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|z 9780128047880 (hbk.)
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|a (OCoLC)969419685
|z (OCoLC)1006507003
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|a 616.9/94/0072
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|a Advances in cancer research
|n Volume 131 /
|c edited by Kenneth D. Tew, Paul B. Fisher.
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264 |
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1 |
|a Cambridge, MA :
|b Academic Press,
|c 2016.
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300 |
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|a 1 online resource (x, 197 pages) :
|b illustrations, some colour
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|a text
|b txt
|2 rdacontent
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|a computer
|b c
|2 rdamedia
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|a online resource
|b cr
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|a Advances in Cancer Research
|v Volume 131
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504 |
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|a Includes bibliographical references and index.
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521 |
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|a Specialized.
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|a Print version record.
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|a 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
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505 |
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|a 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
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505 |
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|a 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
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|a 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
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520 |
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|a 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.
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650 |
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|a Cancer
|x Research.
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650 |
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6 |
|a Cancer
|x Recherche.
|0 (CaQQLa)201-0004697
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650 |
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7 |
|a Cancer
|x Research
|2 fast
|0 (OCoLC)fst00845497
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700 |
1 |
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|a Tew, Kenneth D.,
|e editor.
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700 |
1 |
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|a Fisher, Paul B.,
|e editor.
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776 |
0 |
8 |
|i Print version:
|z 9780128047880
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856 |
4 |
0 |
|u https://sciencedirect.uam.elogim.com/science/bookseries/0065230X/131
|z Texto completo
|