This month’s news from across the specialty

January 1, 2026

In this monthly column, members of the DermWorld Editorial Advisory Workgroup identify exciting news from across the specialty.  

The incidence of melanoma in situ (MIS) has risen sharply in the U.S., surpassing invasive melanoma in 2025 (Cancer J Clin. 2025;75(1):10-45). Despite this sharp rise in MIS detection, mortality remains unchanged, raising concerns for overdiagnosis — cases that meet the histopathologic criteria but would not cause harm if left untreated. Epidemiologic evidence indicates that most MIS are not obligate precursors to invasive melanoma (J Natl Cancer Inst. 2022;114(10):1364-1370), suggesting that aggressive surgical treatment may be unnecessary.

In a retrospective study of 401 cases of MIS, Dessinioti et al. analyzed recurrence, metastasis, and death over a median follow-up period of 5.2 years (range, 1-28 years) (doi:10.1001/jamadermatol.2025.3078). The median size of the lesions was 0.7 cm. The subtypes of MIS with less predictable margins — lentigo maligna and acral MIS — were excluded. All cases underwent excisional biopsies with 2 mm margins, while 372 (92.3%) cases subsequently underwent wide local excision (WLE). Among the 31 cases without subsequent WLE and the 23 cases with margins <5 mm, no recurrence or metastasis was observed. Only one recurrence was observed — an invasive melanoma (0.8 mm) at 14 months in a patient with positive margins who did not undergo WLE.

These findings suggest that WLE may be unnecessary when excisional biopsy margins are clear, especially for small, discrete lesions (“micro-MIS”) and that margins <5 mm may be sufficient. The study contributes to the existing evidence that supports a more conservative surgical management of MIS (Eur J Cancer. 2025;220:115364). Further studies are needed for broader adoption of a conservative surgical approach amid the ongoing U.S. debate favoring margins wider than 5 mm (JAAD. 86 (1), 265).

Biologics: the aging and evolution of the new kids on the block. A recent Journal of Investigative Dermatology study from the United Kingdom introduced a tool to modernize and personalize biologic dosing for psoriasis. It applies therapeutic drug monitoring (TDM) with evolving model-informed precision dosing (MIPD) for risankizumab. The tool is essentially a biologic dosing digital dashboard that incorporates serologic drug levels, clinical progress, and patient-specific parameters (i.e., weight, age, concomitant medications, etc.), extrapolated from clinical trial data from almost 1,900 patients (J Invest Dermat. 2025. 145(9): 2251-60).

I remember when our biologic toolbox included three medication choices, all within the same mechanistic drug class (TNF inhibitors). Now, with over 12 options with varying molecular targets, and approved dosing schedules, we are due for more precise prescribing and long-term management rubrics. Particularly, our ability to taper or widen dosing for biologics remains mainly anecdotal based on an individual patient’s clinical improvement, disease subtype, age, and even their out-of-pocket costs that limit dosing within approved range (J Invest Dermatol. 2025. 145(9): 2120-2).

Although this module is still undergoing prospective study and extrapolation to other biologics, the concept will augment our ability to prescribe the appropriate therapy for targeted patient needs. Perhaps such advances will mitigate insurance formularies from choosing medications and doses for us.

High-throughput sequencing of the T-cell receptor (HTS-TCR) repertoire is emerging as a powerful tool in cutaneous T-cell lymphoma (CTCL) because it can detect malignant T-cell clones with up to 100-fold greater sensitivity than traditional methods, enabling both risk stratification and monitoring of minimal residual disease (MRD). MRD, defined as the small number of malignant cells that persist after therapy, serves as an important biomarker for predicting recurrence and guiding management. Weiner et al. demonstrated that MRD positivity, as detected by HTS-TCR, was strongly associated with disease relapse in Sézary syndrome (SS) (doi:10.1001/jamadermatol.2025.3054).

In another large cohort of 125 patients with mycosis fungoides (MF) and SS, Crisan et al. reported that specific TCR β (TCRB) and γ (TCRG) clonotypes were significantly associated with more aggressive subtypes, advanced disease, and worse overall survival (doi:10.1001/jamadermatol.2025.4081). Together, these findings support the concept that (1) characterization of the dominant TCR clone provides valuable prognostic information, and (2) the persistence or re-emergence of that clone at very low levels after treatment (i.e., MRD) identifies patients at higher risk of recurrence.

In practice, HTS-TCR could be applied to (a) identify patients with high-risk disease based on specific clonotypes and (b) monitor the persistence of malignant clones following therapy — information that could inform closer surveillance or earlier therapeutic intervention.

A new study by Zhang et al. in the Journal of Investigative Dermatology pinpoints a neural IL-17 pathway as the driver of psoriatic itch, reshaping how we think about itch in psoriasis. Through a series of cellular, behavioral, and imaging experiments, they detail that IL-17 receptor signaling at the level of the sensory neuron itself (rather than secondarily via keratinocytes or immune cells) drives chronic itch. Using mouse models of imiquimod-induced psoriasis, the authors found that IL-17RA and IL-17RC are upregulated in peripheral sensory neurons and that conditional deletion of either receptor markedly reduced itch.

They also found that activating IL-17R on neurons triggers intracellular MEK/ERK signaling that in turn drives expression of the ion channel TRPV4. Deleting TRPV4 or selectively suppressing neuronal ERK diminished itch in mouse models of psoriasis, strongly suggesting that this IL-17R/ERK/TRPV4 axis contributes to psoriatic itch. In both instances, however, psoriatic inflammation persisted despite the reduction in itch. The study thus delineates a new axis of type 17 immunity that drives chronic pruritus and is distinct from the pathways that mediate epidermal hyperplasia and inflammation in psoriasis. This work further explains why itch can persist in patients even after visible psoriasis improves clinically, reframing anti-IL-17 therapy as not only anti-inflammatory but also as directly neuromodulatory. Future therapies that specifically modulate neuronal IL-17R or TRPV4 may provide rapid, localized relief of psoriatic itch while bypassing systemic immunosuppression.

Additional DermWorld Resources