{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T08:53:28Z","timestamp":1790931208339,"version":"4.1.0"},"reference-count":38,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2026,6,26]],"date-time":"2026-06-26T00:00:00Z","timestamp":1782432000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"},{"start":{"date-parts":[[2026,6,26]],"date-time":"2026-06-26T00:00:00Z","timestamp":1782432000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Cancer Science"],"published-print":{"date-parts":[[2026,10]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Loss of SMARCB1\/INI1 expression is a common feature of various types of tumors including malignant rhabdoid tumor, an aggressive cancer of children. Because SMARCB1\/INI1 deficiency leads to genome\u2010wide transcriptional dysregulation, identifying a specific therapeutic target that acts on a wide range of SMARCB1\/INI1\u2010deficient tumors has been challenging. This study aimed to establish if the personalized selection of effective drugs against SMARCB1\/INI\u2010deficient tumors is possible by in\u00a0vitro drug sensitivity profiling. The in\u00a0vitro drug sensitivity profiles of tumors from SMARCB1\/INI1\u2010deficient tumor cell line\u2013derived mouse xenograft (CDX) models were evaluated by a short\u2010term collagen gel\u2013embedded three\u2010dimensional culture\u2013drug sensitivity test (3D\u2010DST). With the 3D\u2010DST, molecular targeting drugs, including inhibitors of aurora B kinase, mammalian target of rapamycin, mitogen\u2010activated protein kinase, WNT\/\u03b2\u2010catenin, or mouse double minute 2 homolog (MDM2), were selected as therapeutic drug candidates in SMARCB1\/INI1\u2010deficient tumors. A CDX tumor, which was resistant to MDM2 inhibitors in the 3D\u2010DST, expressed lower\n                    <jats:italic>TP53<\/jats:italic>\n                    compared to an MDM2 inhibitor\u2013sensitive tumor. In cultured cell lines, exposure to MI\u2010773, a MDM2 inhibitor, disturbed the expression of a significant number of genes and induced p21 protein expression in MDM2 inhibitor\u2013sensitive cells. However, such changes were not observed in resistant cells. These results suggest that 3D\u2010DST can predict biologically relevant drug sensitivity profiles in SMARCB1\/INI1\u2010deficient tumors.\n                  <\/jats:p>","DOI":"10.1111\/cas.70451","type":"journal-article","created":{"date-parts":[[2026,6,26]],"date-time":"2026-06-26T09:51:51Z","timestamp":1782467511000},"page":"2852-2862","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["A Three\u2010Dimensional Culture\u2013Drug Sensitivity Test Predicts\n                    <scp>MDM2<\/scp>\n                    Inhibitor\u2013Sensitivity in\n                    <scp>SMARCB1<\/scp>\n                    \/\n                    <scp>INI1<\/scp>\n                    \u2010Deficient Tumors"],"prefix":"10.1111","volume":"117","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6737-1509","authenticated-orcid":false,"given":"Hiroaki","family":"Goto","sequence":"first","affiliation":[{"name":"Division of 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