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|a Emdad, Luni.
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| 245 |
1 |
0 |
|a Pancreatic cancer :
|b basic mechanisms and therapies /
|c edited by Luni Emdad, Azeddine Atfi, Rajan Gogna, Jose G. Trevino, Paul B. Fisher.
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| 264 |
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1 |
|a San Diego :
|b Elsevier Science & Technology,
|c 2023.
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| 264 |
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4 |
|c �2023.
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| 300 |
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|a 1 online resource (392 pages) :
|b illustrations.
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| 336 |
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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
|2 rdacarrier
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| 490 |
1 |
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|a Advances in cancer research;
|v v. 159
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| 504 |
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|a Includes bibliographical references.
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| 588 |
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|a Description based on publisher supplied metadata and other sources.
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| 505 |
8 |
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|a 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.
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| 505 |
8 |
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|a 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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| 650 |
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|a Pancreas
|x Cancer.
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| 650 |
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|a Drug resistance in cancer cells.
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| 650 |
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|a Cellular signal transduction.
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| 650 |
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2 |
|a Pancreatic Neoplasms
|0 (DNLM)D010190
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| 650 |
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2 |
|a Survival Rate
|0 (DNLM)D015996
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| 650 |
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2 |
|a Drug Resistance, Neoplasm
|0 (DNLM)D019008
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| 650 |
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2 |
|a Tumor Microenvironment
|0 (DNLM)D059016
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| 650 |
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2 |
|a Signal Transduction
|0 (DNLM)D015398
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|a Cellules canc�ereuses
|x R�esistance aux m�edicaments.
|0 (CaQQLa)201-0217335
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| 650 |
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6 |
|a Transduction du signal cellulaire.
|0 (CaQQLa)201-0206812
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| 650 |
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6 |
|a Pancr�eas
|x Cancer.
|0 (CaQQLa)201-0288909
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| 700 |
1 |
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|a Atfi, Azeddine.
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| 700 |
1 |
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|a Gogna, Rajan.
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| 700 |
1 |
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|a Trevino, Jose G.
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| 700 |
1 |
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|a Fisher, Paul B.
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| 830 |
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0 |
|a Advances in cancer research ;
|v volume 159.
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| 856 |
4 |
0 |
|u https://sciencedirect.uam.elogim.com/science/bookseries/0065230X/159
|z Texto completo
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| 880 |
8 |
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|6 505-00/(S
|a 3.2. PDAC cells adapt to hypoxic environments -- 3.3. PDAC cells resist mechanical stress by degrading the ECM -- 3.4. Chronic inflammation promotes PDAC growth -- 3.5. Cellular interactions determine the fate of PDAC -- 4. PDAC therapeutic options -- 4.1. Surgery -- 4.2. Chemotherapy -- 4.3. Radiation -- 4.4. Immunotherapy -- 5. Tumor heterogeneity contributes to treatment resistance -- 5.1. Tumor cell heterogeneity -- 5.2. Tumor microenvironment heterogeneity -- 6. Conclusion -- Acknowledgments -- References -- Chapter Eight: Oncogenic signaling pathways in pancreatic ductal adenocarcinoma -- 1. Introduction -- 2. Oncogenic signaling pathways in PDAC -- 2.1. Wnt/β-catenin pathway -- 2.2. KRAS signaling pathway -- 2.3. TGF-β/SMAD signaling pathway -- 2.4. Notch signaling pathway -- 2.5. Sonic hedgehog (SHH) signaling pathway -- 2.6. JNK signaling pathway -- 3. MYC: Master regulator of PDAC aggressiveness -- 3.1. MYC as a reversible driver of PDAC progression -- 3.2. RAS and MYC: Partners in crime -- 3.3. MYC driven epigenetic reprogramming in PDAC -- 3.4. Role of MYC in PDAC metastasis and invasion -- 4. Elucidation of PDAC heterogeneity through single cell genomic approaches -- 5. Conclusions and future directions -- Acknowledgments -- References -- Chapter Nine: Chemoresistance in pancreatic ductal adenocarcinoma: Overcoming resistance to therapy -- 1. Introduction -- 2. PDAC treatment strategies and chemoresistance -- 3. Methods to predict PDAC chemoresistance -- 4. Role of EMT in PDAC chemoresistance -- 5. Role of non-coding RNAs in PDAC chemoresistance -- 5.1. Role of miRNAs in PDAC chemoresistance -- 5.2. Role of lncRNA in PDAC chemoresistance -- 6. Role of the microenvironment in PDAC chemoresistance -- 6.1. Role of the tumor microenvironment and stroma in PDAC chemoresistance.
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| 880 |
8 |
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|6 505-00/(S
|a 6.2. Role of the immune microenvironment in PDAC chemoresistance -- 7. Role of nucleoside transporters in PDAC chemoresistance -- 8. Role of autophagy in PDAC chemoresistance -- 9. Role of metabolism in PDAC chemoresistance -- 10. Role of extracellular vesicles (EV) and exosomes in PDAC chemoresistance -- 11. Role of signaling pathways in PDAC chemoresistance -- 11.1.1. Epidermal growth factor (EGF) -- 11.1.2. Insulin-like growth factor (IGF) -- 11.1.3. Vascular endothelial growth factor (VEGF) -- 11.1.4. Transforming growth factor-beta (TGF-β) -- 11.1.5. Platelet-derived growth factor (PDGF) -- 11.1.6. Hepatocyte growth factor (HGF) -- 11.1.7. Fibroblast growth factor (FGF) -- 11.1.8. Nerve growth factor (NGF) -- 11.1.9. Connective tissue growth factor (CTGF/CCN2) -- 12. Role of pancreatic tumor microbiome in PDAC chemoresistance -- 13. Future directions: Methods to sensitize pancreatic cancer to therapy -- Acknowledgments -- Conflict of interest -- References -- Chapter Ten: Tumor microenvironment interactions with cancer stem cells in pancreatic ductal adenocarcinoma -- 1. Introduction -- 2. Clinical issues in pancreatic ductal adenocarcinoma -- 3. Cancer stem cells in pancreatic ductal adenocarcinoma -- 4. Tumor microenvironment in pancreatic cancer -- 5. Metastasis in pancreatic ductal adenocarcinoma -- 6. Conclusion -- Acknowledgments -- References.
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| 880 |
0 |
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|6 505-00/(S
|a Intro -- Pancreatic Cancer: Basic Mechanisms and Therapies -- Copyright -- Contents -- Contributors -- Preface -- Chapter One: Notch signaling pathway in pancreatic tumorigenesis -- 1. Introduction -- 2. Roles of Notch signaling in pancreatic ductal adenocarcinoma (PDAC) -- 2.1. The cellular origin, initiation, and progression of PDAC -- 2.2. Roles of Notch in PDAC initiation -- 2.3. Roles of Notch in PDAC progression -- 2.4. Differential functions of Notch signaling pathway in PDAC -- 2.5. Roles of Notch modulators in PDAC pathogenesis -- 2.6. Notch signaling in the tumor microenvironment of PDAC -- 2.7. Crosstalk between the Notch and other signaling pathways in PDAC -- 2.7.1. Notch and MEK/ERK -- 2.7.2. Notch and TGF-β -- 2.7.3. Notch and NFκB -- 2.7.4. Notch and Sox9 -- 2.8. Aberrant Notch signaling in human PDAC -- 2.9. Roles of Notch signaling in PDAC resistance to therapeutics -- 2.10. Targeting Notch in PDAC -- 3. Roles of Notch signaling in pancreatic neuroendocrine tumor (PNET) -- 4. Perspective -- References -- Chapter Two: Deciphering epithelial-to-mesenchymal transition in pancreatic cancer -- 1. Significance -- 2. Introduction -- 3. Defining EMT and its molecular mechanisms and pathways -- 3.1. Characteristics of EMT -- 3.2. Molecular regulation of EMT -- 4. The role of EMT in promoting tumor development and metastasis -- 4.1. EMT-driven tumor invasion and metastasis negatively impact patient prognosis -- 4.2. EMT pathways and EMT-transcription factors likely drive oncogenesis -- 5. EMT influences the initiation, survival, and metastasis of pancreatic cancer -- 5.1. EMT drives cancer-initiating cell formation and promotes survival in pancreatic cancer -- 5.2. EMT and PDAC metastasis -- 6. EMT as a therapeutic target for PDAC -- 7. Perspectives, challenges and future directions -- Glossary -- References.
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