Peritoneal tumor microenvironment of cancers on cancer hallmarks : perspectives of translational medicine /

This book offers a comprehensive exploration of peritoneal tumors and cancer hallmarks, with a focus on translational medicine. Edited by leading experts in cancer research from various international institutions, it delves into the formation and clinical significance of peritoneal cancers, includin...

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Detaylı Bibliyografya
Diğer Yazarlar: Song, Yong Sang
Materyal Türü: Ekitap
Dil:İngilizce
Baskı/Yayın Bilgisi: London : Academic Press, 2024.
Konular:
Online Erişim:ScienceDirect
Etiketler: Etiketle
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İçindekiler:
  • Front Cover
  • Peritoneal Tumor Microenvironment of Cancers on Cancer Hallmarks
  • Copyright Page
  • Contents
  • List of Contributors
  • Introduction
  • 1 What is the tumor microenvironment?
  • 1.1 Introduction
  • 1.2 Formation of malignant ascites
  • 1.3 Immune cells
  • 1.4 Fibroblasts and mesenchymal stem cells
  • 1.5 Extracellular matrix
  • 1.6 Hypoxia and reactive oxygen species
  • 1.7 Tumor microenvironment after cancer therapy
  • 1.8 Summary
  • References
  • 2 Clinical significance of peritoneal cancers
  • 2.1 Highlights
  • 2.2 Introduction
  • 2.3 Etiology and epidemiology
  • 2.3.1 Subtypes of peritoneal cancers
  • 2.3.2 Etiology of peritoneal cancers
  • 2.3.3 Pathogenesis of peritoneal cancers
  • 2.3.4 Epidemiology of peritoneal cancers
  • 2.4 Diagnosis and prognosis
  • 2.4.1 Diagnostic symptoms for peritoneal cancers
  • 2.4.2 Diagnostic imaging in peritoneal cancers
  • 2.4.3 Diagnostic biopsies in peritoneal cancers
  • 2.4.4 Staging and prognosis of peritoneal cancers
  • 2.5 Therapy and therapy resistance
  • 2.5.1 Surgery
  • 2.5.2 Systemic chemotherapy
  • 2.5.3 Multimodal therapies
  • 2.5.4 Targeted therapies
  • 2.5.5 Therapy resistance
  • 2.6 Summary and perspective
  • References
  • 3 Tumor microenvironment of peritoneal carcinomatosis: the concept of premetastatic niche altered before tumor implantation
  • 3.1 Highlights
  • 3.2 Introduction
  • 3.3 Peritoneal complex
  • 3.3.1 Anatomy
  • 3.3.2 Histology
  • 3.3.3 Scanning electron microscopy view
  • 3.3.4 Physiology
  • 3.4 Peritoneal wall as a premetastatic environment
  • 3.4.1 Peritoneum and inflammation
  • 3.4.2 Peritoneum and cancer (macroscopic and microscopic analysis)
  • 3.4.2.1 Ovarian cancer cell invasion
  • 3.4.2.2 Digestive cancer cell invasion
  • 3.4.3 Peritoneal liquid in carcinomatosis
  • 3.4.3.1 Noncoagulability ascites character
  • 3.4.3.1.1 Cytokine array analysis.
  • 3.4.3.1.2 Immune cell analysis
  • 3.4.4 Peritoneal wall modification during cancer cell implantation
  • 3.4.4.1 Mesothelial cell transformation (EMT)
  • 3.4.4.2 The submesothelial layer is a target for cancer cells (microscopic analysis)
  • 3.4.4.3 Fibrin in the peritoneal cavity
  • 3.4.4.4 Cluster formation in the peritoneal cavity
  • 3.5 Scar zone on the peritoneal surface as a niche for cancer cell implantation (animal model study)
  • 3.5.1 Inhibition of cancer cell interaction with the peritoneal surface could be a therapeutic target
  • 3.6 Conclusion and perspectives
  • References
  • 4 Cellular models for peritoneal cancer research
  • 4.1 What is peritoneal cancer?
  • 4.1.1 Molecular mechanisms of peritoneal seeding
  • 4.1.2 Why cellular models for peritoneal cancer research is needed?
  • 4.2 Origin of peritoneal carcinoma
  • 4.2.1 Primary peritoneal carcinoma
  • 4.2.2 Pseudomyxoma peritonei
  • 4.2.3 Peritoneal carcinomatosis from gastric cancer
  • 4.2.4 Peritoneal carcinomatosis from ovarian cancer
  • 4.2.5 Peritoneal carcinomatosis from colorectal cancer
  • 4.3 Peritoneal tumor cell line models
  • 4.3.1 Cell line models
  • 4.3.1.1 Peritoneal metastasis cell line establishment from ascites
  • 4.3.1.2 Peritoneal metastasis cell line establishment from omental seeding and matched primary tumor
  • 4.4 Fingerprinting
  • 4.5 Mycoplasma
  • 4.6 Passaging primary cultures and cryopreservation
  • 4.7 Removal of contaminating mesothelial cells and fibroblasts from cultures of isolated peritoneal cells
  • 4.8 Use of established peritoneal tumor cell lines
  • 4.9 3D culture of gastric cancer cell lines derived from ascites
  • References
  • 5 Metabolism of cancer cells altered in peritoneal tumor microenvironment
  • 5.1 Highlights
  • 5.2 Introduction
  • 5.3 Cellular components of peritoneal tumor microenvironment.
  • 5.4 Metabolic crosstalk in the tumor microenvironment
  • 5.5 Peritoneal tumor microenvironment and glucose metabolism
  • 5.6 Peritoneal tumor microenvironment and lipid metabolism
  • 5.7 Peritoneal tumor microenvironment and amino acid metabolism
  • 5.8 Metabolic reprogramming and chemoresistance
  • 5.9 Therapeutic perspectives
  • 5.10 Conclusion
  • References
  • 6 Cell-to-cell interactions in peritoneal tumor microenvironment
  • 6.1 Introduction
  • 6.1.1 Peritoneum cavity and mesothelial cells
  • 6.1.2 Peritoneal carcinomatosis
  • 6.2 Blood and lymphatic vessels
  • 6.3 The omentum
  • 6.4 Key biological functions of omentum
  • 6.4.1 Omentum favors cancer cell implantation
  • 6.5 Sequential events carcinomatosis expansion in peritoneal cavity
  • 6.5.1 Cancer cell nodule on peritoneal surface
  • 6.5.2 Cancer cell cluster and nodule formation
  • 6.6 Peritoneal carcinomatosis and immune response
  • 6.7 Cancer cell clusters in peritoneal liquid
  • 6.8 Hospicells, as a stromal cell-derived from ascites cancer cell clusters
  • 6.9 Origin and markers of hospicells
  • 6.10 Hospicells in the regulation of angiogenesis
  • 6.10.1 Hospicells-associated chemoresistance to chemotherapy for cancer cells via oncological trogocytosis
  • 6.10.2 Hospicells in metastasis of cancer cells
  • 6.10.3 Cross-talk between hospicells and immune cells within tumor microenvironment
  • 6.11 Conclusion and perspective
  • References
  • 7 Diagnostic, prognostic, and therapeutic biomarkers of ovarian cancer
  • 7.1 Introduction
  • 7.2 Ovarian tissue markers
  • 7.2.1 Dynamin-related protein 1
  • 7.2.2 Gelsolin
  • 7.2.3 Hexokinase II
  • 7.2.4 Phosphatidylinositol 3-kinase/Akt
  • 7.2.5 Programmed cell death ligand 1
  • 7.2.6 Folate receptor alpha
  • 7.3 Genetic tissue markers
  • 7.4 Circulatory biomarkers
  • 7.4.1 Protein biomarkers
  • 7.4.1.1 Cancer antigen 125.
  • 7.4.1.2 Human epididymis protein 4
  • 7.4.1.3 Other tumor markers
  • 7.4.1.4 Plasma gelsolin
  • 7.5 Molecular markers
  • 7.5.1 MicroRNAs
  • 7.5.2 Methylated DNA
  • 7.6 Urinary biomarkers
  • 7.7 Human epididymis protein 4
  • 7.8 Matrix metalloproteinase
  • 7.9 Polyamines
  • 7.10 MicroRNAs
  • 7.11 Eosinophil-derived neurotoxin and osteopontin
  • 7.12 Extracellular vesicles as ovarian cancer biomarkers
  • 7.13 The role of CT and MRI in the assessment of peritoneal carcinomatosis
  • 7.14 Detection of peritoneal carcinomatosis
  • 7.15 Prediction of success of cytoreduction
  • 7.16 Treatment response assessment after neoadjuvant chemotherapy (NACT)
  • 7.17 Positron emission tomography and radiogenomics for ovarian cancer detection and prognosis
  • 7.18 Characterization
  • 7.19 T staging
  • 7.20 N &amp
  • M staging
  • 7.21 Detection of recurrence
  • 7.22 Prediction of treatment response
  • 7.23 Prediction of prognosis
  • 7.24 The other tracers for PET imaging
  • 7.25 Radiogenomics
  • 7.26 Artificial intelligence in ovarian cancer detection and prognosis
  • 7.27 Artificial intelligence application in medical imaging and ovarian cancer
  • 7.28 Opportunities and challenges
  • 7.29 Looking into the future
  • 7.30 Summary and conclusions
  • References
  • 8 Current and future perspectives of xenograft models of human ovarian cancer
  • 8.1 Introduction
  • 8.2 Intraperitoneal dissemination of human OC cell lines in murine models
  • 8.3 Human OC xenograft in murine models
  • 8.4 Patient-derived organoid models of OC
  • 8.5 Experimental models of tumor neovascularization and progression using the chick embryo chorioallantoic membrane assay
  • 8.6 Comparison in characteristics of experimental models for ovarian cancer studies
  • 8.7 Conclusion
  • References
  • 9 Tumor microenvironment and chemoresistance
  • 9.1 Introduction.