2012 EDUCATIONAL BOOK - American Society of Clinical Oncology

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ADVANCES IN INFECTION MANAGEMENT IN PEDIATRIC ONCOLOGY CHAIR Andrew Y. Koh, MD University of Texas Southwestern Medical Center Dallas, TX SPEAKERS Lillian Sung, MD, PhD The Hospital for Sick Children Toronto, ON, Canada Theoklis Zaoutis, MD Children’s Hospital of Philadelphia Philadelphia, PA
Prolonged Febrile Neutropenia in the Pediatric Patient with Cancer Overview: Infectious diseases continue to be major causes of morbidity and mortality in pediatric patients with cancer. Yet not all pediatric patients with cancer with fever and neutropenia are at equal risk for substantial morbidity or mortality from infection. Patients at highest risk for developing infectious complications are those with severe and prolonged neutropenia, substantial medical comorbidity, and hematologic malignancy, or recipients of stem-cell transplantation. These “high-risk” patients also have concomitant host immune deficits as well: severe mucositis, lymphopenia, hypogammaglobulinemia, and gut microbial dysbiosis. Because bacterial and fungal infections are the most common infectious complications, continuation of empirical antibacterial antibiotics that were initiated at the onset of febrile neutropenia and prompt initiation of empirical antifungal therapy in ALTHOUGH THE advances of infectious diseases supportive care during the last several decades have permitted patients to successfully recover from the impact of cytotoxic cancer chemotherapy, infectious diseases continue to be major causes of morbidity and mortality in pediatric patients with cancer. This review will address the host immune deficits in pediatric patients with cancer, riskstratification of patients with febrile neutropenia, general management guidelines for patients with prolonged neutropenia, and potential strategies for preventing infectious diseases in patients with prolonged neutropenia. Host Defenses: Innate and Adaptive Immunity To best manage or prevent infectious complications in the patient with cancer with prolonged neutropenia, it is essential to understand the host immune deficits that result from the underlying disease and/or cancer chemotherapy. Mucocutaneous Barriers and Commensal Gut Microbiota Pediatric oncology patients sustain disruptions of the mucocutaneous integrity because of their underlying cancer and its treatment. The disruption of mucocutaneous barriers provides a key portal of entry for bacterial and fungal pathogens (Sidebar 1). Colonization by normal bacterial flora (aerobic gram-positive bacteria and a variety of anaerobic bacteria with relatively low virulence) provides a competitive microbiologic barrier to colonization by extrinsically acquired bacterial and fungal organisms. However, within 24 hours of hospitalization, seriously ill patients undergo a change in their indigenous microflora toward one of aerobic gram-negative organisms. 1 Approximately one-half of the responsible pathogens causing infections are acquired by oncology patients after initial admission to the hospital, and more than 80% of the microbiologically documented infections that occur in adult patients with acute myelogenous leukemia (AML) are caused by organisms that were a component of the endogenous mucosal organisms. 1 Phagocytic Cells By far the most important risk factor in the development of infections in children with cancer remains neutropenia. By Andrew Y. Koh, MD the setting of prolonged fever and neutropenia continue to be the standard of care. In high-risk patients, antibiotic therapy should be maintained until neutrophil counts have recovered. Adjunctive therapies have been shown to be ineffective (e.g., colony-stimulating factors) or necessitate further study (e.g., granulocyte infusions or keratinocyte growth factor treatment to heal mucositis). Prophylactic use of antibacterial and antifungal antibiotics in high-risk patients has shown promise but the fear of inducing antimicrobial-resistant strains remains a deterrent. Finally, the novel concepts of manipulating the host gut microbiota and/or augmenting GI mucosal immunity to prevent invasive bacterial and fungal infections in pediatric patients with cancer offers great promise, but more definitive studies need to be performed. The relationship between neutrophil numbers and the risk of infectious complications in patients with leukemia was first described in the seminal work of Bodey and colleagues in 1966. 2 The investigators concluded that 1) the risk of infection was directly related to the absolute neutrophil count (ANC), severe infections being more prevalent when the ANC fell below 100 cells/mm 3 ; 2) relapse of leukemia was associated with higher rates of infection than was remission; and 3) duration of neutropenia was the single most important factor in predicting risk of infection, with severe neutropenia that lasted longer than 3 weeks being associated with 100% risk of infection and the highest mortality rates. The rate of decline of circulating polymorphonuclear lymphocytes (PMNs) is also critical. For example, patients with rapidly declining ANCs after therapy for acute leukemia seem to be at greater risk for infectious complications than are patients with chronic neutropenia (e.g., aplastic anemia). 3 Risk Assessment in Patients with Cancer with Fever and Neutropenia Not all patients with fever and neutropenia are at equal risk for substantial morbidity or mortality resulting from infection. The identification of a low-risk subset may allow for modifications of therapy in this group, with goals of reduced therapy-related toxicity, improved quality of life, and decreased cost of treatment. Although there is no definitive consensus about the criteria used to prospectively distinguish high risk from low risk, the following key factors that may raise the risk of infectious complications can be surmised from studies that have been conducted: (1) anticipated duration of neutropenia 4 ; (2) substantial medical comorbidity 4 ; (3) cancer status and cancer type; (4) docu- From the University of Texas Southwestern Medical Center, Dallas, TX. Author’s disclosures of potential conflicts of interest are found at the end of this article. Address reprint requests to Andrew Koh, MD, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX 75390-9063; email: Andrew.koh@ utsouthwestern.edu. © 2012 by American Society of Clinical Oncology. 1092-9118/10/1-10 565
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AMERICAN SOCIETY OF CLINICAL ONCOLO
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American Society of Clinical Oncolo
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American Society of Clinical Oncolo
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New Looks and Challenges for Cooper
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Genitourinary Cancer Best Use of Im
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Research and Standard of Care: Lung
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Practice Management and Information
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2012 ASCO Annual Meeting Disclosure
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Matti S. Aapro, MD Clinique De Geno
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Hedy Lee Kindler, MD The University
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Douglas E. Wood, MD University of W
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Mary Lou Smith, JD, MBA Research Ad
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ASCO and Conquer Cancer Foundation
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Letter from the Editor The theme of
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Adjuvant Therapy for Older Women wi
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TREATMENT FOR OLDER WOMEN WITH BREA
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MANAGEMENT OF T1 BREAST CANCERS the
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MANAGEMENT OF T1 BREAST CANCERS Tab
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MANAGEMENT OF T1 BREAST CANCERS Tab
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MANAGEMENT OF T1 BREAST CANCERS 93.
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MANAGEMENT OF T1 BREAST CANCERS 1 c
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ADJUVANT ENDOCRINE THERAPY reductio
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ADJUVANT ENDOCRINE THERAPY which ra
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ADJUVANT ENDOCRINE THERAPY assay is
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A DICKENS TALE OF THE TREATMENT OF
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TREATMENT OF ADVANCED BREAST CANCER
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A FRESH LOOK AT DUCTAL CARCINOMA IN
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Ductal Carcinoma In Situ, and the I
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DCIS AND INFLUENCE OF RISK FACTORS
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KEY QUESTIONS IN THE LOCO-REGIONAL
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POSTMASTECTOMY RADIATION AND PARTIA
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The Appropriate Extent of Surgery f
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SURGERY FOR EARLY-STAGE BREAST CANC
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BIOLOGY AND LOCAL THERAPY DECISIONS
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Clinical and Imaging Surveillance F
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SURVEILLANCE FOLLOWING BREAST CANCE
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SURVEILLANCE FOLLOWING BREAST CANCE
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Advanced Imaging Techniques for the
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IMAGING TECHNIQUES FOR BREAST CANCE
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IMAGING TECHNIQUES FOR BREAST CANCE
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Update of the Oxford Overview: New
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UPDATE OF THE OXFORD OVERVIEW Fig.
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UPDATE OF THE OXFORD OVERVIEW Overv
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Gene Patents and Personalized Medic
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GENE PATENTS AND EFFECTS ON PERSONA
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Chemoprevention for Breast Cancer:
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CHEMOPREVENTION FOR BREAST CANCER T
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CHEMOPREVENTION FOR BREAST CANCER C
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CONTROVERSIES IN PROSTATE CANCER: P
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PROSTATE CANCER RISK REDUCTION men
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PSA SCREENING: HARMS WITHOUT CLEAR
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PSA SCREENING: HARMS WITHOUT CLEAR
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GLIOBLASTOMA: TAKING THE STANDARD O
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GLIOBLASTOMA: BIOLOGY, GENETICS AND
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FUTURE DIRECTIONS IN GBM THERAPY pr
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FUTURE DIRECTIONS IN GBM THERAPY Ch
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ESTABLISHING TREATMENTS FOR GLIOBLA
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Current Concepts in Brain Tumor Ima
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CONCEPTS IN BRAIN TUMOR IMAGING tum
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CONCEPTS IN BRAIN TUMOR IMAGING Aut
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TTF THERAPY IN GLIOBLASTOMA Fig. 1.
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TTF THERAPY IN GLIOBLASTOMA istics.
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Limitations of Adaptive Clinical Tr
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LIMITATIONS OF ADAPTIVE CLINICAL TR
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Capturing the Patient Perspective:
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PATIENT-REPORTED OUTCOMES AS TRIAL
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PATIENT-REPORTED OUTCOMES AS TRIAL
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NEW LOOKS AND CHALLENGES FOR COOPER
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NCI NATIONAL CLINICAL TRIALS NETWOR
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Successful Integration of Cooperati
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COG: GIVING NEW MEANING TO COOPERAT
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A Critical Review of the Enrollment
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BLACK PATIENTS AND CANCER CLINICAL
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BLACK PATIENTS AND CANCER CLINICAL
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Trastuzumab Emtansine (T-DM1): Hitc
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TARGETING CD30 IN HODGKIN LYMPHOMA
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TARGETING CD30 IN HODGKIN LYMPHOMA
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Table 1. Response Rates in Expanded
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Drug Development in the Era of Pers
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that the core pathway is not comple
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This situation is not surprising, g
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Practical Management of Immune-Rela
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TARGETING CRITICAL MOLECULAR ABERRA
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Abl suppression; and 3) the early e
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50% 50% 100% Change in Tumor Size m
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Targeting Molecular Aberrations in
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ETHICAL CHALLENGES OF HEALTH CARE R
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HEALTH CARE REFORM AND ONCOLOGY dev
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INTERNATIONAL VARIATION IN UNDERSTA
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midcareer physician; in one cross-s
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Table 1. Recommendations for Person
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elationship” is also acknowledged
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Conclusion In more individualistic
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The Oncologist’s Duty to Provide
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an external observer, but to the pe
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MEDICAL ERRORS IN CANCER CARE: PREV
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DISCLOSING MEDICAL ERRORS Disclosur
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DISCLOSING MEDICAL ERRORS Author’
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PREVENTING MEDICAL ERRORS more diff
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“PERSONALIZED” ONCOLOGY FOR COL
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0.001), progression-free survival (
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Table 1. Tumor Marker Utility Gradi
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treatment (tx) for metastatic color
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The Interventional Radiologist Role
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effect. The most common drug that h
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gone forever, no further therapy is
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Resection and Thermal Ablation of L
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Author’s Disclosures of Potential
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Minimally Invasive Surgery of Recta
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Authors’ Disclosures of Potential
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CAO/ARO 04 study—which added oxal
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STAGE III COLON CANCER: WHAT WORKS,
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tients with stages II and III color
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A New Direction for Pancreatic Canc
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Table 1. FOLFIRINOX versus Gemcitab
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The Southwest Oncology Group (SWOG)
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A Matter of Timing: Is There a Role
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patients are cared for completely w
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Varying Lymphadenectomies for Gastr
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Conclusion There are clear differen
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Will Disease Heterogeneity Help Def
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Adjuvant Treatments for Localized A
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ADJUVANT TREATMENT FOR GASTRIC CANC
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LIVER-DIRECTED THERAPEUTIC OPTIONS
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THE MANAGEMENT OF LESS COMMON BUT C
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of therapeutic options, patient sel
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combined with concurrent transarter
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to optimize the use of erlotinib by
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Optimal Use of Imaging to Guide Tre
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enhancement seen. Furthermore, the
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CASTRATION-RESISTANT PROSTATE CANCE
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Prognostic, Predictive, and Surroga
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adhesion molecule and further chara
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KIDNEY CANCER BIOLOGY AND THERAPEUT
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Prognostic Factors in Advanced RCC
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cell immunotherapy in which a small
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10. Albers P, Park SI, Niegisch G,
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700 at a dose of 400 mg twice daily
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therapy for nonmetastatic prostate
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ADJUVANT THERAPY FOR OLDER PATIENTS
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Adjuvant Systemic Therapy Adjuvant
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with early-stage breast cancer were
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clinical trials to generate additio
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Adjuvant Treatment of Older Patient
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OLDER PATIENTS WITH ADVANCED CANCER
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RECENT CLINICAL HIGHLIGHTS IN GYNEC
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GLOBAL ADVANCES IN GYNECOLOGIC ONCO
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GLOBAL ADVANCES IN GYNECOLOGIC ONCO
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The European Society of Gynaecologi
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UPFRONT TREATMENT OF OVARIAN CANCER
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ANTIANGIOGENICS AND PARP INHIBITORS
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Intraperitoneal Treatment in Ovaria
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HISTOLOGIC FEATURES AND MANAGEMENT
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PATIENTS WITH HPV-POSITIVE OROPHARY
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HPV-INDUCED OROPHARYNX CANCER analy
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HPV-INDUCED OROPHARYNX CANCER fract
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EARLY ADVANCES IN SCCHN Fig 1. Targ
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Application of Genomic and Proteomi
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GENOMIC AND PROTEOMIC TECHNOLOGIES
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TREATMENT OF THYROID CANCERS: NEW I
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EVALUATION OF ADVANCED THYROID CANC
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EVALUATION OF ADVANCED THYROID CANC
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Systemic Therapeutic Approaches to
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APPROACHES TO ADVANCED THYROID CANC
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AVOIDING OVERDIAGNOSIS AND OVERTREA
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Overdiagnosis and Overtreatment of
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een reached by other modeling effor
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COSTS OF CANCER CARE: AFFORDABILITY
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REDUCING THE COST OF CANCER CARE Fi
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REDUCING THE COST OF CANCER CARE Th
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REDUCING THE COST OF CANCER CARE de
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Why Hasn’t Genomic Testing Change
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MANAGEMENT OF CHRONIC LYMPHOCYTIC L
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PREDICTIVE PARAMETERS IN CLL Table
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Transplant in Chronic Lymphocytic L
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WHEN TO OFFER TRANSPLANTATION IN CL
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NEW DEVELOPMENTS IN MYELOPROLIFERAT
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SMALL-MOLECULE INHIBITORS FOR MPN S
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SMALL-MOLECULE INHIBITORS FOR MPN L
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Insights into the Molecular Genetic
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GENETICS OF MYELOPROLIFERATIVE NEOP
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Classification of Myeloproliferativ
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CLASSIFICATION AND PROGNOSIS OF MPN
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CLASSIFICATION AND PROGNOSIS OF MPN
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AROUND THE WORLD IN ALMOST 80 MINUT
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LUNG CANCER IN BRAZIL Fig. 1. Relat
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LUNG CANCER IN BRAZIL Fig. 3. Chara
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LUNG CANCER IN BRAZIL Author’s Di
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LUNG CANCER IN CHINA Fig 1. Chinese
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LUNG CANCER IN CHINA well equipped
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Research and Standard of Care: Lung
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LUNG CANCER IN ROMANIA ● Protecti
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PHYSICIAN ENGAGEMENT IN ONLINE PATI
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PHYSICIAN ENGAGEMENT IN ONLINE PATI
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LUNG CANCER SCREENING 101 CHAIR Chr
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LUNG CANCER SCREENING The concern i
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LUNG CANCER SCREENING Fig. 1. Guide
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LUNG CANCER SCREENING Fig. 2. Guide
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LUNG CANCER SCREENING 19. Montes RP
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Molecular Testing of Non-Small Cell
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MOLECULAR TESTING AND NSCLC Fig 1.
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MOLECULAR TESTING AND NSCLC logic d
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THYMOMA AND THYMIC CARCINOMA: UPDAT
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MANAGEMENT OF THYMIC CARCINOMA recu
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MANAGEMENT OF THYMIC CARCINOMA Refe
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The Creation of the International T
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ITMIG AS A MODEL FOR RARE DISEASES
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Thymoma: From Chemotherapy to Targe
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SYSTEMIC TREATMENT OF THYMOMA cance
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What Is the Best Strategy for Incor
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TREATMENT OF FOLLICULAR LYMPHOMA Fi
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TREATMENT OF FOLLICULAR LYMPHOMA me
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TREATMENT OF FOLLICULAR LYMPHOMA ou
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TREATMENT OPTIONS IN INDOLENT LYMPH
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ROLE OF HCT FOR INDOLENT LYMPHOMA T
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CONTROVERSIES IN MYELOMA: INDUCTION
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TRANSPLANTATION FOR MYELOMA compare
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TRANSPLANTATION FOR MYELOMA autolog
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CURRENT STATUS OF MYELOMA THERAPY K
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ABFM THERAPY FOR PEDIATRIC ALL Auth
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RADIOTHERAPY FOR PEDIATRIC HODGKIN
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RADIOTHERAPY FOR PEDIATRIC HODGKIN
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Role of Doxorubicin in Rhabdomyosar
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Identification of Novel Biologic Ta
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NOVEL TARGETS IN THE TREATMENT OF D
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Is Biopsy Safe in Children with New
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SAFETY OF DIPG BIOPSY IN CHILDREN F
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SAFETY OF DIPG BIOPSY IN CHILDREN 1
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CHILDREN WITH DIFFUSE INTRINSIC PON
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Communication and Decision Support
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COMMUNICATION AND DECISION SUPPORT
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Planning for the Future: The Role o
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present in the office suite but doe
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Summary and Care Plan are provided.
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DOING IT RIGHT, AND FOR LESS: IMPLE
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CLINICAL PATHWAYS STANDARDIZING PER
Page 749 and 750:
CLINICAL PATHWAYS STANDARDIZING PER
Page 751 and 752:
The Future of Oncology Care with Pe
Page 753 and 754:
quantity. Determining the appropria
Page 755 and 756:
THE ASCO QUALITY ONCOLOGY PRACTICE
Page 757 and 758:
IMPROVING VALUE OF CARE IN ONCOLOGY
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Page 761 and 762:
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PHYSICIAN WELLNESS: COPING WITH REP
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also provides insight on how clinic
Page 767 and 768:
good resource for exploring the pri
Page 769 and 770:
of death or following death and inc
Page 771 and 772:
telephone call to the family, sendi
Page 773 and 774:
New Insights in Cross-Cultural Comm
Page 775 and 776:
CROSS-CULTURAL COMMUNICATION Sideba
Page 777 and 778:
THE ONCOLOGIST, THE PATIENT, AND TH
Page 779 and 780:
estimate of the proportion of their
Page 781 and 782:
exactly the same treatment, even th
Page 783 and 784:
How to Decide Whether to Offer and
Page 785 and 786:
NONSTANDARD THERAPIES FOR ADVANCED
Page 787 and 788:
NONSTANDARD THERAPIES FOR ADVANCED
Page 789 and 790:
TARGETED THERAPIES IN TARGETED OR U
Page 791 and 792:
TARGETED THERAPY IN SARCOMA rates a
Page 793 and 794:
TARGETED THERAPY IN SARCOMA seen in
Page 795 and 796:
TARGETED THERAPY IN SARCOMA recepto
Page 797 and 798:
Adjuvant Treatment of Gastrointesti
Page 799 and 800:
ADJUVANT THERAPY IN HIGH-RISK GASTR
Page 801 and 802:
Management of Tyrosine Kinase Inhib
Page 803 and 804:
TKI-RESISTANT GIST Primary Imatinib
Page 805 and 806:
TKI-RESISTANT GIST Table 2. Clinica
Page 807 and 808:
BIOLOGIC PRINCIPLES OF TARGETED COM
Page 809 and 810:
COMBINING TARGETED AGENTS IN CLINIC
Page 811 and 812:
COMBINING TARGETED AGENTS IN CLINIC
Page 813 and 814:
Combination Therapies Building on t
Page 815 and 816:
COMBINATIONS FOR MELANOMA agents th
Page 817 and 818:
MECHANISMS OF RESISTANCE TO TARGETE
Page 819 and 820:
RESISTANCE MECHANISMS TO MAPK INHIB
Page 821 and 822:
RESISTANCE MECHANISMS TO MAPK INHIB
Page 823 and 824:
Mechanisms of Resistance to Targete
Page 825 and 826:
RESISTANCE TO TARGETED THERAPIES IN
Page 827 and 828:
RESISTANCE TO TARGETED THERAPIES IN
Page 829 and 830:
Translating PI3K-Delta Inhibitors t
Page 831 and 832:
THE STORY OF CAL-101 6% of patients
Page 833 and 834:
PI3 Kinase in Cancer: From Biology
Page 835 and 836:
PI3 KINASE IN CANCER Fig. 1. The PI
Page 837 and 838:
PI3 KINASE IN CANCER Fig. 3. In viv
Page 840:
This publication is supported by an
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2012 EDUCATIONAL BOOK - American Society of Clinical Oncology

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