Cutaneous T-cell lymphomas (CTCLs) are a heterogeneous group of diseases characterised by abnormal neoplastic T-cell growth in the skin. Mycosis fungoides (MF), the most common CTCL, manifests as erythematous skin patches and/or plaques, tumours or erythroderma. The disease may involve blood, lymph nodes and rarely viscera. Sézary syndrome (SS) is a unique leukaemia/lymphoma syndrome related to MF, which presents with blood and skin involvement at diagnosis. The pathogenesis of MF/SS is not fully elucidated. The presence of skin lesions at distant sites underpins a hypothesis that MF/SS lesions may develop through haematogenous seeding. Phenotypic similarities between malignant and normal T-cells led to the notion that disease-initiating mutations occur in specific subtypes of mature T-cells, which are responsible for most CTCLs. However, this mature T-cell precursor model is not always consistent with clinical observations and research on MF/SS pathogenesis. Here, we review evidence supporting an alternative model of pathogenesis for MF/SS involving haematogenous seeding as a key process responsible for the initiation and progression of the disease. According to this hypothesis, malignant transformation occurs at an early stage of T-cell development (probably in bone marrow or thymus), yielding circulating neoplastic T-cells which colonise the skin where the microenvironment is most permissive for proliferation and evolution. These mutated precursor cells seed the skin where they find a suitable niche to develop into clinically perceptible disease. Subsequently, malignant T-cells can re-enter the bloodstream, re-seed pre-existing lesions and seed new areas of the skin, causing synchronous and convergent changes in the transcriptomic profile of lesions and tumours, and clinical disease progression - 'consecutive haematogenous seeding' captures this temporal phenomenon. This model radically changes the current understanding of CTCL pathogenesis, transforming it from a primarily cutaneous disease with secondary involvement of blood, to a systemic disease, where the spread of malignant cells through the blood to the skin is not a phenomenon of advanced disease but is an essential component of pathogenesis. This understanding of MF/SS could have several clinical implications, including standardising our approach to assessing blood tumour burden, potential advances in prognosis and monitoring, and investigating combination treatments to improve patient outcomes.

The lack of evidence under routine clinical settings limited the widespread adoption of adalimumab biosimilars for psoriasis treatment.

Chronic wounds, defined by their prolonged healing process, significantly impair patient quality of life and impose a hefty financial burden on healthcare systems worldwide. Sex/gender-specific mechanisms regulate inflammation and infection, angiogenesis, matrix synthesis, and cell recruitment contribute to cutaneous wound healing, but remain largely understudied. This review is aimed to spotlight the innovative realm of bioengineering and nanomedicine, which is at the helm of revolutionizing complex chronic wound care. It underscores the significance of integrating patient sex into the development and (pre)clinical testing of these avant-garde treatment modalities, in order to enhance healing prospects for both women and men. Moreover, we explore the representation of both sexes in clinical trials of bioengineered and nanomedicine products. Finally, we examine the primary reasons for the historical neglect in translating sex-specific wound healing research into clinical practice and propose strategic solutions. By tackling these issues, the article advocates for advanced treatment frameworks that could significantly improve healing outcomes for individuals of all sexes, thereby optimizing both efficacy and inclusivity in chronic wound management.

The pathogenesis of psoriasis, an inflammatory skin disease, is incompletely understood. Growing evidence substantiates the involvement of stromal cells in the inflammatory process.

Patients with Gorlin (basal cell nevus) syndrome (GS) have numerous phenotypic abnormalities due to over-activity of the hedgehog (HH) signaling pathway, most commonly due to a heritable mutation in the PTCH1 gene, which encodes a major inhibitor of this pathway. HH inhibitors (HHi) taken orally can reverse some of the manifestations, most prominent of which is the development of numerous cutaneous basal cell carcinomas (BCCs). In order to improve the benefit:risk ratio, we have developed a gel containing a small cyclopamine-derived molecule that can be applied topically in expectation that this mode of delivery can reduce the burden of BCCs without producing the systemic adverse effects that cause patients to stop treatment with oral HHis.

Hidradenitis suppurativa (HS) is a chronic, relapsing inflammatory skin disease associated with significant comorbidities and poor quality of life. Despite uncertainty about pathways driving inflammation in HS lesions, the cytokines IL-17A and IL-17F have been shown to be upregulated in patients with HS. Previous studies demonstrated that the monoclonal IgG1 antibody bimekizumab selectively inhibits IL-17F in addition to IL-17A.

Disabling pansclerotic morphea (DPM) is a rare systemic inflammatory disorder at the severe end of the localized scleroderma spectrum which primarily affects children under 14 years of age. The disease is characterized by rapid sclerosis with circumferential involvement that frequently extends to the fascia, muscle, and bone. Disease progression often involves development of sclerotic plaques, chronic skin ulcers, and painful joint contractures leading to patient immobility with a high mortality rate. Internal organ fibrosis is typically absent. The aggressive and systemic nature of the disease leads patients to seek multidisciplinary care where current therapies are targeted towards immunomodulation and measures to preserve mobility while limiting infection, but often have limited efficacy. Here, we summarize all DPM patients in the English literature, common clinical symptoms, laboratory investigations, and treatments reported to date. Assessment of published cases suggest that the number of therapies does not influence disease outcome and that female patients were younger at the time of reported death. Clinician familiarity and awareness of common DPM symptoms are important for an accurate and early diagnosis. Furthermore, knowledge of the treatments that have been reported to be effective in mitigating disease progression may be helpful in expanding the treatment options available to patients.

Artificial daylight photodynamic therapy (ADL-PDT) is an alternative, all-year applicable, nearly painless treatment approach for actinic keratoses (AK) with comparable effectiveness to daylight or conventional PDT. At the time this study was initiated, methyl aminolevulinate (MAL) was the only photosensitizer approved for ADL-PDT in Germany.

Polymorphic light eruption (PLE) is the most frequent photodermatosis in Europe with an estimated prevalence of 10 to 20%, particularly in temperate climates. Itching or burning lesions appear only in sun-exposed areas, predominantly on the chest, the arms and forearms within a few hours following exposure. The disease's cause is still unknown, yet studies have suggested that skin microbial elements may play a role in its pathogenesis.