{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,24]],"date-time":"2026-02-24T12:20:30Z","timestamp":1771935630789,"version":"3.50.1"},"reference-count":64,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,2,16]],"date-time":"2026-02-16T00:00:00Z","timestamp":1771200000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Oncol."],"abstract":"<jats:sec>\n                    <jats:title>Introduction<\/jats:title>\n                    <jats:p>Germ cell tumors (GCTs) are rare neoplasms affecting approximately 3.5% of all pediatric patients, with diverse histological subtypes. Despite their clinical and biological heterogeneity, pediatric GCTs generally exhibit a low mutational burden. Compared to adult GCTs, however, the molecular characterization of pediatric cases remains limited, hindering the development of targeted therapeutic strategies. Therefore, we aimed to elucidate the genomic landscape of pediatric GCT patients via whole exome sequencing (WES).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>WES was performed in 16 pediatric GCTs and respective matched normal samples, including ten ovarian, five testicular, and one mediastinal tumor. The somatic alterations found were described and compared with the clinicopathological characteristics, as well as related to molecular databases.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      The somatic mutations found resemble those observed in adult GCTs and recent pediatric GCTs studies. Genes with predicted oncogenic variants were found in seven samples (43.75%) out of 16 and included\n                      <jats:italic>KIT<\/jats:italic>\n                      (12.5%),\n                      <jats:italic>KRAS<\/jats:italic>\n                      (6.25%),\n                      <jats:italic>MTOR<\/jats:italic>\n                      (12.5%),\n                      <jats:italic>PIK3CA<\/jats:italic>\n                      (6.25%),\n                      <jats:italic>AKT2<\/jats:italic>\n                      (6.25%),\n                      <jats:italic>LARP4B<\/jats:italic>\n                      (6.25%), and\n                      <jats:italic>ACSL6<\/jats:italic>\n                      (6.25%). Copy number alterations were identified on chromosomes 4, 7, 8, 10, 12, 21, and 22, with amplification of\n                      <jats:italic>CDKN1B<\/jats:italic>\n                      ,\n                      <jats:italic>KRAS<\/jats:italic>\n                      ,\n                      <jats:italic>CCND2<\/jats:italic>\n                      ,\n                      <jats:italic>ETV6<\/jats:italic>\n                      , and\n                      <jats:italic>KDM5A<\/jats:italic>\n                      genes, and deletions of\n                      <jats:italic>KIT<\/jats:italic>\n                      and\n                      <jats:italic>PTEN<\/jats:italic>\n                      genes. Clinically significant mutations (\n                      <jats:italic>KIT<\/jats:italic>\n                      : Asp816Val, Ala829Pro; and\n                      <jats:italic>KRAS<\/jats:italic>\n                      : Gln61Leu) suggest potential therapeutic targets for GCT, while\n                      <jats:italic>MTOR<\/jats:italic>\n                      ,\n                      <jats:italic>PIK3CA<\/jats:italic>\n                      , and\n                      <jats:italic>AKT2<\/jats:italic>\n                      emerge as candidates for targeted therapy.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Discussion<\/jats:title>\n                    <jats:p>These findings provide insights into the genomic alterations of pediatric GCTs and emphasize the potential for targeted therapies.<\/jats:p>\n                  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