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| http://dx.doi.org/10.1016/j.immuni.2019.12.008 | DOI Listing |
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Altered chromatin landscape and 3D interactions associated with primary constitutional MLH1 epimutations.
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Hereditary Cancer Group, ONCOBELL Program, Institut d'Investigació Biomèdica de Bellvitge (IDIBELL), L'Hospitalet de Llobregat, Spain.
Background: Lynch syndrome (LS), characterised by an increased risk for cancer, is mainly caused by germline pathogenic variants affecting a mismatch repair gene (MLH1, MSH2, MSH6, PMS2). Occasionally, LS may be caused by constitutional MLH1 epimutation (CME) characterised by soma-wide methylation of one allele of the MLH1 promoter. Most of these are "primary" epimutations, arising de novo without any apparent underlying cis-genetic cause, and are reversible between generations.
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Gastroenterology Department, Shandong Provincial Hospital Affiliated to Shandong First Medical University, No.324 JingwuWeiqi Road, Jinan, Shandong, 250021, China.
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View Article and Find Full Text PDFSpatial transcriptomics reveals unique metabolic profile and key oncogenic regulators of cervical squamous cell carcinoma.
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Tongji Medical College, Maternal and Child Health Hospital of Hubei Province, Huazhong University of Science and Technology, Wuhan, Hubei Province, 430070, China.
Background: As a prevalent and deadly malignant tumor, the treatment outcomes for late-stage patients with cervical squamous cell carcinoma (CSCC) are often suboptimal. Previous studies have shown that tumor progression is closely related with tumor metabolism and microenvironment reshaping, with disruptions in energy metabolism playing a critical role in this process. To delve deeper into the understanding of CSCC development, our research focused on analyzing the tumor microenvironment and metabolic characteristics across different regions of tumor tissue.
View Article and Find Full Text PDFGenetic modulation of RNA splicing rescues BRCA2 function in mutant cells.
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Faculdade de Medicina da Universidade de Lisboa, Lisboa, Portugal
Variants in the hereditary cancer-associated and genes can alter RNA splicing, producing transcripts that encode internally truncated yet potentially functional proteins. However, few studies have quantitatively analyzed variant-specific splicing isoforms. Here, we investigated cells heterozygous and homozygous for the :c.
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