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Cutaneous squamous scell carcinoma (cSCC) is a frequent non-melanoma skin cancer that originates from keratinocytes with increased prevalence. cSCC can be either in situ, as in Bowen's disease, or extended. Advanced age, accumulated sun exposure, light pigmentation, and prior skin cancer diagnosis are all significant risk factors for cSCC.

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A novel oncolytic Vaccinia virus armed with IL-12 augments antitumor immune responses leading to durable regression in murine models of lung cancer.

Front Immunol

January 2025

Sino-British Research Centre for Molecular Oncology, National Centre for International Research in Cell and Gene Therapy, School of Basic Medical Sciences, Academy of Medical Sciences, Zhengzhou University, Zhengzhou, China.

Oncolytic vaccinia viruses (VVs) are potent stimulators of the immune system and induce immune-mediated tumor clearance and long-term surveillance against tumor recurrence. As such they are ideal treatment modalities for solid tumors including lung cancer. Here, we investigated the use of VVL-m12, a next-generation, genetically modified, interleukin-12 (IL-12)-armed VV, as a new therapeutic strategy to treat murine models of lung cancer and as a mechanism of increasing lung cancer sensitivity to antibody against programmed cell death protein 1 (α-PD1) therapy.

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Background: Nocardia infections are rare infections in immunocompetent patients and occur mostly in immunocompromised individuals. Usually, nocardia affects skin, brain, and lungs, but in disseminated forms, which occurred mostly in immunocompromised patients, it can involve every organ. Nocardia sinusitis is extremely rare as our searches returned only a very few related studies.

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Background: Immune checkpoint inhibitors have revolutionized cancer therapy, but many patients fail to respond or develop resistance, often due to reduced T cell activity. Costimulation via 4-1BB has emerged as a promising approach to enhance the effector function of antigen-primed T cells. Bispecific T cell-engaging (TCE) antibodies are an effective way to provide tumor-specific T cell receptor-mediated signaling to tumor-infiltrating lymphocytes.

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Background: Metabolic syndrome represents a pancreatic ductal adenocarcinoma (PDAC) risk factor. Metabolic alterations favor PDAC onset, which occurs early upon dysmetabolism. Pancreatic neoplastic lesions evolve within a dense desmoplastic stroma, consisting in abundant extracellular matrix settled by cancer associated fibroblasts (CAFs).

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