Tumor Hypoxia

Yun Zhong

• Publisher: WSPC
• Year: 2016
• ISBN:
  9789813147331
• Topic: Medicine
• Subtopic: Oncology

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Tumors often start out as a benign growth, but gradually progress toward the malignant stage over a relatively long period of time. Tumor progression results from accumulated genetic mutations and inheritable epigenetic modifications that enable clonal evolution and selection of new clonal populations of tumor cells with aggressive characteristics including metastasis and therapy resistance. Increasing amounts of experimental evidence suggests that tumor microenvironment play a significant role in directing clonal evolution and determining clonal cell fate, which eventually leads to emergence of malignant tumor cell clones. Hypoxia is the most commonly observed feature of tumor microenvironment. Tumor hypoxia is significantly associated with malignant progression and predicts poor patient outcomes. This book provides detailed and up-to-date treaties on the role of hypoxia as a major driving force in tumor microenvironment to elicit cellular adaptation and clonal selection via genetic mutations and epigenetic modifications, to facilitate cancer stem cell maintenance, to enhance metastasis, to augment therapy resistance, and to evade immune surveillance.

--> Editor Yun Zhong 0Tumor Biology, Cancer Biology, Tumor Hypoxia, Oncology, Tumor Microenvironment

• Emerging areas of research: cancer stem cells, epigenetics, immune modulations, post-translational modifications of HIF, cancer metabolism
• Comprehensive discussion of clinical impact as well as new mechanistic paradigms
• Internationally renowned leaders in the field of hypoxia, tumor microenvironment, and cancer biology: Giaccia, Glazer, Pahlman, and Li

Index

A

aberrant DNA synthesis, 171

replicon misfiring, 171

acetylates, 55

acetylation, 54

acidosis, 226

action, 11

adaptive immunity, 80

adaptive responses, 235

adenosine, 263, 275

adult stem cell, 102

adverse prognosis, 207

aerobic, 2, 9–10, 14–16, 32

aggressive phenotypes, 169

aHIF, 196

AIFM3, 202

amino acid metabolism, 231

AML, 103

amyotrophic lateral sclerosis (ALS), 237

angiogenesis, 50, 57, 59, 81, 84, 90, 204–205, 234, 250, 252, 254

leaky vessels, 84

angiopoietin 2, 85

anoikis, 78–79

ERBB2, 79

anoxia, 233

anoxic, 3, 5–8, 10, 14, 16, 32–33

anti-angiogenic factors, 85

anti-oxidant responses, 231

anti-tumor immunity, viii

apoptosis, 131–132, 134–135, 142–143, 202, 226, 252–253, 266

arginine, 254, 256, 261

arrest-defective-1 (ARD1), 54–55

aryl hydrocarbon receptor nuclear translocator (ARNT), 251, 269

ataxia telangiectasia and Rad3-related (ATR), 172–173

ataxia telangiectasia mutated

ATM, 173

ATF6, 227

autophagosome, 236

autophagy, 131–132, 134, 142, 231

autophosphorylation, 229

B

basement membrane, 71, 73

BCL2, 203

Bcl-2-homology domain 3 (BH-3)-only family protein, 79

benzotriazine di-N-oxides, 22

Bevacizumab, 90

biological effect, 7, 19, 27

biological target volume (BTV), 23

biomarker, 208–209

biophysical models, 31, 33

bioreductive drugs, 12

BIX, 239

BNIP3, 79

bone marrow, 104

bone ...

Table of contents

• Cover
• Title
• Copyright
• Preface
• Contents
• Tumor Hypoxia and Radiotherapy
• Post-translational Modifications of the Hypoxia Inducible Factors
• Hypoxia and Metastasis
• Hypoxia and Cancer Stem Cell Regulation
• Hypoxia and Senescence
• Hypoxic Reprograming of Tumor Metabolism, Matching Environmental Supply with Biosynthetic Demand
• Regulation of DNA Repair by Hypoxia
• Regulation of the Hypoxic Response by Non-coding RNAs
• Hypoxia-Induced Endoplasmic Reticulum Stress
• The Hypoxic Tumor Microenvironment and the Anti-cancer Immune Response
• Index