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ArticleVolume 38, Issue 8p1599-1617.e8Open access Affiliations & Notes 1University of Michigan, Department of Molecular & Integrative Physiology, Ann Arbor, MI, United States of America 2University of Michigan, Department of Biological Chemistry, Ann Arbor, MI, United States of America 3University of Michigan, Program in Cellular and Molecular Biology, Ann Arbor, MI, United States of America 4Medical Scientist Training Program, University of Michigan, Ann Arbor, MI, 48109, United States of...
Abstract Chromosome instability is highly prevalent in cancer and drives large-scale chromosomal imbalances, known as aneuploidies1,2,3,4. How aneuploidy contributes to tumorigenesis remains difficult to study due to the vast numbers of genes affected. Here we established a CRISPR knockout- and activation-linked assay (CRISPR-KOALA), enabling high-throughput bidirectional genetic screens in immunocompetent mouse models of cancer.
Abstract Acinar-to-ductal metaplasia (ADM) is a reversible cell state that facilitates pancreas repair following injury. Oncogenic KRAS mutations can progress ADM to pancreatic intraepithelial neoplasia (PanIN) and pancreatic ductal adenocarcinoma (PDAC). However, the metabolic alterations in these precancerous lesions are understudied. Here, we identify global changes in central carbon metabolism genes and metabolites during ADM formation.
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