Skin cancer is the most common malignancy in the United States; however, regional variation in patient demographics, socioeconomic factors, and stage at diagnosis remains incompletely characterized. Defining these disparities is essential to inform targeted prevention and early detection strategies. We performed a cross-sectional analysis of the National Cancer Database (NCDB), including patients diagnosed with skin cancer between 2004 and 2020. Patients were stratified into six United |States geographic regions based on reporting facility location. Demographic, socioeconomic, and clinical variables, including age, sex, race and ethnicity, insurance status, income, urban-rural residence, and American Joint Committee on Cancer (AJCC) stage, were analyzed descriptively. Among 1,048,575 patients (mean age, 70.8 years; 60.3% male), notable regional differences were observed. White patients were 92.5% of the cohort, with the highest representation in the Mountain region (96.2%), whereas Black patients were most prevalent in the Southeast (8.6%). Socioeconomic disparities varied by region; uninsured rates were highest in the Southwest (3.2%) and Southeast (2.1%), while lower-income households predominated in these regions (81.4% and 71.8%). In contrast, higher-income patients were most common in the Northeast (54.7%). The proportion of advanced-stage (III-IV) disease was highest in the Mountain (29.9%) and Pacific (27.6%) regions and lowest in the Midwest (22.0%). Geographic disparities in socioeconomic conditions and healthcare access are associated with variation in stage at diagnosis among patients with skin cancer. These findings highlight the role of structural barriers in delayed presentation and support the need for targeted interventions, including improved insurance coverage, expanded access to dermatologic care, and enhanced early detection strategies, to improve equity in outcomes.

Understanding factors impacting quality of life in patients with keratinocyte carcinoma: A cross-sectional analysis of Mohs surgery patients.

Polymeric-lipid hybrid liposomes co-loaded with curcumin and silver nanoparticles: A strategy for photodynamic therapy in skin cancer.

Treatment of skin cancer: From conventional to nanotechnological approaches.

WNT10A mutations, a major genetic determinant of dental agenesis and ectodermal dysplasia, exert profound effects on craniofacial development. Although classified as rare disorders, these mutations account for more than half of oligodontia cases, reflecting their critical role. The associated phenotypes span a broad clinical spectrum, ranging from isolated tooth agenesis to complex multisystem disorders, including hypodontia, enamel and root defects, palmoplantar keratoderma, alopecia, nail dystrophy, skin xerosis, hypohidrosis, eyelid cysts, and skin cancer, skeletal abnormalities and impaired bone homeostasis, underscoring their systemic impact. This review synthesizes current biological and clinical knowledge by linking phenotypes of WNT10A mutations to disruptions in Wnt/β-catenin signaling and its interactions with BMP, SMAD, RANK/RANKL/OPG, VEGF, and other regulatory pathways. Altered pathway activity affects key processes in tooth morphogenesis, osteogenesis, cellular proliferation, and tissue maintenance, offering mechanistic explanations for the heterogeneity and severity of patient presentations. A clearer understanding of these pathways is essential for improving diagnosis and management of WNT10A-associated oligodontia, particularly in treatment planning for growth-dependent interventions, regenerative strategies, and implant rehabilitation. Despite significant progress, critical gaps remain in defining the molecular basis of variable expressivity and genotype-phenotype relationships. Elucidating these mechanisms will be pivotal for advancing precision approaches in dental and craniofacial care.

Leukotriene receptor antagonist drugs as potential chemopreventive agents: A systematic review and meta-analysis of cancer risk in asthmatic patients.

Expanding the therapeutic applications of PARP inhibitors in cancer by targeting receptor tyrosine kinases.

The costs of superficial radiation therapy are greater than Mohs micrographic surgery for the treatment of nonmelanoma skin cancer: Analysis from the CMS provider and service data set.

Proteomic Discovery of Pathogenesis for Non-Melanoma Skin Cancer in Heart Transplant Recipients

TabFusion: Lightweight early fusion of tabular and image data with graph-convolutional neural networks for skin cancer detection

Anti-virulence and Antitumor Effects of Gold Nanoparticles on Skin Cancer Cell Line A375

Adjuvant therapy with anti-PD-1 monotherapy in melanoma is well established. However, a perioperative approach starting immunotherapy before surgery appears mechanistically more reasonable and emerging research results suggest a clinical benefit. This study aims to provide a comprehensive overview of the current use of perioperative anti-PD-1 monotherapy in Germany. Patients with stageIII melanoma who received perioperative anti-PD-1 monotherapy from April 2019 to March 2025 were included. Data from eight German skin cancer centers were retrospective collected including histological and radiological assessments. We identified 75 melanoma patients with perioperative anti-PD-1 monotherapy. Surgery was conducted in 75% of patients after a median of 11weeks after therapy initiation. Pathological assessment revealed a major pathological response (MPR) in 46.5% of cases, a partial pathological response in 23.2%, and no pathological response in 30.4%. A moderate to strong correlation between radiological and pathological responses was identified. During a median follow up period of 11.6months, melanoma recurrence was observed in 16 patients (21%). The longest recurrence-free survival was seen in the MPR group. Perioperative anti-PD-1 monotherapy has been implemented in routine clinical practice in German skin cancer centers. The observed outcomes are comparable to data reported from prospective studies.

Overexpression of NMNAT3 suppresses melanoma progression by reprogramming NAD⁺ metabolism.

Synergistic effect of chaperone-guided folding and energy allocation for enhancing 5-aminolevulinic acid in engineered Escherichia coli.

Skin Cancer Burden and Recurrence in Lung Transplant Recipients: Associations with Rejection and Clinical Outcomes

Sun-protection awareness, habits, and recommendations of USA Swimming coaches.

Development of a Web-Based App to Predict Risk of Skin Cancer in Cardiac Allograft Recipients

Basal cell carcinomas (BCCs) are thought to reside within an immunosuppressed tumor microenvironment, but a detailed characterization of BCC-associated immune cells was lacking. Utilizing multiplex immunohistochemistry (IHC) (Vectra Polaris, Akoya Biosciences), we designed two staining panels, targeting either T cells (CD3, CD4, CD8, FoxP3, PD1) or myeloid cells (neutrophil elastase, CD68, CD163, HLADR, CD1c). Formalin-fixed paraffin-embedded (FFPE) BCC tumor specimens (n = 30) were analyzed using the panels. The majority of immune cells reside at the peritumoral margin; therefore, a boundary zone of 150 μm around tumor nests was used to capture them. A CD8/T-reg ratio and M1/M2 macrophage ratio of < 0.5 was observed across all BCC specimens, confirming an overall immunosuppressive phenotype. Among different histologic subtypes, infiltrative BCC had significantly lower CD8 T cells (p = 0.038), T-regulatory cells (p = 0.039), and CD8/T-reg ratio (p = 0.048), as well as lower M1/M2 ratio (p = 0.034) compared to non-infiltrative BCC subtypes. The association of infiltrative BCC with a more immunosuppressed microenvironment may contribute to more aggressive biological behavior. Overall, these data demonstrate a method to determine T cell and myeloid profiles in fixed FFPE skin tumor tissues that can identify subtle immune profile differences.

Modeling of Au@rGO enhanced THz photothermal therapy for superficial skin tumors

Merkel cell carcinoma (MCC) is an aggressive neuroendocrine skin malignancy frequently associated with Merkel cell polyomavirus (MCPyV) or ultraviolet (UV) mutagenesis. While immune checkpoint inhibitors (ICIs) targeting the PD-1/PD-L1 axis achieve response rates of 50-60%, primary and acquired resistance remain significant challenges. This review aims to synthesize current evidence on the determinants of ICI resistance in MCC to improve patient stratification and therapeutic strategies. A comprehensive narrative review of scholarly literature was performed using SciSpace, Google Scholar, and PubMed databases. Studies focused on MCC pathogenesis, immunotherapy clinical trials, tumor microenvironment (TME) profiling, and molecular mechanisms of ICI resistance were analyzed. A total of 29 peer-reviewed sources were integrated to provide a multi-layered perspective on resistance. Resistance to ICIs in MCC is multifactorial, driven by TME heterogeneity, MHC-I down-regulation, T-cell exhaustion, and viral status-dependent immune recognition. "Cold" tumors lacking preexisting tissue-resident CD8+ and γδ T-cell circuits are predisposed to failure. Furthermore, tumor cell plasticity - shifting between neuroepithelial and mesenchymal-like states - actively shapes immune evasion. Emerging biomarkers such as circulating tumor DNA (ctDNA) and composite gene expression signatures show promise but require prospective validation. Understanding the interplay between viral status, genomic burden, and the immune landscape is essential for overcoming ICI resistance. Rational combination strategies, particularly ICI plus radiation or epigenetic modulators to restore MHC-I expression, offer pathways to improve outcomes in resistant disease.