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While syngeneic mouse models are commonly used for preclinical validation of these therapeutics, the lack of genetically characterized murine cell lines adds uncertainty to the study of drug\u2010gene interactions in these models. We previously generated a novel murine cell line, A52, from a diethylnitrosamine (DEN)\u2010induced adiponectin\u2010knockout mouse model. Here, we present a comprehensive genomic and transcriptomic characterization of the A52 cell line.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>A52 cells were grown in various culture medium compositions to investigate robustness to simple media. Whole\u2010genome sequencing (WGS) and RNAseq were performed on A52 cells from both cell culture and syngeneic tumor tissue, as well as a reference cell line representing non\u2010tumor cells, AML\u201012.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      A52 was found to show robust growth in all medium compositions. Substantial chromosomal instability was observed in A52, including trisomy 15 and notable amplifications of oncogenic loci such as\n                      <jats:italic>Myc<\/jats:italic>\n                      and\n                      <jats:italic>Cd274<\/jats:italic>\n                      (PDL\u20101), alongside frequent small variants and structural rearrangements. Notably, the cell line harbors the common HCC driver\n                      <jats:italic>Braf<\/jats:italic>\n                      V584E mutation, and a novel\n                      <jats:italic>Plk1<\/jats:italic>\n                      p.R364W variant predicted as a driver mutation. Transcriptomic profiling defined a distinct \u201cA52 gene signature\u201d enriched in EGFR\u2010ERBB signaling and cell migration pathways. Integrative analyses demonstrated that the A52 gene signature aligns closely with a subset of human HCC lacking CTNNB1 mutations.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>This study provides a critical genetic resource, facilitating more precise preclinical modeling and therapeutic validation in HCC.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/ame2.70152","type":"journal-article","created":{"date-parts":[[2026,3,8]],"date-time":"2026-03-08T16:58:50Z","timestamp":1772989130000},"page":"546-557","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Molecular characterization of the\n                    <scp>A52<\/scp>\n                    murine hepatocellular carcinoma cell 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