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Cellular and molecular aspects of myeloproliferative neoplasms. Part B /

Detalles Bibliográficos
Clasificación:Libro Electrónico
Otros Autores: Bartalucci, Niccol�o, Galluzzi, Lorenzo
Formato: Electrónico eBook
Idioma:Inglés
Publicado: [Place of publication not identified] : Academic Press, 2022.
Colección:International review of cell and molecular biology ; 366.
Temas:
Acceso en línea:Texto completo
Tabla de Contenidos:
  • Intro
  • Cellular and Molecular Aspects of Myeloproliferative Neoplasms
  • Part B
  • Copyright
  • Contents
  • Contributors
  • Philadelphia-negative myeloproliferative neoplasms: From origins to new perspectives
  • Acknowledgments
  • Conflict of Interest
  • References
  • Chapter One: The roles of sex and genetics in the MPN
  • 1. Introduction
  • 2. Sex as a factor in MPN epidemiology
  • 3. Biologic basis of sex differences in somatic mutation burden
  • 4. Genetic predisposition to CH and the MPN
  • 5. Heritable risk factors for CH and MPN
  • 5.1. Familial MPN and myeloid malignancy predisposition syndromes
  • 5.2. GWAS identified risk alleles in the general population
  • 6. Inflammation as a risk for CH and MPN
  • 7. Mutation burden and clinical risk
  • 8. Conclusion
  • Funding
  • Conflicts of interest
  • References
  • Chapter Two: Transcriptional configurations of myeloproliferative neoplasms
  • 1. Introduction
  • 2. Studies on the bulk transcriptome of MPN patients
  • 3. From bulk to single cell transcriptomic sequencing of MPN patients
  • 4. Analysis of splicing abnormalities with RNA-seq
  • 5. Analysis of fusion genes in MPN and post-MPN AML patients
  • 6. Concluding remarks and future directions
  • References
  • Chapter Three: Targets in MPNs and potential therapeutics
  • 1. Introduction
  • 2. JAK2 mutations
  • 2.1. Behind JAK2V617F: The molecular background
  • 2.2. JAK2V617F inhibition strategies
  • 2.3. Other JAK inhibitors in MF
  • 2.4. Concerns emerging from JAK2 inhibition in myelofibrosis
  • 3. TPOR/MPL inhibition strategies
  • 4. CALR mutations
  • 4.1. CALR inhibition strategies
  • 4.2. Potential therapies targeting CALR mutants
  • 5. Other targeted therapies
  • 3. Driver mutations and beyond in MPN and leukemic transformation
  • 3.1. Driver mutations
  • 3.2. Non-driver mutations
  • 3.3. Clonal evolution of MPN-BP
  • 3.4. Mutations affecting signal transduction and transcription regulators
  • 3.5. Mutations in epigenetic regulators
  • 3.5.1. Preclinical and clinical studies on combinations targeting epigenetic modifiers
  • 3.6. Mutations in RNA splicing factors
  • 4. Conclusions
  • Acknowledgments
  • Disclosures
  • References
  • Chapter Five: Lessons from mouse models of MPN
  • 1. ``Of mice and Me��n