Clinical and experimental dermatology · 2026
Vitiligo-like leucoderma following treatment with cyclin-dependent kinase 4 and 6 inhibitors: analysis of clinicopathological and immunohistochemical findings.
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Engler Markowitz Maya, Merose Rotem, Didkovski Elena, Doron Alon, Iton-Schwartz Amit, Ben Shitrit Shir, Barzilai Aviv, Nili Gal-Yam Einav, Kidron Debora, Sonnenblick Amir, Snast Igor, Mimouni Daniel, Sherman Shany
Аннотация
BACKGROUND: Vitiligo-like leucoderma is a rare cutaneous adverse event associated with cyclin-dependent kinases 4 and 6 (CDK4/6) inhibitors. However, its clinicopathological and immunohistochemical profiles remain unclear.
OBJECTIVES: To characterize the clinical, pathological and immunohistochemical features of CDK4/6 inhibitor-induced vitiligo-like leucoderma.
METHODS: This retrospective case series describes five female patients with advanced or metastatic breast cancer who developed vitiligo-like leucoderma during CDK4/6 inhibitor therapy. Clinical data and skin biopsies were evaluated, including immunohistochemical analysis of melanocyte markers, cell-cycle protein (p16) and T-cell subsets.
RESULTS: The depigmented lesions appeared primarily in sun-exposed areas. Two patients exhibited an inflammatory phenotype with pruritus and a lichenoid rash. In all patients, the lesions progressed rapidly over several months and then stabilized. This course was maintained regardless of any vitiligo-targeted therapeutic interventions. Histopathological examination revealed complete absence of melanocytes in all biopsies. Three specimens (60%) had inflammatory changes, including lichenoid and perivascular lymphohistiocytic infiltrates, with immunohistochemistry showing a predominance of CD4+ T cells within the infiltrates. Features of chronic actinic damage (epidermal atrophy, orthokeratosis, reactive keratinocytes, dermal solar elastosis) were observed. In two biopsies (40%), there was a patchy distribution of p16 staining within basal and suprabasal keratinocytes. Four patients (80%) demonstrated prolonged (2-4 years) progression-free survival.
CONCLUSIONS: CDK4/6 inhibitor-induced vitiligo-like leucoderma appears to be a distinct clinicopathological entity, characterized by a predictable course and stabilization, consistent inflammatory features, and a CD4-predominant immune profile. These findings suggest a unique pathogenic mechanism, either immune-mediated or associated with actinic damage, that distinguishes this condition from classic vitiligo and immune checkpoint inhibitor-induced vitiligo-like leucoderma.
OBJECTIVES: To characterize the clinical, pathological and immunohistochemical features of CDK4/6 inhibitor-induced vitiligo-like leucoderma.
METHODS: This retrospective case series describes five female patients with advanced or metastatic breast cancer who developed vitiligo-like leucoderma during CDK4/6 inhibitor therapy. Clinical data and skin biopsies were evaluated, including immunohistochemical analysis of melanocyte markers, cell-cycle protein (p16) and T-cell subsets.
RESULTS: The depigmented lesions appeared primarily in sun-exposed areas. Two patients exhibited an inflammatory phenotype with pruritus and a lichenoid rash. In all patients, the lesions progressed rapidly over several months and then stabilized. This course was maintained regardless of any vitiligo-targeted therapeutic interventions. Histopathological examination revealed complete absence of melanocytes in all biopsies. Three specimens (60%) had inflammatory changes, including lichenoid and perivascular lymphohistiocytic infiltrates, with immunohistochemistry showing a predominance of CD4+ T cells within the infiltrates. Features of chronic actinic damage (epidermal atrophy, orthokeratosis, reactive keratinocytes, dermal solar elastosis) were observed. In two biopsies (40%), there was a patchy distribution of p16 staining within basal and suprabasal keratinocytes. Four patients (80%) demonstrated prolonged (2-4 years) progression-free survival.
CONCLUSIONS: CDK4/6 inhibitor-induced vitiligo-like leucoderma appears to be a distinct clinicopathological entity, characterized by a predictable course and stabilization, consistent inflammatory features, and a CD4-predominant immune profile. These findings suggest a unique pathogenic mechanism, either immune-mediated or associated with actinic damage, that distinguishes this condition from classic vitiligo and immune checkpoint inhibitor-induced vitiligo-like leucoderma.