Elena Anghileri, Evelina Miele, Sara Patrizi, Sabina Barresi, Elisabetta Lazzarini, Luisa Maddaloni, Monica Patanè, Lucia Pedace, Rosina Paterra, Antonio Silvani, Franco Locatelli, Stefano Indraccolo, Bianca Pollo
{"title":"胶质母细胞瘤长期幸存者独特的遗传和表观遗传改变:来自两个临床病例的见解","authors":"Elena Anghileri, Evelina Miele, Sara Patrizi, Sabina Barresi, Elisabetta Lazzarini, Luisa Maddaloni, Monica Patanè, Lucia Pedace, Rosina Paterra, Antonio Silvani, Franco Locatelli, Stefano Indraccolo, Bianca Pollo","doi":"10.1111/jcmm.70771","DOIUrl":null,"url":null,"abstract":"<p>The biological mechanisms driving the long survival in glioblastoma (GBM). Five-year long-term survival (LTS) and 10-year survival very long-term survival (VLTS) remain significantly understudied. Here we molecularly detailed two cases. AR10-046 (VLTS) was affected by a giant cell-GBM, classified as the pedHGG_RTK1a subtype according to the v12.5 Heidelberg brain tumor methylation classifier. Somatic and germline MSH6 mutations, typically in Lynch syndrome, and high tumour mutational burden were detected. The copy number variation plots showed chromosome 1q gain and chromosome 13 loss with no other typical GBM alterations. AR10-037 (LTS) suffered from a classical GBM, identified as pedHGG_MYCN subclass. Apart from the canonical chromosome 7 gain and chromosome 10q loss, we observed MDM2 gene amplification and possible rearrangements on chromosome 12 and 18 with the typical aspect of chromothripsis, harbouring two putative new gene fusions: CPSF6::CPM and PTPRR::RAB3IP. We described two patients with peculiar tumour molecular profile, widening the scenario of clinical and molecular variability in such patients.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 20","pages":""},"PeriodicalIF":4.2000,"publicationDate":"2025-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.70771","citationCount":"0","resultStr":"{\"title\":\"Unique Genetic and Epigenetic Alterations in Glioblastoma Long-Term Survivors: Insights From Two Clinical Cases\",\"authors\":\"Elena Anghileri, Evelina Miele, Sara Patrizi, Sabina Barresi, Elisabetta Lazzarini, Luisa Maddaloni, Monica Patanè, Lucia Pedace, Rosina Paterra, Antonio Silvani, Franco Locatelli, Stefano Indraccolo, Bianca Pollo\",\"doi\":\"10.1111/jcmm.70771\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p>The biological mechanisms driving the long survival in glioblastoma (GBM). Five-year long-term survival (LTS) and 10-year survival very long-term survival (VLTS) remain significantly understudied. Here we molecularly detailed two cases. AR10-046 (VLTS) was affected by a giant cell-GBM, classified as the pedHGG_RTK1a subtype according to the v12.5 Heidelberg brain tumor methylation classifier. Somatic and germline MSH6 mutations, typically in Lynch syndrome, and high tumour mutational burden were detected. The copy number variation plots showed chromosome 1q gain and chromosome 13 loss with no other typical GBM alterations. AR10-037 (LTS) suffered from a classical GBM, identified as pedHGG_MYCN subclass. Apart from the canonical chromosome 7 gain and chromosome 10q loss, we observed MDM2 gene amplification and possible rearrangements on chromosome 12 and 18 with the typical aspect of chromothripsis, harbouring two putative new gene fusions: CPSF6::CPM and PTPRR::RAB3IP. We described two patients with peculiar tumour molecular profile, widening the scenario of clinical and molecular variability in such patients.</p>\",\"PeriodicalId\":101321,\"journal\":{\"name\":\"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE\",\"volume\":\"29 20\",\"pages\":\"\"},\"PeriodicalIF\":4.2000,\"publicationDate\":\"2025-10-14\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.70771\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://onlinelibrary.wiley.com/doi/10.1111/jcmm.70771\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","FirstCategoryId":"1085","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1111/jcmm.70771","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Unique Genetic and Epigenetic Alterations in Glioblastoma Long-Term Survivors: Insights From Two Clinical Cases
The biological mechanisms driving the long survival in glioblastoma (GBM). Five-year long-term survival (LTS) and 10-year survival very long-term survival (VLTS) remain significantly understudied. Here we molecularly detailed two cases. AR10-046 (VLTS) was affected by a giant cell-GBM, classified as the pedHGG_RTK1a subtype according to the v12.5 Heidelberg brain tumor methylation classifier. Somatic and germline MSH6 mutations, typically in Lynch syndrome, and high tumour mutational burden were detected. The copy number variation plots showed chromosome 1q gain and chromosome 13 loss with no other typical GBM alterations. AR10-037 (LTS) suffered from a classical GBM, identified as pedHGG_MYCN subclass. Apart from the canonical chromosome 7 gain and chromosome 10q loss, we observed MDM2 gene amplification and possible rearrangements on chromosome 12 and 18 with the typical aspect of chromothripsis, harbouring two putative new gene fusions: CPSF6::CPM and PTPRR::RAB3IP. We described two patients with peculiar tumour molecular profile, widening the scenario of clinical and molecular variability in such patients.
期刊介绍:
The Journal of Cellular and Molecular Medicine serves as a bridge between physiology and cellular medicine, as well as molecular biology and molecular therapeutics. With a 20-year history, the journal adopts an interdisciplinary approach to showcase innovative discoveries.
It publishes research aimed at advancing the collective understanding of the cellular and molecular mechanisms underlying diseases. The journal emphasizes translational studies that translate this knowledge into therapeutic strategies. Being fully open access, the journal is accessible to all readers.