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Cancer cells restrict immunogenicity of retrotransposon expression via distinct mechanisms.
Immunity
December 2024
Halvorsen Center for Computational Oncology, Department of Epidemiology and Biostatistics, Memorial Sloan Kettering Cancer Center, New York, NY, USA; Physiology, Biophysics & Systems Biology, Weill Cornell Medicine, New York, NY, USA. Electronic address:
To thrive, cancer cells must navigate acute inflammatory signaling accompanying oncogenic transformation, such as via overexpression of repeat elements. We examined the relationship between immunostimulatory repeat expression, tumor evolution, and the tumor-immune microenvironment. Integration of multimodal data from a cohort of pancreatic ductal adenocarcinoma (PDAC) patients revealed expression of specific Alu repeats predicted to form double-stranded RNAs (dsRNAs) and trigger retinoic-acid-inducible gene I (RIG-I)-like-receptor (RLR)-associated type-I interferon (IFN) signaling.
View Article and Find Full Text PDFCTLA4 blockade abrogates KEAP1/STK11-related resistance to PD-(L)1 inhibitors.
Nature
November 2024
Department of Thoracic and Head and Neck Medical Oncology, University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Article Synopsis
- Dual immune checkpoint blockade (ICB) using CTLA4 and PD-(L)1 inhibitors shows improved anti-tumor effectiveness and immune toxicity compared to PD-(L)1 inhibitors alone in advanced non-small-cell lung cancer (NSCLC) patients.
- Patients with mutations in STK11 and/or KEAP1 genes benefit more from the combination treatment compared to those receiving only PD-(L)1 inhibitors, as shown in the POSEIDON trial.
- The loss of KEAP1 serves as a strong predictor for the success of dual ICB, as it leads to a more favorable outcome by changing the tumor's immune environment to better engage CD4 and CD8 T cells for anti-tumor activity. *
The investigation of SNP in SOCS2 gene and its effect on milk yield, fat, protein, and somatic cell count in Awassi ewes.
Trop Anim Health Prod
September 2024
Tarım Bilimleri ve Teknolojileri Fakültesi, Hayvansal Üretim ve Teknolojileri Bölümü, Niğde Ömer Halisdemir Üniversitesi, 12345, Niğde, Türkiye.
Background: Livestock farmers face financial losses every year because milk yield and components are severely affected by udder diseases. These udder infections attract the immune response from the host and lead to the influx of neutrophils into milk to fight infection and thus the number of somatic cell count (SCC) is increased. The SCC value of milk could be used as an important indicator in detecting clinical mastitis in dairy animals.
View Article and Find Full Text PDFTwo Distinct Characteristics of Immune Microenvironment in Human Hepatocellular Carcinoma with Wnt/β-Catenin Mutations.
Liver Cancer
June 2024
Department of Gastroenterology and Hepatology, Kindai University Faculty of Medicine, Osakasayama, Japan.
Introduction: Immunotherapy is becoming a promising approach for unresectable-hepatocellular carcinoma (HCC); the anti-tumor response is affected by the tumor microenvironment (TME). Although Wnt/β-catenin mutations are reported to cause non-inflamed phenotype, their role on TME remains controversial. We aimed to clarify the heterogeneity of immunophenotype in HCC with Wnt/β-catenin mutations.
View Article and Find Full Text PDFKSR1 Knockout Mouse Model Demonstrates MAPK Pathway's Key Role in Cisplatin- and Noise-induced Hearing Loss.
J Neurosci
May 2024
Departments of Pharmacology and Neuroscience, Creighton University, Omaha, Nebraska 68178
Hearing loss is a major disability in everyday life and therapeutic interventions to protect hearing would benefit a large portion of the world population. Here we found that mice devoid of the protein kinase suppressor of RAS 1 (KSR1) in their tissues (germline KO mice) exhibit resistance to both cisplatin- and noise-induced permanent hearing loss compared with their wild-type KSR1 littermates. KSR1 is a scaffold protein that brings in proximity the mitogen-activated protein kinase (MAPK) proteins BRAF, MEK1/2 and ERK1/2 and assists in their activation through a phosphorylation cascade induced by both cisplatin and noise insults in the cochlear cells.
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