{"title":"在新发现的婴儿白血病细胞系和ACIN1::NUTM1诱导模型中,ACIN1::NUTM1融合调控的特征基因表达谱","authors":"Minori Tamai, Chiaki Komatsu, Keiko Kagami, Shin Kasai, Atsushi Watanabe, Koshi Akahane, Kumiko Goi, Chihiro Tomoyasu, Toshihiko Imamura, Satoshi Oguri, Sumio Iwasaki, Takanori Teshima, Yasushi Yatabe, Takeshi Inukai","doi":"10.1111/bjh.70130","DOIUrl":null,"url":null,"abstract":"<p><p>NUTM1-rearranged (NUTM1-R) infant acute lymphoblastic leukaemia (ALL) is a newly identified subgroup of non-KMT2A-R infant ALL, with ACIN1::NUTM1 the most frequent fusion. KMT2A-R and NUTM1-R infant ALL are characterized by fewer copy number alterations. Moreover, the gene expression profile in NUTM1-R infant ALL characteristically reveals upregulation of the genes that are involved in KMT2A-R infant ALL development, including HOXA9 and HOXA10. However, the direct association of NUTM1-fusion with this gene expression remains unexplored. Clinically, in sharp contrast to KMT2A-R infant ALL, the prognosis of NUTM1-R infant ALL is excellent, although its drug sensitivity profile remains unclear. Here, we newly identified an ACIN1::NUTM1-positive ALL cell line, KOPN32, which was previously established from a relapsed infant-ALL case, as the only cell line with NUTM1-fusion. KOPN32 had fewer copy number alterations, like KMT2A-R ALL cell lines. Both KOPN32 and an ACIN1::NUTM1-inducible ALL model, which was established using the ACIN1::NUTM1 fusion cDNA subcloned from KOPN32, revealed upregulation of HOXA9, HOXA10, SKIDA1 and BMI1, indicating direct involvement of ACIN1::NUTM1 fusion in the upregulation of these genes. In the drug sensitivity to eight standard agents, KOPN32 showed high sensitivity to both daunorubicin and vincristine; both are crucial agents in the induction therapy for infant ALL.</p>","PeriodicalId":135,"journal":{"name":"British Journal of Haematology","volume":" ","pages":""},"PeriodicalIF":3.8000,"publicationDate":"2025-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"A characteristic gene expression profile regulated by ACIN1::NUTM1 fusion in a newly identified infant leukaemic cell line and an ACIN1::NUTM1-inducible model.\",\"authors\":\"Minori Tamai, Chiaki Komatsu, Keiko Kagami, Shin Kasai, Atsushi Watanabe, Koshi Akahane, Kumiko Goi, Chihiro Tomoyasu, Toshihiko Imamura, Satoshi Oguri, Sumio Iwasaki, Takanori Teshima, Yasushi Yatabe, Takeshi Inukai\",\"doi\":\"10.1111/bjh.70130\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>NUTM1-rearranged (NUTM1-R) infant acute lymphoblastic leukaemia (ALL) is a newly identified subgroup of non-KMT2A-R infant ALL, with ACIN1::NUTM1 the most frequent fusion. KMT2A-R and NUTM1-R infant ALL are characterized by fewer copy number alterations. Moreover, the gene expression profile in NUTM1-R infant ALL characteristically reveals upregulation of the genes that are involved in KMT2A-R infant ALL development, including HOXA9 and HOXA10. However, the direct association of NUTM1-fusion with this gene expression remains unexplored. Clinically, in sharp contrast to KMT2A-R infant ALL, the prognosis of NUTM1-R infant ALL is excellent, although its drug sensitivity profile remains unclear. Here, we newly identified an ACIN1::NUTM1-positive ALL cell line, KOPN32, which was previously established from a relapsed infant-ALL case, as the only cell line with NUTM1-fusion. KOPN32 had fewer copy number alterations, like KMT2A-R ALL cell lines. Both KOPN32 and an ACIN1::NUTM1-inducible ALL model, which was established using the ACIN1::NUTM1 fusion cDNA subcloned from KOPN32, revealed upregulation of HOXA9, HOXA10, SKIDA1 and BMI1, indicating direct involvement of ACIN1::NUTM1 fusion in the upregulation of these genes. In the drug sensitivity to eight standard agents, KOPN32 showed high sensitivity to both daunorubicin and vincristine; both are crucial agents in the induction therapy for infant ALL.</p>\",\"PeriodicalId\":135,\"journal\":{\"name\":\"British Journal of Haematology\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":3.8000,\"publicationDate\":\"2025-08-29\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"British Journal of Haematology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1111/bjh.70130\",\"RegionNum\":2,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"HEMATOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"British Journal of Haematology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1111/bjh.70130","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"HEMATOLOGY","Score":null,"Total":0}
A characteristic gene expression profile regulated by ACIN1::NUTM1 fusion in a newly identified infant leukaemic cell line and an ACIN1::NUTM1-inducible model.
NUTM1-rearranged (NUTM1-R) infant acute lymphoblastic leukaemia (ALL) is a newly identified subgroup of non-KMT2A-R infant ALL, with ACIN1::NUTM1 the most frequent fusion. KMT2A-R and NUTM1-R infant ALL are characterized by fewer copy number alterations. Moreover, the gene expression profile in NUTM1-R infant ALL characteristically reveals upregulation of the genes that are involved in KMT2A-R infant ALL development, including HOXA9 and HOXA10. However, the direct association of NUTM1-fusion with this gene expression remains unexplored. Clinically, in sharp contrast to KMT2A-R infant ALL, the prognosis of NUTM1-R infant ALL is excellent, although its drug sensitivity profile remains unclear. Here, we newly identified an ACIN1::NUTM1-positive ALL cell line, KOPN32, which was previously established from a relapsed infant-ALL case, as the only cell line with NUTM1-fusion. KOPN32 had fewer copy number alterations, like KMT2A-R ALL cell lines. Both KOPN32 and an ACIN1::NUTM1-inducible ALL model, which was established using the ACIN1::NUTM1 fusion cDNA subcloned from KOPN32, revealed upregulation of HOXA9, HOXA10, SKIDA1 and BMI1, indicating direct involvement of ACIN1::NUTM1 fusion in the upregulation of these genes. In the drug sensitivity to eight standard agents, KOPN32 showed high sensitivity to both daunorubicin and vincristine; both are crucial agents in the induction therapy for infant ALL.
期刊介绍:
The British Journal of Haematology publishes original research papers in clinical, laboratory and experimental haematology. The Journal also features annotations, reviews, short reports, images in haematology and Letters to the Editor.