Cutaneous adverse events associated with new cancer therapies

Modern oncologic therapies, including immune checkpoint inhibitors (ICIs), targeted kinase inhibitors (TKIs), antibody-drug conjugates (ADCs), bispecific antibodies, and adoptive cellular therapies, have transformed cancer care while introducing diverse cutaneous adverse events (cAEs). This review summarizes recent advances in the mechanistic understanding, clinical patterns, and management of dermatologic toxicities associated with contemporary cancer therapeutics.

Emerging evidence indicates that therapy-associated cAEs often reflect distinct biological mechanisms rather than nonspecific drug reactions. These toxicities can be conceptually organized into four major mechanistic paradigms: immune disinhibition, epithelial signaling inhibition, cytotoxic epithelial injury, and cytokine-driven immune activation. While immune checkpoint inhibitors remain the most extensively characterized model, newer therapeutic platforms, including ADCs and immune-engaging cellular therapies, have introduced additional toxicity patterns that are only beginning to be systematically characterized. Recent clinicopathologic studies have clarified cytotoxic epithelial injury patterns associated with ADCs, while early clinical series suggest cytokine-mediated inflammatory eruptions may occur during cellular immunotherapies. At the same time, advances in immunopathologic profiling have supported the development of mechanism-directed management strategies, including targeted cytokine blockade for steroid-refractory immune-mediated dermatoses.

Cutaneous adverse events associated with modern cancer therapies increasingly represent mechanism-based toxicities linked to therapy-specific biological pathways. Integrating clinical morphology with treatment class and immunologic mechanisms provides a practical framework for diagnosis and management. Mechanism-directed dermatologic care, including early recognition, targeted immunomodulation, and multidisciplinary collaboration, may improve toxicity control while preserving oncologic efficacy.