Radiation Biology
Molecular Foundations and Clinical Applications
- 1st Edition - September 1, 2026
- Latest edition
- Authors: Barry S. Rosenstein, Jerome M. Karp
- Language: English
Radiation Biology: Molecular Foundations and Clinical Applications is a comprehensive exploration of the effects of radiation on living organisms, delving into the molecular… Read more
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Description
Description
Radiation Biology: Molecular Foundations and Clinical Applications is a comprehensive exploration of the effects of radiation on living organisms, delving into the molecular mechanisms underlying cellular responses. This book examines critical topics such as radiation-induced DNA damage, repair processes, and molecular signaling pathways. It provides a detailed look at how cells respond to radiation, addressing cell cycle control, apoptosis, and the effects of radiation on immune system functionality. As a resource for researchers, it bridges the gap between molecular biology and clinical oncology, offering insights into radiation's role in both therapeutic contexts and its broader impact on human biology.
In addition to its focus on molecular responses, the book covers topics like tumor microenvironment and metabolism, the role of epigenetics in radiation biology, and the hallmarks of cancer relevant to radiation therapy. It also provides discussions on chemotherapeutic agents, radiation carcinogenesis, and the complex interplay between radiation and cancer biology. The later sections extend the scope to tissue, organ, and systemic effects of radiation, making it an invaluable reference for professionals in molecular biology, oncology, and related fields striving to push the boundaries of radiation research.
Key features
Key features
Focuses on the topic of radiation biology at the cellular and molecular level
Addresses the topic from fundamentals through to clinical application
Considers the latest advances in the field of radiation biology and radiation oncology
Readership
Readership
Table of contents
Table of contents
1.1 Types of ionizing radiations
1.2 Description of electromagnetic radiation
1.3 Directly and indirectly ionizing radiations
1.4 Direct and indirect action of radiation
1.5 Photoelectric effect, Compton process and pair production
1.6 Exposure, absorbed dose, equivalent dose and effective dose
1.7 Radiation chemistry
2. Radiation-Induced DNA Damages and DNA Repair Processes
2.1 Evidence suggesting DNA as the target for ionizing radiation
2.2 Radiation-induced DNA damages
2.3 Multiply damages sites/clustered DNA damages
2.4 DNA repair mechanisms
2.5 Homologous recombination/gene conversion
2.6 Non-homologous end-joining
2.7 Single-strand annealing
2.8 Alternative end-joining/micro-homology mediated end-joining/theta mediated end-joining
2.9 Chromosome instability syndromes
2.10 Nucleotide, base and mismatch repair
2.11 Synthetic lethality
2.12 Chromosome and chromatid-type aberrations
2.13 Telomeres and telomerase2.14 Chromothripsis
3. Molecular Pathways of Cell Death
3.1 Cell Death Morphotypes
3.2 Main Forms of Regulated Cell Death Induced by Radiation
3.3 Morphological Changes of Regulated Cell Death
3.4 Cross-regulation Among Regulated Cell Death Pathways
3.5 Possible Cell Fates Following Irradiation
3.6 Senescence
3.7 Mitotic death/catastrophe
3.8 Necrosis3.9 Apoptosis
3.10 Caspases
3.11 Apoptotic intrinsic pathway
3.12 Apoptotic extrinsic pathway
3.13 Necroptosis
3.14 Autophagy
4. Radiotherapy and Immune Checkpoint Blockade
4.1 Immune System Overview
4.2 Blockade of CTLA-4, PD-1 and PD-L1 to induce antitumor responses
4.3 The prevalence of somatic mutations across human cancer types
4.4 Radiation causes activation of the STING pathway
4.5 Mechanisms by which radiation enhances immunotherapy
4.6 Radiation-induced secretion of IFN-I is critical for abscopal responses
4.7 DNA exonuclease Trex1 regulates radiotherapy-induced tumor immunogenicity
4.8 Immunosuppressive pathways enhanced by RT in the TME
4.9 Use of immune checkpoint blockade to enhance the abscopal effect
5. Molecular Signaling in Irradiated Cells
5.1 Cellular signaling pathways
5.2 Growth factors
5.3 Growth factor receptors
5.4 RAS
5.5 PTEN
5.6 MAPK core signaling module
5.7 Phosphoinositide metabolism in growth factor signaling
5.8 Cytoplasmic tyrosine kinase pathways
5.9 Developmental signaling pathways – WNT, Notch and Hedgehog
5.10 Transcription factor DNA-binding domain classes
5.11 NF-kappaB
6. Cell-Survival Curves
6.1 Determination of in vitro cell survival curves
6.2 Target theory6.3 Linear quadratic models
6.4 The α/β value and the effect of dose fractionation
6.5 Effective dose response curves6.6 Survival curve calculations
6.7 Principles of tumor control probability and dose response relationships
6.8 Tumor control probability calculations
6.9 Tumor control versus risk of normal tissue complications – Risk-benefit analysis
7. Impact of Cell Cycle Phase, Dose Rate and Kinetic Factors on Radiation Responses
7.1 Production of a synchronous population of cells
7.2 Cell cycle stage and radiation response
7.3 CDKs and cyclins
7.4 Potentially lethal damage repair
7.5 Sublethal damage repair
7.6 Effects of hypoxia and LET on PLDR and SLDR
7.7 Dose rate effect
7.8 Radiolabeled immunoglobin therapy
7.9 Brachytherapy – LDR and HDR; interstitial and intracavitary use
7.10 DNA damage and ATM regulation of the cell cycle
7.11 Mitotic and labeling index
7.12 Calculation of cell cycle phases
7.13 Growth fraction and cell loss factor
7.14 Use of Tpot to predict tumor response
8. The Role of Oxygen in Irradiated Cells
8.1 Oxygen enhancement ratio
8.2 OER and LET
8.3 OER and oxygen concentration
8.4 Paired survival cures and determination of tumor hypoxic cell fraction
8.5 Reoxygenation
8.6 Hypoxia and tumor progression
9. The Use of Hypofractionation, Hyperfractionation and Accelerated Treatment in Radiotherapy
9.1 Strandquist plots
9.2 NSD, TDF and CRE and problems with their use
9.3 Evidence supporting the theory that the α/β ratio for early responding tissues and tumors is greater than the α/β ratio for late responding tissues
9.4 Relationship between biologically effective dose, total dose and fraction size
9.5 Hyperfractionation
9.6 Accelerated treatment
9.7 Hypofractionation
9.8 SBRT/SABR
9.9 Flash radiotherapy
9.10 Biologically effective dose
10. Angiogenesis, Microenvironment and Metastasis and Radiation Responses
10.1 Tumor microenvironment
10.2 Differences in vasculature between normal tissue and tumors
10.3 Angiogenesis
10.4 The angiogenic switch
10.5 Hypoxia, angiogenesis and HIF-1α
10.6 The angiogenic balance
10.7 Anti-angiogenic drugs
10.8 The normalization hypothesis
10.9 Methods to detect hypoxia
10.10 Metastasis
10.11 Matrix metalloproteinases
10.12 E-cadherin and catenins
10.13 Integrins
10.14 Aerobic glycolysis
11. Linear Energy Transfer and Relative Biological Effectiveness
11.1 Track and energy average calculation of LET
11.2 Factors that affect RBE
11.3 RBE as a function of LET, explanation for shape of curve
12. Radiation Sensitizers
12.1 Enhancement ratio
12.2 Halogenated pyrimidines
12.3 5-Fluorouracil and fluorodeoxyuridine
12.4 Gemcitabine12.5 Platinum analogues
12.6 Topoisomerase I inhibitors - irinotecan
12.7 Epidermal growth factor receptor inhibitors – cetuximab
12.8 Radiosensitizers undergoing clinical development
12.9 Hypoxic cell sensitizers
12.10 Bioreductive drugs
13. Radioprotectors and Radiomitigators
13.1 Dose reduction factor
13.2 Antioxidants
13.3 Sulfhydryl compounds
13.4 Pentoxifylline
13.5 Superoxide dismutase
13.6 Nitroxides
13.7 Naturally occurring antioxidants
13.8 Cytokines & growth factors
13.9 Palifermin
13.10 Angiotensin-converting enzyme inhibitors
13.11 Radiprotectors undergoing development
14. Particle Beam Radiotherapy
14.1 Protons
14.2 Carbon ions
15. Predictive Assays in Radiotherapy
15.1 Intrinsic cellular radiosensitivity
15.2 Oxygen status
15.3 Molecular markers
15.4 Gene expression tumor assays
15.5 Normal tissue assays
15.6 Radiogenomics
16. Interaction of Heat and Radiation
16.1 Methods to achieve localized heating
16.2 Possible targets for heat-induced lethality
16.3 Effect of pH and nutrient deficiency on sensitivity to heat
16.4 Hypoxia and hyperthermia
16.5 Thermotolerance
16.6 Hyperthermia combined with irradiation
16.7 Thermal enhancement ratio
16.8 Time sequence of heat and irradiation
16.9 Mild temperature hyperthermia
17. Classical and Targeted Chemotherapeutic Agents and Interaction with Radiation
17.1 Biological basis of chemotherapy
17.2 Alkylating agents
17.3 Antibiotics and other natural products
17.4 Antimetabolites
17.5 Hormonal therapies
17.6 mTOR inhibitors
17.7 Monoclonal antibodies
17.8 Histone deacetylase inhibitors
17.9 Small molecule tyrosine kinase inhibitors
17.10 Phosphoinositide-3 kinase (PI3K) inhibitors
17.11 Radioisotopes
17.12 Proteasome inhibitors
17.13 Fusion proteins
17.14 Immunotherapy and immunomodulatory agents
17.15 Hedgehog signaling pathway inhibitors
17.16 Protein synthesis inhibitors
17.17 CDK inhibitors
17.18 Oncolytic viral therapy
17.19 PARP inhibitors
17.20 BCL-2 inhibitors
17.21 The oxygen effect for chemotherapy agents
17.22 Drug resistance
17.23 Comparison of chemotherapeutic agents with radiation
17.24 Adjunct use of chemotherapeutic agents with radiation
17.25 Spatial cooperation
18. Radiation Carcinogenesis
18.1 Stochastic and non-stochastic effects of radiation
18.2 Epidemiologic studies of irradiated populations
18.3 Models for carcinogenesis
18.4 Cancer incidence as a function of dose; leukemia, breast, thyroid, bone, skin and lung
18.5 Second/Subsequent malignancies following radiotherapy
18.6 Low dose exposures and cancer risk
19. Hereditary Effects of Radiation
19.1 Radiation-induced genetic effects
19.2 Measurement of genetic risks
19.3 Megamouse project
19.4 Genetic risk in humans
20. In Utero Radiation Effects
20.1 Stages of development
20.2 Intrauterine death, congenital abnormalities and neonatal death
20.3 Mental retardation and microcephaly
20.4 Dependence upon dose-rate and stage of gestation
20.5 Sensitivity of the developing embryo and fetus to radiation-induced carcinogenesis
21. Radiation Protection Guidelines
21.1 Sources of radiation to the human population
21.2 Dose equivalent
21.3 Effective dose equivalent
21.4 Committed Dose
21.5 Collective Dose
21.6 Genetically significant dose
21.7 Doses from diagnostic radiology and nuclear medicine
21.8 Estimation of fatal cancers and genetic effects in an irradiated population
21.9 Limits for occupational exposure
21.10 ALARA21.11 Protection of the embryo and fetus
21.12 Emergency occupational exposure
21.13 Non-occupational limits
21.14 Exposure to indoor radon
21.15 Negligible individual dose
22. Normal Tissue and Organ Radiation Responses
22.1 Molecular basis of acute and late effects
22.2 Cell population kinetics of normal tissues
22.3 Hierarchical or type H tissues
22.4 Flexible or type F tissues
22.5 Functional Subunits
22.6 Categories of cell sensitivity
22.7 Organ radiation responses
22.8 Tolerance doses
22.9 QUANTEC
23. Whole-Body Radiation Effects
3.1 Radiologic Terrorism
23.2 The latent period
23.3 Central nervous system syndrome
23.4 Gastrointestinal syndrome
23.5 Hematopoietic syndrome
23.6 LD50
23.7 Treatment of radiation accident victims and patients receiving TBI
24. Topics in Cancer Biology Relevant to Radiation Oncology
24.1 Hallmarks of cancer
24.2 Cell cycle regulation – cyclins and CDKs
24.3 Cancer stem cells24.4 Multistage oncogenesis
24.5 Mechanisms of carcinogenesis
24.6 Oncogenes and mechanisms of oncogene activation
24.7 Tumor suppressor genes24.8 Hereditary disorders that predispose to cancer
24.9 Loss of heterozygosity
24.10 pRb
24.11 p53
24.12 INK4a/ARF
24.13 ATM and regulation of the G1/S, S and G2/M checkpoints
24.14 ATR and Seckel syndrome
Product details
Product details
- Edition: 1
- Latest edition
- Published: September 1, 2026
- Language: English
About the authors
About the authors
BR
Barry S. Rosenstein
Dr. Rosenstein is a Professor of Radiation Oncology and a Professor of Genetics & Genomic Sciences at the Icahn School of Medicine at Mount Sinai. The focus of Dr. Rosenstein’s research program for the past 25 years has been the identification of genetic/genomic markers associated with the development of adverse effects resulting from radiotherapy. In this context, he was one of the first investigators to hypothesize that possession of single nucleotide polymorphisms in certain genes may render some cancer patients more susceptible to injuries resulting from radiotherapy. Dr. Rosenstein established and co-led for 14 years the Radiogenomics Consortium (RGC), representing an international consortium currently with 240 members in 33 countries across 135 institutions. Through his efforts, Dr. Rosenstein, has been in the forefront of research in the use of big data in radiation oncology and has collaborated with investigators possessing expertise in bioinformatics and statistics to employ machine learning-based modeling approaches in radiogenomic studies.
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