Hye-Jung Chung, Sharika Rajan, Zhichao Wu, Christina K. Ferrone, Mark Raffeld, Ina Lee, Jeffrey Gagan, Christopher Dampier, Zied Abdullaev, Manoj Tyagi, Patrick. J. Cimino, Martha Quezado, Kenneth Aldape
{"title":"MYB/MYBL1基因改变的神经胶质瘤经常携带MYB和MYBL1基因的截断和非生产性融合","authors":"Hye-Jung Chung, Sharika Rajan, Zhichao Wu, Christina K. Ferrone, Mark Raffeld, Ina Lee, Jeffrey Gagan, Christopher Dampier, Zied Abdullaev, Manoj Tyagi, Patrick. J. Cimino, Martha Quezado, Kenneth Aldape","doi":"10.1007/s00401-024-02803-0","DOIUrl":null,"url":null,"abstract":"<div><p>Astrocytomas that harbor recurrent genomic alterations in <i>MYB</i> or <i>MYBL1</i> are a group of Pediatric-type diffuse low-grade gliomas that were newly recognized in the 2021 WHO Classification of Tumors of the Central Nervous System. These tumors are described in the WHO classification as harboring fusions in <i>MYB</i> or <i>MYBL1</i>. In this report, we examine 14 consecutive cases in which a <i>MYB</i> or <i>MYBL1</i> alteration was identified, each with diagnostic confirmation by genome-wide DNA methylation profiling (6 Angiocentric gliomas and 8 Diffuse astrocytomas, <i>MYB-</i> or <i>MYBL1</i>-altered), for their specific genomic alterations in these genes. Using RNA sequencing, we find productive in-frame fusions of the <i>MYB</i> or <i>MYBL1</i> genes in only 5/14 cases. The remaining 9 cases show genomic alterations that result in truncation of the gene, without evidence of an in-frame fusion partner. Gene expression analysis showed overexpression of the <i>MYB</i>(<i>L1</i>) genes, regardless of the presence of a productive fusion. In addition, <i>QKI,</i> a recognized fusion partner common in angiocentric glioma, was generally up-regulated in these 14 cases, compared to a cohort comprising >1000 CNS tumors of various types, regardless of whether a genomic alteration in <i>QKI</i> was present. Overall, the results show that truncations, in the absence of a productive fusion, of the <i>MYB</i>(<i>L1</i>) genes can likely drive the tumors and have implications for the analysis and diagnosis of Angiocentric glioma and Diffuse astrocytoma, <i>MYB-</i> or <i>MYBL1</i>-altered, especially for cases that are tested on panels designed to focus on fusion detection.</p></div>","PeriodicalId":7012,"journal":{"name":"Acta Neuropathologica","volume":"148 1","pages":""},"PeriodicalIF":9.3000,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s00401-024-02803-0.pdf","citationCount":"0","resultStr":"{\"title\":\"MYB/MYBL1-altered gliomas frequently harbor truncations and non-productive fusions in the MYB and MYBL1 genes\",\"authors\":\"Hye-Jung Chung, Sharika Rajan, Zhichao Wu, Christina K. Ferrone, Mark Raffeld, Ina Lee, Jeffrey Gagan, Christopher Dampier, Zied Abdullaev, Manoj Tyagi, Patrick. J. Cimino, Martha Quezado, Kenneth Aldape\",\"doi\":\"10.1007/s00401-024-02803-0\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p>Astrocytomas that harbor recurrent genomic alterations in <i>MYB</i> or <i>MYBL1</i> are a group of Pediatric-type diffuse low-grade gliomas that were newly recognized in the 2021 WHO Classification of Tumors of the Central Nervous System. These tumors are described in the WHO classification as harboring fusions in <i>MYB</i> or <i>MYBL1</i>. In this report, we examine 14 consecutive cases in which a <i>MYB</i> or <i>MYBL1</i> alteration was identified, each with diagnostic confirmation by genome-wide DNA methylation profiling (6 Angiocentric gliomas and 8 Diffuse astrocytomas, <i>MYB-</i> or <i>MYBL1</i>-altered), for their specific genomic alterations in these genes. Using RNA sequencing, we find productive in-frame fusions of the <i>MYB</i> or <i>MYBL1</i> genes in only 5/14 cases. The remaining 9 cases show genomic alterations that result in truncation of the gene, without evidence of an in-frame fusion partner. Gene expression analysis showed overexpression of the <i>MYB</i>(<i>L1</i>) genes, regardless of the presence of a productive fusion. In addition, <i>QKI,</i> a recognized fusion partner common in angiocentric glioma, was generally up-regulated in these 14 cases, compared to a cohort comprising >1000 CNS tumors of various types, regardless of whether a genomic alteration in <i>QKI</i> was present. Overall, the results show that truncations, in the absence of a productive fusion, of the <i>MYB</i>(<i>L1</i>) genes can likely drive the tumors and have implications for the analysis and diagnosis of Angiocentric glioma and Diffuse astrocytoma, <i>MYB-</i> or <i>MYBL1</i>-altered, especially for cases that are tested on panels designed to focus on fusion detection.</p></div>\",\"PeriodicalId\":7012,\"journal\":{\"name\":\"Acta Neuropathologica\",\"volume\":\"148 1\",\"pages\":\"\"},\"PeriodicalIF\":9.3000,\"publicationDate\":\"2024-10-18\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://link.springer.com/content/pdf/10.1007/s00401-024-02803-0.pdf\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Acta Neuropathologica\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://link.springer.com/article/10.1007/s00401-024-02803-0\",\"RegionNum\":1,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"CLINICAL NEUROLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Acta Neuropathologica","FirstCategoryId":"3","ListUrlMain":"https://link.springer.com/article/10.1007/s00401-024-02803-0","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CLINICAL NEUROLOGY","Score":null,"Total":0}
MYB/MYBL1-altered gliomas frequently harbor truncations and non-productive fusions in the MYB and MYBL1 genes
Astrocytomas that harbor recurrent genomic alterations in MYB or MYBL1 are a group of Pediatric-type diffuse low-grade gliomas that were newly recognized in the 2021 WHO Classification of Tumors of the Central Nervous System. These tumors are described in the WHO classification as harboring fusions in MYB or MYBL1. In this report, we examine 14 consecutive cases in which a MYB or MYBL1 alteration was identified, each with diagnostic confirmation by genome-wide DNA methylation profiling (6 Angiocentric gliomas and 8 Diffuse astrocytomas, MYB- or MYBL1-altered), for their specific genomic alterations in these genes. Using RNA sequencing, we find productive in-frame fusions of the MYB or MYBL1 genes in only 5/14 cases. The remaining 9 cases show genomic alterations that result in truncation of the gene, without evidence of an in-frame fusion partner. Gene expression analysis showed overexpression of the MYB(L1) genes, regardless of the presence of a productive fusion. In addition, QKI, a recognized fusion partner common in angiocentric glioma, was generally up-regulated in these 14 cases, compared to a cohort comprising >1000 CNS tumors of various types, regardless of whether a genomic alteration in QKI was present. Overall, the results show that truncations, in the absence of a productive fusion, of the MYB(L1) genes can likely drive the tumors and have implications for the analysis and diagnosis of Angiocentric glioma and Diffuse astrocytoma, MYB- or MYBL1-altered, especially for cases that are tested on panels designed to focus on fusion detection.
期刊介绍:
Acta Neuropathologica publishes top-quality papers on the pathology of neurological diseases and experimental studies on molecular and cellular mechanisms using in vitro and in vivo models, ideally validated by analysis of human tissues. The journal accepts Original Papers, Review Articles, Case Reports, and Scientific Correspondence (Letters). Manuscripts must adhere to ethical standards, including review by appropriate ethics committees for human studies and compliance with principles of laboratory animal care for animal experiments. Failure to comply may result in rejection of the manuscript, and authors are responsible for ensuring accuracy and adherence to these requirements.