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Cover
Title Page
Editorial Board
1. Reviewers
2. American Cancer Society Content Staff
List of Contributors
Introduction
Section 1: Cancer Causes, Prevention, and Early Detection
1. 1 Descriptive Epidemiology
  1. Introduction
  2. Cancer Surveillance in the US
  3. Measuring the Cancer Burden
  4. Cancer Occurrence Patterns in the US
  5. Demographic and Geographic Patterns
  6. Conclusion
  7. References
2. 2 Fundamentals of Cancer Epidemiology
  1. Introduction
  2. Exposures and Disease Occurrence
  3. Study Designs
  4. Measures of Association
  5. Threats to Validity
  6. Summarizing or Combining Data from Multiple Studies
  7. “Proof” of Causality
  8. Summary
  9. References
3. 3 Socioeconomic Inequalities in Cancer Incidence and Mortality
  1. Introduction
  2. Data Sources and Methodology
  3. Socioeconomic Disparities in Cancer Mortality Based on Aggregate County‐Level Data
  4. Socioeconomic Disparities in Cancer Mortality Based on Individual‐level Data
  5. Socioeconomic Disparities in Site‐Specific Cancer Incidence
  6. Summary and Conclusions
  7. References
4. 4 The Global Burden of Cancer
  1. Introduction
  2. International Cancer Data Sources
  3. All Cancer Sites
  4. Lung Cancer
  5. Colon and Rectum Cancer
  6. Breast Cancer
  7. Prostate Cancer
  8. Liver Cancer
  9. Cervical Cancer
  10. Stomach Cancer
  11. Esophageal Cancer
  12. Oral Cavity and Pharyngeal Cancers
  13. Conclusion
  14. References
5. 5 Counseling and Testing for Inherited Predisposition to Cancer
  1. Introduction
  2. Genetic Counseling and Testing
  3. Hereditary Breast and Gynecologic Cancer Syndromes
  4. Hereditary Colorectal Cancer Syndromes
  5. Hereditary Upper Gastrointestinal Cancer Syndromes
  6. Hereditary Endocrine Syndromes
  7. Hereditary Kidney Cancer Syndromes
  8. New Directions and Research
  9. References
6. 6 Tobacco
  1. Introduction
  2. Epidemiology
  3. Current Approaches to the Control of Tobacco Use
  4. What “Works” in Tobacco Control?
  5. Special Emphasis Section: Treatment of Tobacco Dependence
  6. Current Issues and Controversies in Tobacco Control
  7. Global Tobacco Control Issues and Considerations
  8. Conclusion
  9. References
7. 7 Microbial Carcinogens
  1. Introduction
  2. Epstein–Barr Virus
  3. Hepatitis B Virus
  4. Hepatitis C Virus
  5. Kaposi Sarcoma Herpesvirus
  6. Human Immunodeficiency Virus Type‐1
  7. Human Papillomavirus
  8. Human T‐cell Lymphotropic Virus
  9. Helicobacter Pylori
  10. Schistosoma Haematobium
  11. Opisthorchis Viverrini and Clonorchis Sinesis
  12. Conclusions
  13. References
8. 8 Environmental and Occupational Carcinogens
  1. Introduction
  2. Criteria for Classifying Agents as Carcinogenic to Humans
  3. Selected Occupational and Environmental Exposures
  4. Importance of Continued Research
  5. Perspectives That May Be Helpful for Clinicians in Discussing Occupational and Environmental Carcinogens with Their Patients and the General Public
  6. References
9. 9 Nutrition and Physical Activity for Cancer Prevention
  1. Introduction
  2. Overweight and Obesity
  3. Physical Activity and Cancer Prevention
  4. Nutrition, Dietary Factors, and Alcohol Consumption and Cancer Prevention
  5. Community Action
  6. References
10. 10 Sun Protection
  1. Introduction
  2. Epidemiology
  3. Risk Factors
  4. Mechanisms of UVR‐induced Carcinogenesis
  5. Host Phenotype
  6. Prevention of Skin Cancers
  7. Chemoprevention
  8. Screening for Skin Cancer
  9. Conclusion
  10. References
11. 11 Screening and Early Detection
  1. Introduction
  2. The Decision to Screen – Key Criteria
  3. Research Designs for the Evaluation of Screening
  4. Measures of Screening Performance
  5. The Acceptability of the Screening Test
  6. Common Screening Tests
  7. Conclusion
  8. References
Section 2: Cancer Biology
1. 12 The Principles and Drivers of Cancer
  1. Introduction – The Causal Chain of Cancer
  2. Endogenous Alteration to DNA
  3. Exogenous Factors Affecting DNA
  4. DNA Repair
  5. The Drivers of Cancer
  6. Cell Death and its Resistance in Cancer Cells
  7. Induction of Angiogenesis
  8. Tissue Invasion and Metastasis
  9. The Tumor Microenvironment
  10. Conclusion
  11. References
Section 3: Diagnosis
1. 13 Imaging in Oncology
  1. Introduction
  2. Technical Principles
  3. Imaging in Different Clinical Settings
  4. Radiation Protection
  5. References
2. 14 The Pathologic Evaluation of Neoplastic Diseases
  1. Introduction
  2. Interactions Between Clinicians and Pathologists
  3. Definitions of Tumor Types
  4. Macroscopic Examination of Tissue Specimens
  5. Histologic Study of Human Malignancies
  6. Staging and Grading
  7. Frozen Section Examination
  8. Cytopathology
  9. Special Slide‐Based Procedures
  10. Evaluation of Tumor Markers in Tissue and Biofluids
  11. Flow Cytometry
  12. Cytogenetics
  13. Molecular Biologic Techniques
  14. Microarray Analysis
  15. Polymerase Chain Reaction
  16. DNA Sequence Analysis
  17. Summary
  18. References
3. 15 Cancer Staging
  1. Introduction
  2. Characteristics of the TNM System
  3. Application of Prognostic Factors
  4. Rating Prognostic Factors
  5. Managing Change
  6. Residual Tumor Classification
  7. Isolated Tumor Cells Versus Micrometastases
  8. Staging and Large Data Sets
  9. Literature Review
  10. Staging and Neoadjuvant Therapy
  11. The Future
  12. References
Section 4: Treatment Modalities
1. 16 Surgical Oncology Overview
  1. Introduction
  2. Diagnosis
  3. Staging
  4. Surgery with Curative Intent
  5. Management of Metastatic Disease
  6. Palliation
  7. Reconstructive and Plastic Surgery
  8. Surgical Prophylaxis
  9. Access Surgery
  10. Recent Surgical Technical Innovations
  11. Minimally Invasive Surgery
  12. Robot‐Assisted Surgery
  13. Summary
  14. References
2. 17 Radiotherapy
  1. Historical Viewpoint
  2. Radiation Physics
  3. Radiation Biology Interactions and Considerations
  4. Radiotherapy Processes: Indication, Planning, and Delivery
  5. Modalities in Radiotherapy
  6. Conclusion
  7. References
3. 18 Cytotoxic Chemotherapy
  1. Introduction
  2. The Scientific Basis for Cytotoxic Chemotherapy Use in Cancer
  3. Principles of Cytotoxic Chemotherapy Pharmacology
  4. Practical Aspects of Chemotherapy Administration
  5. Classes of Agents (Table 18.1)
  6. Conclusion
  7. References
4. 19 Hormonal Therapy for Cancer
  1. Historical Background of Hormonal Therapy for Breast Cancer
  2. General Therapeutic Strategies for Metastatic Breast Cancer
  3. Current Hormonal Therapies for Breast Cancer
  4. Current Hormonal Therapies for Prostate Cancer
  5. Conclusions
  6. References
5. 20 Immunotherapy of Cancer
  1. Introduction
  2. Tumor Immunogenicity
  3. Role of the Immune System in Cancer
  4. Nonspecific Immunostimulants
  5. Cytokines
  6. Immunotherapy Targeting T‐cell Cosignaling Checkpoints
  7. Adoptive Cellular Therapy
  8. Vaccine‐Based Immunotherapy
  9. Active Immunotherapeutic Options
  10. Immunotherapy Targeting T‐cell Cosignaling Checkpoints: Melanoma, NSCLC, RCC, Classical Hodgkin Lymphoma, Bladder Cancer and HNSCC
  11. Conclusion
  12. References
6. 21 Targeted Therapies
  1. Introduction
  2. Types of Targeted Agents
  3. Signal Transduction Pathways Targeted in Cancer
  4. Basic Cellular Processes Targeted in Cancer
  5. Angiogenesis
  6. Conclusion
  7. References
7. 22 Hematopoietic Stem Cell Transplantation for Cancer
  1. Introduction
  2. Autologous Hematopoietic Stem Cell Transplantation
  3. Allogeneic Hematopoietic Stem Cell Transplantation (alloHSCT)
  4. References
8. 23 Diet, Physical Activity, and Weight Control for Cancer Patients and Survivors
  1. Introduction
  2. Current ACS Guidelines
  3. Lifestyle Behaviors Among Cancer Survivors
  4. Implementing Healthy Lifestyle Change in Cancer Survivors
  5. Conclusion
  6. References
9. 24 Clinical Trials
  1. Introduction: Definition and Importance of Clinical Trials
  2. Clinical Trial Types and Designs
  3. Ethical Considerations for Clinical Trials
  4. Phases of Clinical trials
  5. Clinical Trials involving Radiation Therapy, Surgery, and Multidisciplinary Therapy
  6. Cancer Prevention Trials
  7. Limitations and Challenges of Clinical Trials
  8. Public versus Commercial Sponsors of Clinical Trials
  9. National Clinical Trials Network
  10. Clinical Trials in the Era of Genomic Medicine and Personalized Medicine
  11. References
10. 25 Complementary and Alternative (Integrative) Oncology
  1. Introduction
  2. Definitions: Alternative, Complementary, Integrative
  3. Prevalence of CIM
  4. CIM and Symptom Management
  5. Communicating about CIM
  6. CIM Modalities
  7. Nutrition and Exercise
  8. Summary
  9. References
Section 5: Geriatric Oncology
1. 26 Geriatric Oncology
  1. Introduction
  2. “Geriatric”
  3. Assessing the Older Patient with Cancer
  4. Coordination of Care: Role of the Multidisciplinary Team
  5. Diminished Physiological Capacity and Reserve
  6. Predicting Chemotherapy‐Associated Toxicity
  7. Approach to the Older Patient with Cancer
  8. References
Section 6: Symptom Management, Palliative Care, Complications and Toxicities of Treatment, Patient‐Reported Outcomes, etc.
1. 27 Palliative and Supportive Care
  1. Introduction
  2. Definitions of Palliative Medicine
  3. Components for a Palliative Care Program
  4. Palliative Care in the Intensive Care Unit
  5. Growth of a Palliative Care Program
  6. Barriers to Access Palliative Care
  7. Benefits of Palliative Care
  8. Access and Integration of Palliative Care with Cancer Therapy
  9. Models of Delivery of Palliative Medicine
  10. Communication
  11. Symptoms Assessment and Management
  12. End‐of‐Life Care
  13. Palliative Sedation
  14. Conclusion
  15. References
2. Chapter 28: Sexuality and Fertility
  1. Introduction
  2. Cancer and Sexuality
  3. Reproductive Issues
  4. Communication
  5. Conclusions
  6. References
3. Chapter 29: Psychiatric Issues in Cancer Patients
  1. Introduction
  2. Major Psychiatric Disorders in Oncology
  3. Symptoms and Situations not Otherwise Classified in Oncology Settings
  4. Conclusion
  5. Acknowledgment
  6. References
4. Chapter 30: Oncologic Emergencies
  1. Introduction
  2. Infectious Emergencies
  3. Neurologic Emergencies
  4. Metabolic Emergencies
  5. Cardiovascular Emergencies
  6. Respiratory Emergencies
  7. Chemotherapeutic Emergencies
  8. Hematologic Emergencies
  9. References
5. 31 Patient‐Reported Outcomes in Cancer
  1. Introduction
  2. What are PROs and What are Their Advantages?
  3. Use of PROs in Clinical Practice
  4. How are PROs used in Clinical and Public Health Research?
  5. Challenges and Considerations in the Use of PRO Measures
  6. Summary
  7. References
6. 32 Survivorship Care
  1. Introduction
  2. Breast Cancer Survivors
  3. Prostate Cancer Survivors
  4. Colorectal Cancer Survivors
  5. Lymphoma Survivors
  6. Testicular Cancer Survivors
  7. Head and Neck Cancer Survivors
  8. Lung Cancer Survivors
  9. Special Therapeutic Modality: Allogeneic Hematopoietic Stem Cell Transplantation
  10. Special Population: The Childhood Cancer Survivor
  11. Special Population: The Elderly Cancer Survivor
  12. Conclusions
  13. Acknowledgments
  14. References
Index
End User License Agreement

List of Tables

Chapter 01
1. Table 1.1 Trends in 5‐year relative survival rates (%) by race, US, 1975–2012.
2. Table 1.2 Incidence rates by site, race, and ethnicity, US, 2009–2013.
3. Table 1.3 Death rates by site, race, and ethnicity, US, 2010–2014.
Chapter 02
1. Table 2.1 Basic measures of cancer occurrence or burden used in epidemiology.
2. Table 2.2 Hypothetical data from 1 year of follow‐up in a cohort study of 400,000 men.
3. Table 2.3 Relative risk and attributable risk of cancer mortality by pipe smoking.
4. Table 2.4 Criteria for assessing causality between an exposure and cancer incidence and/or mortality.
Chapter 03
1. Table 3.1 Age‐adjusted all‐cancer and site‐specific cancer mortality rates per 100,000 population and relative risk (RR) of mortality among those aged ≥25 years by educational attainment and poverty status.
2. Table 3.2 Prevalence (%) of current smoking, obesity, and cancer screening by education and income/poverty level in the United States.
Chapter 04
1. Table 4.1 Incidence and mortality rates and number of cases and deaths by sex and cancer site for more and less developed areas, 2012.
2. Table 4.2 Five‐year net survival(%) for selected cancers among adults aged 15 and older in select countries, 2005–2009.
Chapter 05
1. Table 5.1 Major adult cancer predisposition syndromes, with associated features and genes. Associated malignancies are listed first, followed by less common tumors and benign features. Modified from Weitzel et al. [1]. The incidences of these syndromes are listed elsewhere [138]. Human Genome Organisation (HUGO)‐approved gene abbreviations can be found at http://www.genenames.org/. This list is not exhaustive. Syndromes and familial clusters that are poorly characterized genetically are not included (see text).
2. Table 5.2 Tumors/cancers that are strongly associated with a germline cancer predisposition. Each of the tumors/cancers listed here (organized by organ system) should trigger a referral for genetic counseling [139], regardless of other medical/family history. This list is not meant to be comprehensive, and does not include combinations of different tumor types.
Chapter 06
1. Table 6.1 Guidance for use of the seven first‐line, FDA‐approved medications.
Chapter 07
1. Table 7.1 Microbial carcinogens: summary of biologic mechanisms.
2. Table 7.2 Microbial carcinogens and their associated cancer sites.
3. Table 7.3 Number of new cancer cases in 2008 attributable to infection, by infectious agent and development status.
Chapter 08
1. Table 8.1 Agents that the IARC has classified as having sufficient evidence of causing lung cancer in humans based on IARC Monograph 100 and subsequent monographs. Highlighted agents or exposure circumstances are discussed in the text.
2. Table 8.2 Agents that the IARC has classified as having sufficient evidence of causing leukemia or lymphoma in humans based on IARC Monograph 100 and subsequent monographs. Highlighted agents or exposure circumstances are discussed in the text.
3. Table 8.3 Agents that the IARC has classified as having sufficient evidence of causing cancer of the urinary bladder in humans based on IARC Monograph 100 and subsequent monographs. Highlighted agents or exposure circumstances are discussed the in text.
4. Table 8.4 Agents that the IARC has classified as having sufficient evidence of causing cancer sites other than lung, leukemia/lymphoma or urinary bladder in humans based on IARC Monograph 100 and subsequent monographs. Highlighted agents or exposure circumstances are discussed in the text.
Chapter 09
1. Table 9.1 ACS Guidelines on Nutrition and Physical Activity for Cancer Prevention.
2. Table 9.2 Examples of moderate and vigorous physical activity.
Chapter 11
1. Table 11.1 Key factors in the decision to introduce screening.
2. Table 11.2 Measures of screening performance.
3. Table 11.3 The randomized controlled trials of breast cancer screening.
4. Table 11.4 ACS and USPSTF guidelines for breast cancer screening in average risk women.
5. Table 11.5 ACS and USPSTF guidelines for colorectal cancer screening in average risk adults ages 50 years and older.
6. Table 11.6 The 2001 Bethesda System.
7. Table 11.7 ACS and USPSTF guidelines for cervical cancer screening in average risk women ages 21 years and older.
8. Table 11.8 ACS and USPSTF guidelines for lung cancer screening with LDCT in current and former smokers aged 55–74.
9. Table 11.9 Key discussion points for the process of shared decision making related to screening for early lung cancer detection with low dose helical CT.
10. Table 11.10 ACS and USPSTF guidelines for prostate cancer screening.
11. Table 11.11 Core elements of the information to be provided to men to assist with their decision about prostate cancer screening.
Chapter 12
1. Table 12.1 DNA damage and repair.
Chapter 14
1. Table 14.1 Nomenclature pertaining to neoplastic diseases.
2. Table 14.2 Selected antigenic moieties of diagnostic value in practical immunohistochemistry.
3. Table 14.3 Example of the use of selected monoclonal antibodies for the classification of a lymphoma by flow cytometry.
4. Table 14.4 Examples of chromosomal translocations in hematopoietic and soft tissue/bone tumors.
Chapter 16
1. Table 16.1 Selected results from cytoreduction and hyperthermic intraperitoneal chemotherapy for peritoneal carcinomatosis literature.
2. Table 16.2 Comparison of laparoscopic colectomy versus open colectomy randomized controlled trials.
Chapter 17
1. Table 17.1 Examples of fractionation regimens.
2. Table 17.2 QUANTEC summary: approximate dose/volume/outcome data for several organs following conventional fractionation.
3. Table 17.3 Therapeutic isotopes.
Chapter 18
1. Table 18.1 Cytotoxic chemotherapy and cell cycle activity.
Chapter 20
1. Table 20.1 Tumor antigens [1].
2. Table 20.2 Registration trials of immunotherapeutic agents in bladder cancer, melanoma, RCC, and prostate cancer.
3. Table 20.3 Ongoing Phase III trials of cytokines singly or in combination.
4. Table 20.4 Registration trials of PD‐1 and CTLA‐4 inhibitors in melanoma, NSCLC, RCC, Hodgkin’s lymphoma and SCCHN.
5. Table 20.5 Recently completed and ongoing Phase III trials of cancer vaccines.
Chapter 21
1. Table 21.1 Targeted therapies.
Chapter 22
1. Table 22.1 Indications for an autologous hematopoietic stem cell transplantation.
2. Table 22.2 Neoplastic indications for an allogeneic hematopoietic stem cell transplantation.
3. Table 22.3 Common toxicities post allogeneic hematopoietic stem cell transplantation.
Chapter 23
1. Table 23.1 American Cancer Society Guidelines on Nutrition and Physical Activity for Cancer Survivors.
2. Table 23.2 Sample strategies to promote healthy lifestyles.
Chapter 24
1. Table 24.1 Major components of a clinical trial protocol.
2. Table 24.2 Clinical trial phases.
3. Table 24.3 Goals of therapeutic clinical trials.
4. Table 24.4 Role of publicly funded trials.
Chapter 25
1. Table 25.1 National Institutes of Health – National Center for Complementary and Integrative Health.
2. Table 25.2 Recommended websites for evidence‐based resources (all accessed 21 August 2017).
Chapter 26
1. Table 26.1 ADLs and IADLs [27, 28].
Chapter 27
1. Table 27.1 Recommendation for patient‐centered communication when discussing bad news [100–102].
2. Table 27.2 Selected studies supporting use of common antiemetics.
Chapter 28
1. Table 28.1 Resources for oncology providers and patients.
2. Table 28.2 Communication models for addressing sexual health.
Chapter 29
1. Table 29.1 Medications frequently used to treat depression in cancer patients.
2. Table 29.2 Commonly prescribed benzodiazepines in cancer patients.
Chapter 30
1. Table 30.1 Multinational Association of Supportive Care in Cancer (MASCC) score.
2. Table 30.2 Patchell Criteria for operative intervention in cord compression.
3. Table 30.3 Treatment of hypercalcemia.
4. Table 30.4 Laboratory definition of tumor lysis syndrome using Cairo‐Bishop classification.
5. Table 30.5 Grading of tumor lysis syndrome complications.
6. Table 30.6 Treatment of metabolic alterations in tumor lysis syndrome.
Chapter 31
1. Table 31.1 Classification of PROs and selected measures. Ahmed et al. 2012 [11]. Reproduced with permission of Wolters Kluwer Health, Inc.
Chapter 32
1. Table 32.1 Late and long‐term effects among breast cancer survivors.

List of Illustrations

Chapter 01
1. Figure 1.1 Long‐term trends in age‐adjusted cancer incidence and death rates, 1930–2014.
2. Figure 1.2 Leading new cancer cases and deaths in the US in 2017. Ranking is based on modeled projections and may differ from the most recent observed data. *Estimates are rounded to the nearest 10 and cases exclude basal cell and squamous cell skin cancers and in situ carcinoma except urinary bladder.
3. Figure 1.3 Long‐term trends in age‐adjusted cancer incidence rates among men, 1975–2013.
4. Figure 1.4 Long‐term trends in age‐adjusted cancer incidence rates among women, 1975–2013.
5. Figure 1.5 Long‐term trends in age‐adjusted male cancer death rates by site, 1930–2014.
6. Figure 1.6 Long‐term trends in age‐adjusted female cancer death rates by site, 1930–2014.
Chapter 03
1. Figure 3.1 Weighted correlations between area socioeconomic index and county‐level age‐adjusted cancer mortality rates, US, 1950–2007.
2. Figure 3.2 Trends in (a) lung, (b) colorectal, (c) female breast, and (d) cervical cancer mortality rates by area socioeconomic deprivation index, US, 1950–2013.
Chapter 04
1. Figure 4.1 Most commonly diagnosed cancers worldwide by sex, 2012.
2. Figure 4.2 Estimated radiotherapy availability worldwide, 2013. *Countries with 100% of patients able to access radiotherapy may also include countries where radiotherapy supply is greater than demand, although disparities in access may still exist within these countries.
Chapter 05
1. Figure 5.1 Estimated proportions of familial (a) breast, (b) ovarian cancer. Most cancer is sporadic, although familial aggregation is also observed for most cancer types. Most familial cancer remains unexplained. The proportion attributable to known, high‐risk syndromes (BRCA1/2, MMR genes, TP53) is not large. Past genome‐wide association studies (GWAS) have identified numerous low‐penetrance loci (pre‐iCOGS), and recent international consortia, such as the Illumina Collaborative Oncological Gene‐environment Study (iCOGS), are uncovering additional loci. In the figure, “pre‐iCOGS” and “iCOGS” refer to susceptibility loci (SNPs) identified before and after use of the iCOGS array, respectively. “Other iCOGS estimated” refers to loci anticipated to be discovered as studies with the array progress [140]. SNP, single nucleotide polymorphism.
2. Figure 5.2 Elements of hereditary/familial cancer genetic counseling.
3. Figure 5.3 Sample pedigree, suggestive of Lynch syndrome. Typical pedigree taken during genetic counseling, used for risk assessment. Arrow indicates the proband (consultant); circles represent women; squares men. Horizontal alignment indicates a generation; vertical lines show offspring/parents. Shading indicates a cancer diagnosis. Diagonal line indicates individual is deceased. Here, the proband was diagnosed with colorectal cancer at age 51 and his maternal family history meets Amsterdam criteria [47] for Lynch syndrome.
4. Figure 5.4 The utility of different methods of genetic and genomic analyses used to define cancer susceptibility factors plotted as a function of penetrance and population frequency. Traditional approaches such as linkage analysis in large affected families have successfully defined the established rare and highly penetrant cancer syndromes, discussed in this chapter (shown at the top left). GWAS (genome‐wide association studies) of large numbers of individuals affected and unaffected with common sporadic cancers have identified common variants with small effects (bottom right). The anticipated utility of NGS (next‐generation sequencing) stems from its potential to identify additional moderate‐to‐high risk cancer susceptibility genes in smaller cancer families.
Chapter 07
1. Figure 7.1 Global prevalence of chronic hepatitis B virus infection.
2. Figure 7.2 Global prevalence of hepatitis C virus infection.
Chapter 11
1. Figure 11.1 The relationship between sojourn time and lead time in cancer screening. The cancer is asymptomatic, but detectable by screening, i.e., the sojourn time (t₀ – t₂). Lead time gained = (t₂ – t₁).
2. Figure 11.2 Cancer survival, lead time, and lead time bias. In this example, there are two hypothetical patients, A and B. Their cancers are undetectable before t₀; asymptomatic but detectable by screening at t₁ between t₀ and t₂; and detectable with symptoms after t₂. The lead time gained = (t₂ – t₁). At t₃ death occurs for both hypothetical patients, A and B, but patient A appears to have longer survival because screening advanced the time of diagnosis.
3. Figure 11.3 The relationship between sojourn time and length bias in cancer screening. Cancers that are intersected by the vertical lines (screening events) are screen detected, while those not intersected are missed by screening. Note that some cancers with long sojourn times are detectable at consecutive screening rounds.
Chapter 13
1. Figure 13.1 A 61‐year‐old male with clear cell renal carcinoma (pathological stage T3b). The patient had previously undergone right radical nephrectomy for tumor. (a) Longitudinal, color‐encoded transabdominal Doppler ultrasound of the left kidney shows a 4‐cm tumor in the posterior renal cortex (star). Note the hypovascularity of the tumor compared to normal renal cortical parenchyma, recognizable by the lack of Doppler signal within the tumor. (b) Coronal contrast‐enhanced CT shows that the renal tumor (star) is in direct contact with renal sinus fat (arrow). Such contact is associated with a high probability of muscular venous branch invasion, which was histologically proven in this case. An enlarged, enhancing paraaortic mass is suspicious for lymph node metastasis (curved arrow). An incidental simple cyst in the lower pole of the left kidney (arrowhead) shows a thin wall, homogeneous water‐like attenuation, and no contrast enhancement.
2. Figure 13.2 A 53‐year‐old female with advanced cervical cancer (FIGO stage IVB). (a) Sagittal T2‐weighted MRI demonstrates a cervical mass (arrows) with extension into the lower uterine segment (arrowhead) and a distended endometrial cavity (star). (b) Coronal T2‐weighted MRI demonstrates bilateral parametrial invasion (arrows) and distended endometrial cavity (star). (c) Axial CT image with oral contrast demonstrates subcentimeter left para‐aortic and aortocaval lymph nodes (arrows). (d, e) Axial fused FDG PET and CT images demonstrate abnormal FDG tracer uptake in left para‐aortic and aortocaval lymph nodes consistent with metastatic involvement (arrows) and in a right anterior peritoneal tumor implant (dashed arrow). The fused images also show physiologic tracer accumulation in the liver (star) and bone marrow (asterisk), as well as excreted tracer in the renal collecting systems bilaterally (arrowheads).
Chapter 14
1. Figure 14.1 Imaging studies of a child with hematuria show an intravesical mass (a). The resected tumor manifests a multiply polypoid “grape cluster”‐like appearance (b), which is contextually diagnostic of botryoid embryonal rhabdomyosarcoma.
2. Figure 14.2 Well‐differentiated papillary noninvasive urothelial carcinoma shows minimal morphological differences from hyperplastic, non‐neoplastic urothelium (a). Poorly differentiated urothelial carcinoma with sarcomatoid (spindle‐cell) features has little microscopic resemblance to normal urothelium (b).
3. Figure 14.3 Gleason scoring of prostatic carcinoma is done by observing the range of microscopic growth patterns in the tumor, which are segregated into five groups (a). The first and second most dominant patterns are summed to yield the Gleason “score” (e.g., 3 + 4, 4 + 5, etc.). Gleason pattern 1 and 2 tumors are well differentiated (b); pattern 3 lesions are moderately differentiated (c); and pattern 4 and 5 neoplasms are poorly differentiated (d).
4. Figure 14.4 This bronchial brushing cytology specimen shows a cluster of highly atypical epithelioid cells that are three‐dimensional and show prominent nucleoli. The image is that of adenocarcinoma. A fragment of non‐neoplastic bronchial epithelium is seen for comparison at the far left of the photograph.
5. Figure 14.5 Fine‐needle aspiration of a thyroid mass yielded this specimen, in which cohesive, cytologically monotonous cells are present with nuclear grooves. The image is diagnostic of papillary thyroid carcinoma.
6. Figure 14.6 A broad range of nuclear sizes, shapes, and densities is represented in this fine needle aspiration specimen from an adenosquamous carcinoma of the lung.
7. Figure 14.7 Poorly differentiated malignant neoplasms can be markedly similar to one another under the microscope, despite having different cellular lineages. As examples, poorly differentiated sinonasal carcinoma (a), amelanotic sinonasal melanoma (b), and sinonasal large‐cell non‐Hodgkin lymphoma (c) are shown here, the histologic images of which are mutually superimposable. Special studies are necessary to separate them diagnostically; for example, an immunostain for CD45 (leukocyte common antigen) is shown in (d) in large‐cell lymphoma
8. Figure 14.8 Spindle‐cell sarcomas also may exhibit markedly similar microscopic growth patterns, despite different cellular lineages. A leiomyosarcoma is shown in (a), and a monophasic synovial sarcoma is depicted in (b). Their histological appearances are virtually identical. However, immunostains for desmin (a myogenic marker) are positive in leiomyosarcoma (c) and others for transducin‐like enhancer protein of split 1 (TLE1) are reactive in monophasic synovial sarcoma (d). Those findings are mutually exclusive.
9. Figure 14.9 Metastatic carcinoma is present in this bone biopsy (a); the patient previously had no history of malignancy, and, therefore, the source of the tumor was unknown. Immunostaining for prostate‐specific antigen (b) establishes the identity of the lesion as metastatic prostatic adenocarcinoma.
10. Figure 14.10 This uterine cervical squamous carcinoma has been studied by chromogenic in situ hybridization for human papillomavirus type 18. The tumor cells show a positive integration signal (blue) in virtually all the neoplastic cells.
11. Figure 14.11 Examples of gene amplification detected by fluorescent in situ hybridization. Right panel: glioblastoma with epidermal growth factor receptor (EGFR) amplification in a so‐called “double minute” pattern with small individual red signals (the green signal represents a centromeric probe for chromosome 7 while the red signal is the gene specific probe for EGFR). Left panel: invasive breast cancer with HER‐2/neu amplification showing numerous red gene signals and considerably fewer green CEP17 signals (the green signal represents a centromeric probe for chromosome 17 while the red signal is the gene specific probe for Her2/neu; in this example, the HER‐2/neu to CEP17 signal ratio is >2.0).
12. Figure 14.12 Example of the classification of a lymphoma by flow cytometry (see Table 14.3). (a) Section of spleen from a 61‐year‐old woman showing effacement of the parenchyma by large malignant lymphocytes. (b) Scattergram of the malignant infiltrate obtained by flow cytometry. Note the presence of two gated regions corresponding to small lymphoctyes and large lymphocytes (arbitrarily labeled R1 and R3, respectively). The results of multiparametric analysis of the cells within region R3 when combined with the morphology of the tumor are diagnostic of large cell lymphoma, B cell type.
13. Figure 14.13 Example of molecular genetic analysis of Ewing sarcoma/peripheral neuroectodermal tumor (ES/PNET) arising in the kidney of a 60‐year‐old woman. (a) Hematoxylin and eosin stained section of the tumor. (b) Reverse transcriptase polymerase chain reaction (RT‐PCR) of formalin‐fixed paraffin‐embedded tissue demonstrates the presence of an EWSR1‐FLI1 gene fusion transcript that is characteristic of ES/PNET. Lane 1, molecular size markers; lane 2, positive control RT‐PCR product from an ES/PNET cell line (EWSR1 exon 7 to FLI1 exon 5 fusion); lane 3, renal tumor (EWSR1 exon 7 to FLI1 exon 8 fusion); lane 4, negative control.
14. Figure 14.14 Example of the use of Sanger sequencing to characterize the genotype of a gastrointestinal stromal tumor (GIST). (a) Hematoxylin and eosin stained section of the tumor. (b) DNA was extracted from formalin‐fixed paraffin embedded sections of the tumor, and direct DNA sequence analysis of the KIT gene was performed. The computer‐generated base sequence (top) inferred from the automated sequencing electropherogram (bottom) is shown; comparison with the wild‐type KIT sequence demonstrates a six base deletion that changes codons 552 through 554 but maintains the gene’s open reading frame, a mutation characteristic of GIST.
15. Figure 14.15 Example of the use of DNA sequence analysis of a panel of 50 genes by next generation sequencing to identify unexpected sequence changes that suggest the use of a targeted therapy. The thymic carcinoma in this patient (a) was no longer responsive to standard therapies; next generation sequence testing identified a 3 bp deletion of KIT resulting in p.D579del (b), a deletion known to be responsive to tyrosine kinase inhibitor therapy with imatinib in other tumor types. The patient was treated with imatinib as part of a clinical trial, with a resulting decrease in tumor size that lasted over 2 years.
Chapter 15
1. Figure 15.1 The REMARK checklist for reporting of prognostic factors.
Chapter 16
1. Figure 16.1 Example of peritoneal carcinomatosis with heavy disease burden present within the abdominal cavity.
2. Figure 16.2 Example of locally advanced breast cancer with skin involvement and necrosis present.
Chapter 17
1. Figure 17.1 The electromagnetic spectrum extending over several orders of magnitude and identifying some of the more commonly noted regions of the spectrum.
2. Figure 17.2 X‐ray interactions in matter: the Compton effect and the photoelectric effect. The first step in the absorption of a photon of X‐rays or gamma rays is the conversion of the energy of the photon into the kinetic energy of an electron or electron‐positron pair. At higher energies, when the energy of the incident photon greatly exceeds the binding energy of the bound electrons in the atoms of the absorber, Compton scatter dominates. Part of the photon energy is given to the electron as kinetic energy, whereas the photon is deflected and has reduced energy. At lower energies, when the binding energy of the bound electrons of the atoms of the absorber is not small compared to the photon energy, the photoelectric effect is most important. The photon disappears completely as it interacts with a bound electron. The electron is ejected with kinetic energy equal to the photon energy, less the energy required to overcome the electron bond. The vacancy caused by the removal of the electron must be filled by an electron dropping from an outer orbit, giving rise to a photon of characteristic radiation.
3. Figure 17.3 Percentage depth‐dose curves for a variety of radiation types used in clinical radiation therapy. These include X‐rays and γ‐rays (110 kV to 18 MV) and various energies of electrons (6–20 MeV). The inset shows the pattern of absorption at shallow depths and provides an illustration of the skin‐sparing effect of photons.
4. Figure 17.4 Cell survival curve and the linear quadratic model. (a) Typical survival curve for mammalian cells exposed to radiation (X‐rays or gamma rays) of low linear energy transfer (low‐LET). The curve is described by the initial slope D1, the final slope D0, and some expression of the width of the shoulder (either n, the extrapolation number, or D0, the quasi‐threshold dose). (b) Typical survival curve for mammalian cells exposed to low‐LET radiation, expressed in terms of the linear‐quadratic model. In this model, two components contribute to cell killing: one is proportional to dose (αD), and the other is proportional to the square of the dose (βD²). The ratio at which these two components are equal is the ratio of α/β.
5. Figure 17.5 Cell cycle and radiosensitivity. Cells are most sensitive to radiation during late G2 and M phases, moderately sensitive during late G1 and S phases, and most resistant in mid S and early G2 phases.
6. Figure 17.6 Typical prostate IMRT treatment plan using volumetric modulated arc therapy showing conformal avoidance of the rectum (brown), bladder (yellow), and femoral heads (orange and green), while delivering the dose prescription (79.2 Gy) to the clinical (magenta) and planning (navy) target volumes. (a) Axial cross‐section with dose color wash. (b) Corresponding dose‐volume histograms of the target volumes and organs‐at‐risk.
7. Figure 17.7 Depth‐dose distributions for a proton beam compared with other photon beams. The dose for the proton beam is limited for the entrance tissues, reaches a Bragg peak at the desired depth, then displays an extremely sharp fall‐off.
8. Figure 17.8 Color wash dose distributions comparing intensity modulated radiotherapy (IMRT) with photons (b) and uniform scanning proton therapy (a) for a patient with a gluteal soft tissue sarcoma, with a preoperative prescription dose of 50.0 Gy (RBE). Note the reduction in integral dose with the proton plan, particularly to the abdominopelvic organs.
Chapter 18
1. Figure 18.1 The Norton–Simon hypothesis [9]. The repeated administration of chemotherapy (arrows) leads to tumor volume regression that is proportional to the rate of growth. Minimizing the time between therapies will increase the likelihood of continued cell death across heterogeneous cell types.
2. Figure 18.2 The cell cycle. Cells progress through a cycle that consists of phases for growth (G1, S, and G2) and division (M), and they become quiescent when they exit this cycle (G0). The lines depict the relative length of time in each phase, and conventional cytotoxic chemotherapy works in each portion of the cycle, except G0, depending on mechanism of action.
3. Figure 18.3 Intrinsic and extrinsic pathways of apoptosis [13]. Both pathways of apoptosis activate caspases, which initiate and execute the apoptotic function. Caspase 3 catalyzes nuclear apoptosis, and caspase 9 is critical for the apoptosome, which further activates caspase 3. Other downstream caspases induce cleavage of protein kinases, cytoskeletal proteins, DNA repair proteins and inhibitory subunits of endonucleases. They also alter cytoskeleton integrity and cell cycle signaling, which cause morphological changes and eventual phagocytosis.
4. Figure 18.4 Folate metabolism and enzymatic reactions [104]. Inhibition of dihydrofolate reductase leads to depletion of intracellular reduced folate reserves, and accumulation of dihydrofolate. Increased amounts of dihydrofolate polyglutamates and can inhibit another key enzyme in DNA synthesis, thymidylate synthase. These effects in concert lead to reduced DNA synthesis in cancer cells following dihydrofolate reductase inhibition with antifolates.
Chapter 21
1. Figure 21.1 Sites of action of antibodies and tyrosine kinase inhibitors.
2. Figure 21.2 Mitogen‐activated protein kinase (MAPK) pathway and PI3K pathway with downstream effectors.
Chapter 27
1. Figure 27.1 Model of palliative care for patients with cancer.
2. Figure 27.2 Growth of palliative care clinical encounters from fiscal years 2000–2010. IP, inpatient; OP, outpatient; CO, palliative care consultation; FU, follow‐up clinical visit; PCU, palliative care unit. *Name change (supportive care from palliative care).
3. Figure 27.3 Conceptual framework for “Supportive Care”, “Palliative Care”, and “Hospice Care”. “Hospice Care” is part of “Palliative Care”, which in turn is under the umbrella of “Supportive Care”. “Palliative Care” predominantly addresses the care needs for patients with advanced cancer in both acute care facilities and the community, whereas “Supportive Care” provides an even broader range of services for patients throughout various stages of the disease, including diagnosis, active treatment, end of life, and survivorship.
4. Figure 27.4 Percentage of patients with access to palliative care according to tumor type.
5. Figure 27.5 The cancer care package. (a) In the Solo Practice Model, the oncologist provides both cancer assessment and treatment, and addresses a variety of supportive care issues such as pain and dyspnea. However, the lack of time and expertise means that these issues may not be managed adequately. (b) In the Congress Practice Model, the oncologist refers the patient to various specialities for all the supportive care issues. This could result in fragmented and expensive care. (c) In the Integrated Care Model, the oncologist routinely refers patients to palliative care for their supportive care needs. This helps to ensure patients receive comprehensive and integrated care, and it streamlines the provision of care.
6. Figure 27.6 Edmonton Symptom Assessment System.
7. Figure 27.7 WHO’s Pain Relief Ladder.
8. Figure 27.8 Interrelationships between neural pathway that mediate nausea and vomiting. GI, gastrointestinal. GERD, gastroesophageal reflux disease.
9. Figure 27.9 Memorial Delirium Assessment Scale (MDAS).
Chapter 30
1. Figure 30.1 Spinal cord compression from metastatic breast cancer.
Chapter 31
1. Figure 31.1 Conceptual model of health‐related quality of life in cancer survivors.
Chapter 32
1. Figure 32.1 Sample cancer treatment summary and survivorship care plan.

The American Cancer Society’s Principles of Oncology

Prevention to Survivorship

Editorial Board

Ted Gansler, MD, MBA, MPH (Principal Editor)

Reviewers

American Cancer Society Content Staff