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- •Contents
- •Preface
- •About the Editors
- •Contributors
- •1.1 Tumor Microenvironment (TME)
- •1.3 TME Components
- •1.3.1 Cells
- •References
- •1.3.2 Noncellular Components
- •1.4 Discussion
- •2.1 Introduction
- •2.2 Key Immune Phenomena Shaping the TIME
- •2.2.1 Phagocytosis
- •2.2.2 Antigen Presentation
- •2.2.3 Cancer Immunoediting
- •2.2.4 Cytokine-Chemokine-Complement Mediated Networks in the TIME
- •2.3 Innate Immune Networks in the TIME
- •2.4 Adaptive Immunity Networks in the TIME
- •2.5 Discussions
- •References
- •3.1 Introduction
- •3.1.1 Definition and Overview of Cancer-Associated Fibroblasts
- •3.1.2 Importance of Studying CAFs in Cancer Research
- •3.2 Origin of CAFs
- •3.3 CAF Biomarkers
- •3.3.1 Cancer-Promoting CAF Biomarkers
- •3.3.2 Cancer-Restraining CAF Biomarkers
- •3.3.3 CAF Biomarkers with a Dual Role
- •3.3.4 Other CAF Markers with Unclear Functions
- •3.4 Heterogeneity and Plasticity of CAFs
- •3.4.1 Molecular Mechanisms Regulating CAF Heterogeneity
- •3.4.2 Functional Heterogeneity of CAFs
- •3.5 Tumor Microenvironment in Glioblastoma
- •3.6 Cancer-Associated Fibroblasts in Glioblastoma
- •3.7 Therapeutic Targeting of CAFs
- •References
- •4.1 Introduction
- •4.2 Endothelial Cells (ECs)
- •4.3 Tumor Endothelial Cells (TECs)
- •4.4 Heterogeneity of TECs
- •4.5 Modulation of TEC Characteristics by the TME
- •4.6 Immunomodulatory Endothelial Cells
- •4.7 Role of Tumor Endothelial Cells in Angiogenesis
- •4.8 Endothelial Cells in Cancer Therapy
- •4.9 Discussion
- •References
- •5.1 Introduction
- •5.2 TME Therapies
- •5.2.1 Tumor-Associated Immune Cells
- •5.2.2 Therapies Directed Toward the Tumor-Associated Vasculature
- •5.2.3 Therapies Directed Against Extracellular Matrix and Tumor Stroma
- •5.3 Discussion
- •References
- •6.1 Introduction
- •6.3 Cancer and Traditional Drug
- •6.4 Drug Repurposing
- •6.5 The TME and Drug Repurposing
- •6.6 Drug Repurposing in Cancer
- •6.7 Discussion
- •References
- •7.2 Cellular Components
- •7.3 Noncellular Components
- •7.4 TME-Driven Support of Cancer Hallmarks
- •7.4.3 Immunomodulation in the TME
- •7.4.4 The TME in Therapeutic Response and Resistance
- •7.5 Metabolic Reprogramming in the TME
- •7.6 Therapeutic Targeting of the TME
- •7.7 Artificial Intelligence and Machine Learning
- •7.8 Direction of Future Research in AI
- •7.9.1 Digital Pathology and Computer Vision
- •7.9.2 Multi-Omics Integration
- •7.9.3 Predictive Modeling of TME Features
- •7.9.4 Clinical Applications of AI/ML for the TME
- •7.9.5 Emerging Frontiers in AI/ML for TME Analysis
- •References
- •Index

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115
6
Drug Repurposing and
Tumor Microenvironment
in Cancer
Waliza Ansar
6.1 INTRODUCTION
Cancer is one of the world’s critical health distresses with high clinical burden. Cancer
is a complex heterogeneous multiple disorders earmarked by several hallmarks: sus-
taining proliferative signaling, instability of genomic makeup, enhancing replicative
immortality, preventing cell death, inammation, de novo angiogenesis, evading the
immune system, invasion and metastasis (Stanta et al 2016). Cancer cells do not
simply escape the immune supervision by host cells or themselves. Cancer cells can
craft an immunosuppressive vibrant microenvironment encompassing the surround-
ing cells to impede tumor growth. This microenvironment is known as tumor micro-
environment (TME) (Malik et al 2022).
Tumorigenesis is a complex and multilayered process, in which consecutive muta-
tions in tumor-suppressor genes and oncogenes virtually causes in prolic growth
and resistance to cell death. Most of the known human tumor types were dened
by has a range of hallmarks, which were all mentioned in Table6.1 (Hanahan and
Weilberg 2000, 2011).
The integrated network of tumor microenvironment and its multifaceted interac-
tions creates a spotlight of modern research rather than malignant cancer. The tumor
microenvironment with all its components also contributes to the development of
cancer (Hanahan and Coussens 2012). Studies have provided some evidence that
human tumor cells in due course creates a mass of malignant cancer cells. Tumor
cells secrete chemokines, cytokines, and growth factors to competently recruit
immune cells, vascular cells, and stromal cells. These recruited cells release inter-
mediate metabolites and growth-promoting signals to recreate the tumor microenvi-
ronment. The interactive communication between the microenvironment and cancer
cells causes proliferation, metastasis and nally death (Zhang et al 2020).
Recent progress in the tumor microenvironment research includes its compo-
sition, its components, cellular crosstalk to unveil the heterogeneity of this niche,
variable stages of their differentiation and proliferative purposes. The TME encom-
passes a assorted range of immune and non-immune cells that diverge in oncogenic,
phylogenic, phenotypic expressions and functional distinctiveness, immune commu-
nications, tumor potential for proliferation, and response to therapeutic modalities.
DOI: 10.1201/9781003405023-6
Соседние файлы в папке Библиотека им академика М.И. Перельмана
