Cellular and molecular aspects of myeloproliferative neoplasms. Part B /
Clasificación: | Libro Electrónico |
---|---|
Otros Autores: | , |
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