f03298fecc152cc506fe2316b27ab311 270606.pdf 3f38da9c630feffacae6831882f9e2c950ecec64 270606.pdf b903e3f1a46f28d81afb6311b469e5f9d75ba0f3f9a27d340178bd907344a9bc 270606.pdf Title: Genomic and Epigenomic Landscape of Juvenile Myelomonocytic Leukemia Subject: Juvenile myelomonocytic leukemia (JMML) is a rare myelodysplastic/myeloproliferative neoplasm of early childhood. Most of JMML patients experience an aggressive clinical course of the disease and require hematopoietic stem cell transplantation, which is currently the only curative treatment. JMML is characterized by RAS signaling hyperactivation, which is mainly driven by mutations in one of five genes of the RAS pathway, including PTPN11, KRAS, NRAS, NF1, and CBL. These driving mutations define different disease subtypes with specific clinico-biological features. Secondary mutations affecting other genes inside and outside the RAS pathway contribute to JMML pathogenesis and are associated with a poorer prognosis. In addition to these genetic alterations, JMML commonly presents aberrant epigenetic profiles that strongly correlate with the clinical outcome of the patients. This observation led to the recent publication of an international JMML stratification consensus, which defines three JMML clinical groups based on DNA methylation status. Although the characterization of the genomic and epigenomic landscapes in JMML has significantly contributed to better understand the molecular mechanisms driving the disease, our knowledge on JMML origin, cell identity, and intratumor and interpatient heterogeneity is still scarce. The application of new single-cell sequencing technologies will be critical to address these questions in the future. Keywords: juvenile myelomonocytic leukemia; RAS pathway; DNA methylation; experimental therapeutics Author: Claudia Fiñana, Noel Gómez-Molina, Sandra Alonso-Moreno and Laura Belver Creator: LaTeX with hyperref Producer: pdfTeX-1.40.21 CreationDate: Thu Mar 10 09:08:43 2022 CET ModDate: Thu Mar 10 09:25:58 2022 CET Tagged: no UserProperties: no Suspects: no Form: none JavaScript: no Pages: 20 Encrypted: no Page size: 595.276 x 841.89 pts (A4) Page rot: 0 File size: 1281504 bytes Optimized: no PDF version: 1.7 name type encoding emb sub uni object ID ------------------------------------ ----------------- ---------------- --- --- --- --------- SOZKOC+VnURWPalladioL-Bold Type 1 Custom yes yes no 10 0 LCWQHR+URWPalladioL-Bold Type 1 Custom yes yes no 15 0 QHTFDD+URWPalladioL-Roma Type 1 Custom yes yes no 20 0 CPFMRT+URWPalladioL-Ital Type 1 Custom yes yes no 24 0 MCBCCI+SourceSansRoman-Regular Type 1C Custom yes yes no 32 0 MCBCCM+SourceSansRoman.613wght Type 1C Custom yes yes no 36 0 MCBCCO+SourceSansRoman-Bold Type 1C Custom yes yes no 40 0 LCJEVJ+TimesNewRomanPS-BoldItalicMT Type 1C WinAnsi yes yes no 53 0 SDEUHD+CMSY10 Type 1 Builtin yes yes no 75 0 KMRAPL+VnURWPalladioL Type 1 Custom yes yes no 95 0 VCIXZP+EURM10 Type 1 Builtin yes yes no 114 0 Jhove (Rel. 1.22.1, 2019-04-17) Date: 2023-04-29 02:33:20 CEST RepresentationInformation: 270606.pdf ReportingModule: PDF-hul, Rel. 1.12.1 (2019-04-17) LastModified: 2023-04-28 16:40:05 CEST Size: 1281504 Format: PDF Version: 1.7 Status: Well-Formed and valid SignatureMatches: PDF-hul MIMEtype: application/pdf PDFMetadata: Objects: 656 FreeObjects: 1 IncrementalUpdates: 0 DocumentCatalog: PageLayout: SinglePage PageMode: UseNone Outlines: Item: Title: Introduction Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@44c8afef Item: Title: Genetic Alterations in JMML Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@7b69c6ba Children: Item: Title: PTPN11 Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@46daef40 Item: Title: NRAS and KRAS Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@12f41634 Item: Title: CBL Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@13c27452 Item: Title: NF1 Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@262b2c86 Item: Title: Other Driver Genetic Alterations in the RAS Pathway Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@371a67ec Item: Title: Secondary Genetic Alterations in JMML Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@5ed828d Item: Title: Epigenetic Alterations in JMML Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@50d0686 Children: Item: Title: Early Studies on DNA Methylation in JMML Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@7a3d45bd Item: Title: The JMML Methylation Landscape Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@1e7c7811 Item: Title: DNA Methylation as a Prognostic Tool in JMML Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@77ec78b9 Item: Title: Genetic and Epigenetic Therapeutic Targets for the Treatment of JMML Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@1a3869f4 Children: Item: Title: JMML Therapeutic Targets on Signaling Pathways Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@a38d7a3 Children: Item: Title: RAS Pathway Targeting Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@77f99a05 Item: Title: Targeting of Other Signaling Pathways Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@63440df3 Item: Title: Epigenetic Therapeutic Targets in JMML Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@3aeaafa6 Item: Title: Current Challenges and Future Perspectives in JMML Research Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@76a3e297 Children: Item: Title: JMML Experimental Models Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@4d3167f4 Item: Title: State-of-the-Art Methods to Explore JMML Tumor Origin, Heterogeneity and Evolution Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@ed9d034 Item: Title: Conclusions Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@6121c9d6 Item: Title: References Destination: edu.harvard.hul.ois.jhove.module.pdf.PdfSimpleObject@87f383f Info: Title: Genomic and Epigenomic Landscape of Juvenile Myelomonocytic Leukemia Author: Claudia Fiñana, Noel Gómez-Molina, Sandra Alonso-Moreno and Laura Belver Subject: Juvenile myelomonocytic leukemia (JMML) is a rare myelodysplastic/myeloproliferative neoplasm of early childhood. Most of JMML patients experience an aggressive clinical course of the disease and require hematopoietic stem cell transplantation, which is currently the only curative treatment. JMML is characterized by RAS signaling hyperactivation, which is mainly driven by mutations in one of five genes of the RAS pathway, including PTPN11, KRAS, NRAS, NF1, and CBL. These driving mutations define different disease subtypes with specific clinico-biological features. Secondary mutations affecting other genes inside and outside the RAS pathway contribute to JMML pathogenesis and are associated with a poorer prognosis. In addition to these genetic alterations, JMML commonly presents aberrant epigenetic profiles that strongly correlate with the clinical outcome of the patients. This observation led to the recent publication of an international JMML stratification consensus, which defines three JMML clinical groups based on DNA methylation status. Although the characterization of the genomic and epigenomic landscapes in JMML has significantly contributed to better understand the molecular mechanisms driving the disease, our knowledge on JMML origin, cell identity, and intratumor and interpatient heterogeneity is still scarce. The application of new single-cell sequencing technologies will be critical to address these questions in the future. 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