Epigenetic regulation of cancer. Part A /

Detalles Bibliográficos
Clasificación:Libro Electrónico
Formato: eBook
Idioma:Inglés
Publicado: [S.l.] : Academic Press, 2023.
Colección:International review of cell and molecular biology ; v. 380
Temas:
Cancer > Gene therapy.
Epigenetics.
Cancer > Th�erapie g�enique.
�Epig�en�etique.
Acceso en línea:Texto completo
Tabla de Contenidos:
  • Front Cover
  • Series page
  • International Review of CELL AND MOLECULARBIOLOGY
  • Copyright
  • Contents
  • Contributors
  • Epigenetic regulation of cancer
  • Acknowledgments
  • Competing interests
  • References
  • Chapter One: Epigenetic regulation of epithelial-mesenchymal transition during cancer development
  • 1 Introduction
  • 2 Epigenetic modifications and human cancers
  • 2.1 A brief overview of epigenetic modifications
  • 2.1.1 Histone modifications
  • 2.1.2 Modifications at DNA level
  • 2.1.3 Modifications at mRNA and ncRNA levels
  • 2.2 Roles of epigenetic modifications in cancer development
  • 3 EMT and human cancers
  • 3.1 A brief overview of EMT
  • 3.1.1 EMT process
  • 3.1.2 Transcription factors and signaling pathways involved in the EMT process
  • 3.2 Roles of EMT in cancer development
  • 4 Epigenetic regulation of EMT in human cancers
  • 4.1 Regulation of EMT by histone modifications in human cancers
  • 4.2 Regulation of EMT by DNA modifications in human cancers
  • 4.3 Regulation of EMT by mRNA and ncRNA modifications in human cancers
  • 5 Epigenetic therapy targeting EMT for management of human cancers
  • 6 Conclusions and future perspectives
  • Acknowledgements
  • Declaration of competing interest
  • References
  • Chapter Two: Novel insights into DNA methylation-based epigenetic regulation of breast tumor angiogenesisNovel insights into DNA methylation-based epigenetic regulation of breast tumor angiogenesis
  • 1 Introduction
  • 1.1 DNA methylation-based regulation of breast tumor angiogenesis: What is known?
  • 1.1.1 Identification of pro-angiogenic genes regulated by DNA methylation
  • 1.1.2 Promoters of pro-angiogenic genes are hypomethylated and anti-angiogenic genes are hypermethylated in breast tumors
  • 2 Conclusion
  • 3 Future perspectives
  • Acknowledgements
  • Conflict of interest
  • References.
  • Chapter Three: Super-enhancer landscape rewiring in cancer: The epigenetic control at distal sites
  • 1 Introduction
  • 2 Promoters and typical enhancers
  • 3 Super-enhancers (SEs)
  • 4 Super-enhancers identification
  • 5 eRNAs
  • 6 The Mediator complex
  • 7 Chromatin remodelers
  • 8 TADs, chromatin organization and distal CREs
  • 9 Super-enhancer, phase separation and membraneless organells
  • 10 SEs in cancer an introduction
  • 11 SEs expansion or contraction in cancer
  • 12 Subversion of hierarchically organization of SEs in cancer
  • 12.1 SEs hierarchy in gastric adenocarcinoma
  • 12.2 SEs hierarchy in breast cancer
  • 12.3 SEs hierarchy in prostate cncer
  • 12.4 SEs hierarchy in ovarian cancer
  • 12.5 SEs hierarchy in colorectal cancer (CRC)
  • 12.6 SEs hierarchy in hepatocellular carcinoma (HCC)
  • 12.7 SEs hierarchy in sarcomas
  • 12.8 SEs hierarchy in neuroblastoma and glioblastoma
  • 12.9 SEs hierarchy in DLBCL
  • 12.10 SEs hierarchy in leukemia
  • 13 SEs and ncRNAs, dangerous liaisons in cancer progression
  • 14 SEs and ncRNAs, altered circuits in resistance to therapy
  • 15 SEs for classification of tumors subtypes or cancer ethnicity, predicts subclonal evolution and identify new druggable targets
  • 15.1 Targeting specific SEs in cancer: going over to JQ-1 and THZ1
  • 16 Conclusions
  • Acknowledgments
  • Conflict of interest
  • References
  • Chapter Four: Non-coding RNAs in the epigenetic landscape of cutaneous T-cell lymphomaNon-coding RNAs in CTCL
  • 1 Introduction
  • 2 miRNAs in CTCL
  • 2.1 miRNA role in diagnosis, progression, and prognosis
  • 2.1.1 Diagnosis
  • 2.1.2 Progression
  • 2.1.3 Prognosis
  • 2.2 Oncogenic miRNAs in CTCL
  • 2.2.1 miR-155
  • 2.2.2 miR-21
  • 2.3 Tumor-suppressive miRNAs in CTCL
  • 2.3.1 miR-337
  • 2.3.2 miR-150
  • 3 Long non-coding RNAs in CTCL
  • 3.1 Oncogenic lncRNA in CTCL
  • 3.1.1 MALAT1.
  • 3.2 Tumor-suppressive lncRNAs in CTCL
  • 3.2.1 MEG3
  • 4 Non-coding RNAs in CTCL patients
  • 5 Conclusion and future perspectives
  • Conflict of interest statement
  • Funding
  • References
  • Chapter Five: Epigenetic mechanism of therapeutic resistance and potential of epigenetic therapeutics in chemorefractory prostate cancer
  • 1 Introduction
  • 1.1 Chemotherapy: target, mode of action, limitation(s)
  • 1.2 Androgen deprivation therapy
  • 1.3 Androgen receptor blocker therapy
  • 1.4 Immunotherapy
  • 2 Epigenetic reprogramming-dependent aberrant regulation of genes during therapeutic resistance development in prostate cancers
  • 3 Aberrant expression of epigenetic regulatory genes during therapeutic resistance in prostate cancer
  • 4 Epigenetic regulation of DNA repair genes in prostate cancer chemoresistance
  • 5 Epigenetic regulation of androgen-dependent growth in ADT in prostate cancer
  • 6 Epigenetic regulation of genes associated with cellular plasticity during chemoresistance in prostate cancer
  • 6.1 Epigenetic reprogramming of stem cell marker genes in chemotherapy resistance in prostate cancer
  • 6.2 Epigenetic reprogramming of EMT marker genes in chemotherapy resistance in prostate cancer
  • 7 Potential of epigenetics-based therapeutics in prostate cancer treatment
  • 8 Summary
  • References
  • Chapter Six: Epigenetic inhibitors and their role in cancer therapy
  • 1 Introduction
  • 2 Epigenetic modifications
  • 2.1 DNA methylation
  • 2.2 Mechanisms of DNA methylation
  • 2.3 Histone modifications
  • 2.4 Histone methylation
  • 2.5 Histone acetylation
  • 2.6 Histone phosphorylation
  • 2.7 Histone ubiquitination
  • 2.8 RNA modifications
  • 2.9 Non-coding RNA modifications
  • 3 The role of epigenetics in cancer development
  • 4 Epigenetics as a target for cancer therapies
  • 5 Epi-drugs
  • 5.1 DNA methyltransferase inhibitors.
  • 5.1.1 Nucleoside analog inhibitors
  • 5.1.2 Non-nucleoside inhibitors
  • 5.2 Histone methyltransferase inhibitors
  • 5.3 Histone deacetylase inhibitors (HDACi)
  • 6 Small non-coding RNAs
  • 6.1 Small molecule inhibitors of miRNAs (SMIRs)
  • 6.2 miRNA-based therapy
  • 6.2.1 Epi-drugs combined therapy
  • 6.3 Epi-drugs combined with chemotherapy
  • 6.4 Epi-drugs combined with immunotherapy
  • 7 Conclusion and future perspectives
  • Acknowledgments
  • CRediT authorship contribution statement
  • Conflict of interest
  • Funding
  • References
  • Backcover.

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