Ariane Huang, Sofia R Beer, Christopher A Eide, Brian J Druker, Jeffrey W Tyner, Jessica Leonard, Cristina E Tognon
{"title":"确定ZMYM2: FGFR1融合阳性白血病的药物联合策略","authors":"Ariane Huang, Sofia R Beer, Christopher A Eide, Brian J Druker, Jeffrey W Tyner, Jessica Leonard, Cristina E Tognon","doi":"10.1080/28354311.2025.2530229","DOIUrl":null,"url":null,"abstract":"<p><p>Myeloid/lymphoid neoplasms with eosinophilia and tyrosine kinase gene fusions (MLN-TK) are a class of fusion protein-driven, poor prognosis leukemias. Leukemias harboring FGFR1 fusions have previously been referred to as 8p11.2 myeloproliferative syndrome (EMS) or stem cell leukemia/lymphoma (SCLL) and are currently referred to as Myeloid/lymphoid neoplasms with FGFR1 rearrangement based on the most recent WHO classification system. To identify new therapeutic options for MLN-TK patients, we evaluated clinical and <i>ex vivo</i> drug response data from a <i>ZMYM2:FGFR1</i>-positive patient who was successfully treated with FGFR kinase-targeting inhibitors. After initially responding to ponatinib, the patient was switched to pemigatinib which eventually transitioned them to a successful transplant. Leukemia cells isolated from the patient exhibited ex vivo sensitivity to ponatinib, bortezomib and axitinib. ZMYM2:FGFR1-transformed Ba/F3 cells were exquisitely sensitive to next generation FGFR inhibitors, and combinations of FGFRi plus trametinib or midostaurin were found to be synergistic, suggesting novel therapeutic options for FGFR1-fusion positive patients.</p>","PeriodicalId":521021,"journal":{"name":"Precision oncogenomics","volume":" ","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12379768/pdf/","citationCount":"0","resultStr":"{\"title\":\"Identifying Drug Combination Strategies for <i>ZMYM2: FGFR1</i> Fusion Positive Leukemia.\",\"authors\":\"Ariane Huang, Sofia R Beer, Christopher A Eide, Brian J Druker, Jeffrey W Tyner, Jessica Leonard, Cristina E Tognon\",\"doi\":\"10.1080/28354311.2025.2530229\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Myeloid/lymphoid neoplasms with eosinophilia and tyrosine kinase gene fusions (MLN-TK) are a class of fusion protein-driven, poor prognosis leukemias. Leukemias harboring FGFR1 fusions have previously been referred to as 8p11.2 myeloproliferative syndrome (EMS) or stem cell leukemia/lymphoma (SCLL) and are currently referred to as Myeloid/lymphoid neoplasms with FGFR1 rearrangement based on the most recent WHO classification system. To identify new therapeutic options for MLN-TK patients, we evaluated clinical and <i>ex vivo</i> drug response data from a <i>ZMYM2:FGFR1</i>-positive patient who was successfully treated with FGFR kinase-targeting inhibitors. After initially responding to ponatinib, the patient was switched to pemigatinib which eventually transitioned them to a successful transplant. Leukemia cells isolated from the patient exhibited ex vivo sensitivity to ponatinib, bortezomib and axitinib. ZMYM2:FGFR1-transformed Ba/F3 cells were exquisitely sensitive to next generation FGFR inhibitors, and combinations of FGFRi plus trametinib or midostaurin were found to be synergistic, suggesting novel therapeutic options for FGFR1-fusion positive patients.</p>\",\"PeriodicalId\":521021,\"journal\":{\"name\":\"Precision oncogenomics\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2025-07-16\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12379768/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Precision oncogenomics\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1080/28354311.2025.2530229\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Precision oncogenomics","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1080/28354311.2025.2530229","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Identifying Drug Combination Strategies for ZMYM2: FGFR1 Fusion Positive Leukemia.
Myeloid/lymphoid neoplasms with eosinophilia and tyrosine kinase gene fusions (MLN-TK) are a class of fusion protein-driven, poor prognosis leukemias. Leukemias harboring FGFR1 fusions have previously been referred to as 8p11.2 myeloproliferative syndrome (EMS) or stem cell leukemia/lymphoma (SCLL) and are currently referred to as Myeloid/lymphoid neoplasms with FGFR1 rearrangement based on the most recent WHO classification system. To identify new therapeutic options for MLN-TK patients, we evaluated clinical and ex vivo drug response data from a ZMYM2:FGFR1-positive patient who was successfully treated with FGFR kinase-targeting inhibitors. After initially responding to ponatinib, the patient was switched to pemigatinib which eventually transitioned them to a successful transplant. Leukemia cells isolated from the patient exhibited ex vivo sensitivity to ponatinib, bortezomib and axitinib. ZMYM2:FGFR1-transformed Ba/F3 cells were exquisitely sensitive to next generation FGFR inhibitors, and combinations of FGFRi plus trametinib or midostaurin were found to be synergistic, suggesting novel therapeutic options for FGFR1-fusion positive patients.