Improvement of psoriasis in a patient with metastatic colon cancer after treatment with panitumumab

Shiraishi, Ken; Akiyama, Shoko; Tohyama, Mikiko; Sayama, Koji

doi:10.1111/ajd.13203

Cited by 2 publications

(1 citation statement)

References 5 publications

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“…An antagonist of EGFR tyrosine kinase improved the psoriatic phenotype but had no significant effect on nonpsoriatic skin [15]. Applying EGFR tyrosine kinase inhibitors [16,17] or anti-EGFR monoclonal antibodies [18,19] has remarkably improved chronic psoriasis in some cancer patients. These results suggest that EGFR signaling plays a critical role in the pathogenesis of psoriasis; however, the mechanisms involved remain unclear.…”

Section: Introductionmentioning

confidence: 99%

EGFR ligands synergistically increase IL‐17A‐induced expression of psoriasis signature genes in human keratinocytes via IκBζ and Bcl3

et al. 2022

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Various epidermal growth factor receptor (EGFR) ligands are highly expressed in the epidermis of psoriasis lesions, and abnormal EGFR activation appears to be involved in the pathogenesis of psoriasis. However, how EGFR signaling contributes to the development of psoriasis is unclear. Interleukin (IL)‐17A, a critical effector of the IL‐23/IL‐17A pathway, increases the expression of psoriasis signature genes in keratinocytes and plays an essential role in the pathogenesis of psoriasis by inducing IκBζ, a critical transcriptional regulator in psoriasis. In this study, we stimulated primary human keratinocytes with IL‐17A and various EGFR ligands to investigate whether EGFR ligands regulate the expression of psoriasis signature genes. In cultured normal human keratinocytes and a living skin equivalent, EGFR ligands did not induce psoriasis‐related gene expression, but significantly enhanced the IL‐17A‐mediated induction of various psoriasis signature genes, including antimicrobial peptides, cytokines, and chemokines. This was dependent on an EGFR activation‐mediated synergistic increase in IL‐17A‐induced IκBζ expression and was partially mediated by the EGFR‐dependent upregulation of Bcl3. Therefore, EGFR ligands can act as synergistic agents of IL‐17A signaling by stimulating the epidermal production of psoriasis signature genes in psoriasis lesions. This study reveals a potential mechanism by which EGFR signaling contributes to the pathogenesis of psoriasis.

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Section: Introductionmentioning

confidence: 99%

EGFR ligands synergistically increase IL‐17A‐induced expression of psoriasis signature genes in human keratinocytes via IκBζ and Bcl3

et al. 2022

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Psoriasis in the Era of Targeted Cancer Therapeutics: A Systematic Review on De Novo and Pre-existing Psoriasis in Oncologic Patients Treated with Emerging Anti-neoplastic Agents

Madan,

Ortiz-López,

Sakunchotpanit

et al. 2024

Dermatol Ther (Heidelb)

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New advancements in medicine have paved the way for targeted therapies and immune checkpoint inhibitors (ICIs), which have become mainstays of cancer therapy. Targeted therapies work by pinpointing specific molecules in cancer pathways and inhibiting their function, while ICIs target irregularities in the immune system and DNA repair, participating in the induction of cell death. Although these agents have demonstrated great efficacy in treating a diverse set of cancers, they can frequently provoke serious dermatologic adverse effects. The side effects caused by an ICI are classified as immune-related adverse events since ICIs are immunomodulating, while the cutaneous side effects of targeted therapies are known as dermatologic adverse effects. Multiple studies have reported psoriasis and psoriasiform eruptions among the side effects observed in neoplastic patients receiving targeted therapies or ICIs. Psoriasis is an immune-mediated disease characterized by overactive T-cells and keratinocytes. To conduct this review, we retrieved 1363 studies from the PubMed database published between 2008 and 2023 using the terms “psoriasis” AND “cancer treatment.” Many of these studies aimed to understand how patients with cancer receiving treatment may develop or even achieve psoriasis remission. Given that cancer and psoriasis involve a delicate balance between immune activation and suppression, ICIs and targeted therapies might produce varying effects. The aim of this review was to explore the relationship between psoriasis and cancer therapeutics while also highlighting the need to prioritize proper management of cutaneous side effects in neoplastic patients.

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Improvement of psoriasis in a patient with metastatic colon cancer after treatment with panitumumab

Cited by 2 publications

References 5 publications

EGFR ligands synergistically increase IL‐17A‐induced expression of psoriasis signature genes in human keratinocytes via IκBζ and Bcl3

EGFR ligands synergistically increase IL‐17A‐induced expression of psoriasis signature genes in human keratinocytes via IκBζ and Bcl3

Psoriasis in the Era of Targeted Cancer Therapeutics: A Systematic Review on De Novo and Pre-existing Psoriasis in Oncologic Patients Treated with Emerging Anti-neoplastic Agents

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