{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\n Recent genomic studies have identified alterations in the gene C10orf53 in distinct cancer types, suggesting that it may represent a novel candidate with potential relevance to tumorigenesis. In an acute myeloid leukemia (AML) cohort analyzed by whole‐genome sequencing, C10orf53 was detected among several novel somatic mutations alongside other genes implicated in leukemogenesis, highlighting it as an emerging factor in the molecular landscape of AML."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": " In a separate study examining sporadic multiple meningiomas, a mutation in C10orf53 was observed in an individual tumor nodule, pointing toward its possible contribution to tumor evolution; however, its precise role—whether as a driver of tumorigenesis or as a passenger mutation—remains to be further elucidated."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": "\n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n Although other cancer genomic investigations (including exome sequencing studies in congenital pouch colon and prostate cancer) did not report alterations in C10orf53, they underscore the value of comprehensive high‐throughput sequencing in uncovering novel genetic alterations that may serve as future diagnostic biomarkers or therapeutic targets. Taken together, these findings advocate for additional functional studies to define the biological role of C10orf53 in oncogenesis and to clarify its potential impact across various malignancies.\n "}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Jae-Woong Min, Youngil Koh, Dae-Yoon Kim, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Identification of Novel Functional Variants of SIN3A and SRSF1 among Somatic Variants in Acute Myeloid Leukemia Patients."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Mol Cells (2018)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.14348/molcells.2018.0051"}], "href": "https://doi.org/10.14348/molcells.2018.0051"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "29764005"}], "href": "https://pubmed.ncbi.nlm.nih.gov/29764005"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Miguel Torres-Martín, M Elena Kusak, Alberto Isla, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Whole exome sequencing in a case of sporadic multiple meningioma reveals shared NF2, FAM109B, and TPRXL mutations, together with unique SMARCB1 alterations in a subset of tumor nodules."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Cancer Genet (2015)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.cancergen.2015.03.012"}], "href": "https://doi.org/10.1016/j.cancergen.2015.03.012"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "25981829"}], "href": "https://pubmed.ncbi.nlm.nih.gov/25981829"}]}]}]}