Photodynamic therapy reduces the burden of small ultraviolet-induced epidermal clones in human and mouse skin.

Actinic keratoses (AKs) and keratinocyte carcinomas (KCs) arise from prolonged UV exposure, with precursor UV-induced clonal mutations (CMs) appearing in sun-damaged skin. Photodynamic therapy (PDT) is a common field treatment for AKs and early KCs, but its impact on subclinical CMs is unknown. This study examines CMs using targeted ultra-deep sequencing on epidermal samples.

Mutation Hotspots Found in Bladder Cancer Aid Prediction of Carcinogenic Risk in Normal Urothelium.

More than 80,000 new cases of bladder cancer are estimated to be diagnosed in 2023. However, the 5-year survival rate for bladder cancer has not changed in decades, highlighting the need for prevention. Numerous cancer-causing mutations are present in the urothelium long before signs of cancer arise.

HotSPOT: A Computational Tool to Design Targeted Sequencing Panels to Assess Early Photocarcinogenesis.

Mutations found in skin are acquired in specific patterns, clustering around mutation-prone genomic locations. The most mutation-prone genomic areas, mutation hotspots, first induce the growth of small cell clones in healthy skin. Mutations accumulate over time, and clones with driver mutations may give rise to skin cancer.

Diagnostic and Prognostic Deep Learning Applications for Histological Assessment of Cutaneous Melanoma.

Melanoma is among the most devastating human malignancies. Accurate diagnosis and prognosis are essential to offer optimal treatment. Histopathology is the gold standard for establishing melanoma diagnosis and prognostic features.

Blockade of p38 kinase impedes the mobilization of protumorigenic myeloid populations to impact breast cancer metastasis.

Patients with metastatic breast cancer (MBC) have limited therapeutic options and novel treatments are critically needed. Prior research implicates tumor-induced mobilization of myeloid cell populations in metastatic progression, as well as being an unfavorable outcome in MBC; however, the underlying mechanisms for these relationships remain unknown. Here, we provide evidence for a novel mechanism by which p38 promotes metastasis.