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Advances in cancer research Volume 131 /
Advances in Cancer Research provides invaluable information on the exciting and fast-moving field of cancer research. Here, once again, outstanding and original reviews are presented on a variety of topics.
| Clasificación: | Libro Electrónico |
|---|---|
| Otros Autores: | , |
| Formato: | Electrónico eBook |
| Idioma: | Inglés |
| Publicado: |
Cambridge, MA :
Academic Press,
2016.
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| Colección: | Advances in Cancer Research
Volume 131 |
| Temas: | |
| Acceso en línea: | Texto completo |
Tabla de Contenidos:
- Front Cover; Advances in Cancer Research; Copyright; Contents; Contributors; Chapter One: The Dual Role of Senescence in Pancreatic Ductal Adenocarcinoma; 1. Introduction; 1.1. Pancreatic Ductal Adenocarcinoma: An Overview; 1.2. The Biological Relevance of Cellular Senescence; 2. Senescent Cells in Pancreatic Cancer; 2.1. Senescence in Pancreatic Tumor Cells; 2.2. Senescence as Barrier to PDAC Progression; 2.3. Senescence Bypass in PDAC; 2.4. Epigenetic Regulation of the Senescent State in PDAC; 2.5. Senescence in Pancreatic Stellate Cells; 3. Senescence and Inflammation in Pancreatic Cancer
- 3.1. The SASP Links Senescence to Inflammation3.2. Senescence-Inflammation Interface in PDAC; 4. Conclusions and Some Unanswered Questions; 4.1. Oncogenic Kras as Primary Inducer of Senescence in PDAC; 4.2. Bidirectional Reversibility of the Senescent State; 4.3. On the Pro- and Antitumorigenic Roles of Senescence; 4.4. Senescent Cell-Immune Cell Interactions; Acknowledgments; References; Chapter Two: Small-Molecule Targeting of BET Proteins in Cancer; 1. Introduction; 2. BET Proteins; 2.1. The Bromodomain; 2.2. BET Function; 2.3. BETs in Health and Disease; 3. BET Inhibitors; 3.1. Discovery
- 3.2. Chemistry3.3. Tolerability; 4. BET Inhibition in NMC; 4.1. NUT Midline Carcinoma; 4.2. BRD4-NUT Function; 4.3. Inhibition of BRD4-NUT by BET Inhibitors; 4.4. Clinical Trials with BET Inhibitors; 4.5. Other Cancers; 5. Resistance to BET Inhibitors; 6. Future of BET Inhibitors; 6.1. Combinations; 6.2. Novel BET Inhibitor Derivatives; 7. Concluding Remarks; References; Chapter Three: H3K27 Methylation: A Focal Point of Epigenetic Deregulation in Cancer; 1. Introduction; 2. Histone H3 Mutations; 3. Alterations in H3K27me "Writers"; 3.1. EZH2 Overexpression; 3.2. EZH2 Mutations
- 3.3. Mutations in Polycomb Group-Associated Proteins4. Alterations in H3K27me "Readers"; 5. Alterations in H3K27 "Erasers"; 6. Cross Talk with Other Chromatin Regulators; 6.1. MMSET Overexpression; 6.2. SWI/SNF Chromatin-Remodeling Complex Inactivation; 6.3. Histone Acetylation; 6.4. Wilms' Tumor 1 Mutations; 6.5. MLL Oncofusions; 6.6. H2A Monoubiquitination; 7. Targeting Deregulated H3K27me; 8. Conclusions and Future Perspectives; Acknowledgments; References; Chapter Four: AEG-1/MTDH/LYRIC: A Promiscuous Protein Partner Critical in Cancer, Obesity, and CNS Diseases; 1. Introduction