Risk of Malignant Transformation Arising From Giant Congenital Melanocytic Nevi: A 20-year Single-center Study.

BACKGROUND: Although giant congenital melanocytic nevus (GCMN) is regarded as premalignant, the incidence and risk factors of malignant transformation are controversial. OBJECTIVE: This study aimed to share the authors' surgical experience with GCMNs and provide data on their demographics, malignant transformation, and prognosis. METHODS: This single-center, consecutive study included 152 patients with GCMN who visited this center from March 2000 to February 2020. Their medical documentation was reviewed retrospectively, and the nevi were classified according to the size as follows: Group 1, 10 to 19.9 cm (n = 45); Group 2, 20 to 39.9 cm (n = 62); and Group 3, ≥40 cm (n = 45). RESULTS: Seven malignancies were found (4.6%; 4 melanomas, 2 rhabdomyosarcomas [RMS], and 1 malignant peripheral nerve sheath tumor [MPNST]). The risk increased according to the nevus size (2.2% in Group 1, 3.2% in Group 2, and 8.9% in Group 3) but the difference was not statistically significant (p = .3305). CONCLUSION: Malignant transformation from GCMN cannot be ignored. It can include transformation into melanoma, RMS, and MPNST. Early surgical resection and regular follow-up should be performed in patients with nevi ≥10 cm.

Stimulation of Toll-Like Receptor 3 Diminishes Intracellular Growth of Salmonella Typhimurium by Enhancing Autophagy in Murine Macrophages.

The Salmonella enterica serovar Typhimurium (S. Typhimurium) is a facultative Gram-negative bacterium that causes acute gastroenteritis and food poisoning. S. Typhimurium can survive within macrophages that are able to initiate the innate immune response after recognizing bacteria via various pattern-recognition receptors (PRRs), such as Toll-like receptors (TLRs). In this study, we investigated the effects and molecular mechanisms by which agonists of endosomal TLRs-especially TLR3-contribute to controlling S. Typhimurium infection in murine macrophages. Treatment with polyinosinic:polycytidylic acid (poly(I:C))-an agonist of TLR3-significantly suppressed intracellular bacterial growth by promoting intracellular ROS production in S. Typhimurium-infected cells. Pretreatment with diphenyleneiodonium (DPI)-an NADPH oxidase inhibitor-reduced phosphorylated MEK1/2 levels and restored intracellular bacterial growth in poly(I:C)-treated cells during S. Typhimurium infection. Nitric oxide (NO) production increased through the NF-κB-mediated signaling pathway in poly(I:C)-treated cells during S. Typhimurium infection. Intracellular microtubule-associated protein 1A/1B-light chain 3 (LC3) levels were increased in poly(I:C)-treated cells; however, they were decreased in cells pretreated with 3-methyladenine (3-MA)-a commonly used inhibitor of autophagy. These results suggest that poly(I:C) induces autophagy and enhances ROS production via MEK1/2-mediated signaling to suppress intracellular bacterial growth in S. Typhimurium-infected murine macrophages, and that a TLR3 agonist could be developed as an immune enhancer to protect against S. Typhimurium infection.