreak characterized by firm violaceous papules on the trunk and extremities along with conjunctival injection and periorbital inflammation. Biopsy of affected tissue from both the cutaneous and ophthalmologic sources demonstrated increased numbers of CD30 + large atypical cells amid a mixed inflammatory cell infiltrate, consistent with lymphomatoid papulosis. A review of the literature reveals a plausible mechanism for the induction of persistent JAK signaling in the presence of a JAK inhibitor. We discuss this mechanism in depth because it pertains to this patient and recommend continued vigilance with the use of these immunologic agents.

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“…An increased occurrence of non‐melanoma skin cancer (NMSC), such as cutaneous squamous cell carcinoma (cSCC), has not only been described following the long‐term treatment with the anti‐metabolite hydroxyurea (HU) but also under Janus kinase 1 and 2 inhibitors (JAKi) therapy for haematological malignancies. It has been reported that NMSC developing in patients on ruxolitinib therapy exhibit a more aggressive and metastatic profile 1–6 . We report a polycythaemia vera (PV) and long‐term HU and ruxolitinib therapy who developed highly aggressive cSCC not responding to cetuximab and pembrolizumab treatment.…”

Section: Introductionmentioning

confidence: 93%

“…It has been reported that NMSC developing in patients on ruxolitinib therapy exhibit a more aggressive and metastatic profile. [1][2][3][4][5][6] We report a polycythaemia vera (PV) and long-term HU and ruxolitinib therapy who developed highly aggressive cSCC not responding to cetuximab and pembrolizumab treatment.…”

Section: Introductionmentioning

confidence: 99%

Aggressive cutaneous squamous cell carcinoma in a hydroxyurea‐ and ruxolitinib‐pretreated patient with polycythaemia vera

Gambichler

Stockfleth

Susok

2021

Acad Dermatol Venereol

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Hydroxyurea and ruxolitinib are frequently used to treat myeloproliferative disorders, including polycythaemia vera, and chronic treatment is associated with many cutaneous adverse effects such as the development of aggressive non‐melanoma skin cancer (NMSC). We report an 85‐year‐old man with a history of hydroxyurea‐ and ruxolitinib‐treated polycythaemia vera who was referred for the management of progressively growing tumours on his scalp. Histopathology of the largest scalp lesion revealed a partly desmoplastic cutaneous squamous carcinoma with perineural invasion. Initial imaging revealed metastatic disease in cervical lymph nodes, bones and lungs. The scalp lesions were successfully treated with bleomycin‐based electrochemotherapy. Under initial systemic therapy using four cycles of cetuximab, metastatic disease progressed. Following the approval by the health insurance, compassionate use of pembrolizumab monotherapy was initiated. After three cycles of pembrolizumab, however, metastatic disease further progressed and the patient finally died from global respiratory insufficiency. The present case exemplifies the cutaneous adverse effects of long‐term hydroxyurea and ruxolitinib therapy, frequently resulting in highly aggressive NMSCs that are usually not responsive to systemic treatments even such as immune checkpoint inhibitors.

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Development of Aggressive Squamous Cell Carcinoma With Perineural Invasion During Ruxolitinib Treatment

Cited by 4 publications

References 0 publications

Diverse landscape of dermatologic toxicities from small‐molecule inhibitor cancer therapy

Diverse landscape of dermatologic toxicities from small‐molecule inhibitor cancer therapy

A Case of Tofacitinib-Induced Lymphomatoid Papulosis With Ocular Involvement

Aggressive cutaneous squamous cell carcinoma in a hydroxyurea‐ and ruxolitinib‐pretreated patient with polycythaemia vera

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