Pancreatic cancer : basic mechanisms and therapies /

Detalles Bibliográficos
Clasificación:Libro Electrónico
Autor principal: Emdad, Luni
Otros Autores: Atfi, Azeddine, Gogna, Rajan, Trevino, Jose G., Fisher, Paul B.
Formato: Electrónico eBook
Idioma:Inglés
Publicado: San Diego : Elsevier Science & Technology, 2023.
Colección:Advances in cancer research ; volume 159.
Temas:
Pancreas > Cancer.
Drug resistance in cancer cells.
Cellular signal transduction.
Pancreatic Neoplasms
Survival Rate
Drug Resistance, Neoplasm
Tumor Microenvironment
Signal Transduction
Cellules canc�ereuses > R�esistance aux m�edicaments.
Transduction du signal cellulaire.
Pancr�eas > Cancer.
Acceso en línea:Texto completo
Tabla de Contenidos:
  • Chapter Three: In vivo models of pancreatic ductal adenocarcinoma
  • 1. Introduction
  • 2. Spontaneous tumor models
  • 2.1. Chemical-induced models
  • 2.1.1. N-nitrosobis (2-oxopropyl)amine (BOP)
  • 2.1.2. Additional nitrosamines
  • 2.1.3. Azaserine (O-diazoacetyl-l-serine)
  • 2.1.4. 7,12-Dimethylbenz[a]anthracene (DMBA)
  • 2.2. Genetically engineered mouse models (GEMM)
  • 2.2.1. Conditional gene knockout
  • 2.2.2. Cre-Lox recombination
  • 2.2.3. KC/KIC model
  • 2.2.4. KPC model
  • 2.2.5. TGF/SMAD pathway models
  • 2.2.6. Tet (tetracycline) expression systems
  • 2.2.7. Tetracycline-induced PDAC models
  • 2.2.8. CRISPR-based GEMMs
  • 3. Implantation models
  • 3.1. Subcutaneous implantation
  • 3.2. Orthotopic implantation
  • 3.3. Metastatic models
  • 3.4. Patient-derived xenograft (PDX) protocols
  • 3.5. Patient derived organoid xenograft (PDOX) models
  • 3.6. Humanized PDX models
  • 3.7. Syngeneic models
  • 4. Conclusions
  • Acknowledgments/Funding
  • References
  • Chapter Four: Interplay between MAP kinases and tumor microenvironment: Opportunity for immunotherapy in pancreatic cancer
  • 1. Introduction
  • 2. Current treatments and drug resistance in pancreatic cancer
  • 3. Pancreatic cancer TME and drug resistance
  • 4. Expression and function of ICPs in pancreatic cancer
  • 5. MAP4KMAP3KMAP2KMAPK signaling module in pancreatic cancer
  • 5.1. Expression and function of MAP4Ks in pancreatic cancer
  • 5.2. Expression and function of MAP3Ks in pancreatic cancer
  • 5.3. Expression and function of MAP2Ks in pancreatic cancer
  • 5.4. Expression and function of MAPKs in pancreatic cancer
  • 6. Targeting ICPs and MAPKs in pancreatic cancer
  • 7. Summary
  • Acknowledgments
  • Author contributions
  • Competing interests
  • References
  • Chapter Five: Targeting KRAS in pancreatic cancer: Emerging therapeutic strategies
  • 1. Introduction.
  • 2. Biochemistry of KRAS
  • 3. KRAS signaling pathways
  • 3.1. Receptor tyrosine kinase (RTK) pathway
  • 3.2. RAF/MEK/ERK pathway
  • 3.3. PI3K/AKT/mTOR pathway
  • 3.4. Non-canonical pathways
  • 4. KRAS mutations in PC
  • 4.1. Metabolic effects
  • 4.2. Tumor microenvironmental and immune modulatory effects
  • 5. Emerging KRAS-targeted therapies
  • 5.1. Direct KRAS inhibitors
  • 5.2. Indirect KRAS inhibitors
  • 5.3. PROTACs
  • 6. KRAS-targeted combination strategies
  • 6.1. KRAS inhibitor combinations with targeted therapy
  • 6.2. KRAS inhibitor combinations with immunotherapy
  • 6.3. KRAS inhibitor combinations with chemotherapy
  • 7. KRAS and cellular senescence
  • 7.1. Dual role of KRAS in senescence
  • 7.2. Senescence-associated drug resistance and therapeutic vulnerabilities
  • 8. Challenges for effectively targeting KRAS in PC
  • 9. Future perspectives and conclusions
  • Acknowledgments
  • Conflict of interest
  • References
  • Chapter Six: Racial disparities in pancreatic cancer clinical trials: Defining the problem and identifying solutions
  • 1. Introduction
  • 2. Racial implicit bias as a barrier to enrollment
  • 3. Access to trials and study design barriers
  • 4. Impediments to clinical trial recruitment
  • 4.1. Patient awareness
  • 4.2. Community engagement to increase participation
  • 5. Increasing pancreatic cancer trial diversity-A way forward
  • References
  • Chapter Seven: Tumor heterogeneity: An oncogenic driver of PDAC progression and therapy resistance under stress conditions
  • 1. Introduction
  • 2. PDAC tumoral heterogeneity
  • 2.1. Inter-tumor heterogeneity in PDAC
  • 2.2. Intratumoral heterogeneity in PDAC
  • 2.3. The role of intratumoral heterogeneity in metastasis
  • 3. PDAC adapts to grow in stress conditions
  • 3.1. PDAC cells use metabolic reprogramming to meet their energy needs.

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