2012 EDUCATIONAL BOOK - American Society of Clinical Oncology

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IMAGING IN NEURO-ONCOLOGY: PRACTICAL PRIMER FOR THE PRACTICING PHYSICIAN CHAIR Susan M. Chang, MD University of California, San Francisco San Francisco, CA SPEAKERS Whitney B. Pope, MD, PhD University of California, Los Angeles Los Angeles, CA Andrew D. Norden, MD, MPH Dana-Farber Cancer Institute Boston, MA
Current Concepts in Brain Tumor Imaging By Andrew D. Norden, MD, MPH, Whitney B. Pope, MD, PhD, and Susan M. Chang, MD Overview: Magnetic resonance imaging (MRI) is the most useful imaging tool in the evaluation of patients with brain tumors. Most information is supplied by standard anatomic images that were developed in the 1980s and 1990s. More recently, functional imaging including diffusion and perfusion MRI has been investigated as a way to generate predictive and prognostic biomarkers for high-grade glioma evaluation, but additional research is needed to establish the added benefits of these indices to standard MRI. Response critieria for high-grade gliomas have recently been updated by the Response Assessment in Neuro-Oncology (RANO) working THE FIRST published magnetic resonance image (MRI) was from a paper in the journal Nature by Nobel Prize Laureate Paul Lauterbur in 1973. 1 By 1981, magnetic resonance had been used for imaging the brain, demonstrated the pathologic appearance of glioblastoma (GBM), and compared favorably to computed tomography (CT) as the “posterior fossa was visualized with substantially less artifact. ...” 2 MRI was noted to detect tumors not seen on CT as early as 1982, and this led quickly to an explosion of articles evaluating MRI of brain tumors and other intracranial pathology. T1- and T2-weighted images were quickly adopted as standard imaging along with multiple planar scanning. Gadolinium-based contrast agents were introduced around 1984, 3 as were high-field strength superconducting (1.5 Tesla) scanners. 4 Another advance in brain tumor imaging occurred in the late 1990s with the introduction of fluid-attenuated inversion recovery (FLAIR) sequences that generated strongly T2-weighted images although signal associated with cerebrospinal fluid (CSF) was suppressed. 5 Today, MRI remains the imaging modality of choice for tumor diagnosis, characterization, and assessment of treatment response. Conventional MRI in Neuro-Oncology MRI has traditionally been used to evaluate tumor location, size and extent, mass effect, involvement of critical structures such as adjacent blood vessels, and compromise of the blood-brain barrier (which results in contrast enhancement). The typical MR scan for a patient with glioma includes sagittal T1, axial T1, T2, FLAIR and postcontrast axial and coronal T1-weighted images. Recently pulse sequences sensitive to physiology, rather than just anatomy, are being more commonly used (see following). Changes in enhancing tumor size based on bidimensional measurements of postcontrast T1-weighted images are the basis for both the Macdonald and later RANO criteria for evaluating tumor response. 6 Conversely, nonenhancing tumor is assessed qualitatively in RANO, but not at all in the Macdonald criteria. Nonenhancing tumor is typified by areas of increased T2 signal intensity associated with mass effect and architectural distortion such as blurring of the graywhite interface. 7 Edema and treatment effect including gliosis also result in increased T2 signal, which can make nonenhancing tumor difficult to quantify. FLAIR is more sensitive to T2 signal abnormalities, as a result of the nulling of CSF, thereby overcoming the limitation of partial volume averaging in the cortical and periventricular regions group. The new criteria account for nonenhancing tumor in addition to the contrast-enhancing abnormalities on which older criteria relied. This issue has recently come to the fore with the introduction of the antiangiogenic agent bevacizumab into standard treatment for recurrent glioblastoma. Because of its potent antipermeability effect, contrast enhancement is markedly reduced in patients who receive bevacizumab. The RANO criteria also address the phenomenon of pseudoprogression, in which there may be transient MRI worsening of a glioblastoma following concurrent radiotherapy and temozolomide. as can be seen in standard T2 images. However, FLAIR also reduces gray-white differentiation in comparison to typical T2-weighted images, which can diminish the image reader’s ability to distinguish the T2 changes that are a result of tumor compared with T2 changes that are the result of edema and/or gliosis. Thus, T2 and FLAIR images can provide complementary information, and both should be acquired for evaluation of patients with brain tumors. Although relying on changes in enhancing tumor previously worked well for evaluating treatment response, the widespread adoption of bevacizumab therapy for recurrent GBM highlights the limitations of this approach. This limitation stems largely from bevacizumab’s antipermeability effect. GBMs are characterized by extensive abnormal vasculature with a leaky blood-brain barrier. 8 As a result, contrast material extravasates out of tumor vessels, leading to increased signal on gadolinium-enhanced T1-weighted images. Bevacizumab sequesters vascular endothelial growth factor (VEGF), a potent permeability factor and promoter of angiogenesis, and thereby acts to diminish contrast enhancement. Therefore a reduction in contrast enhancement following bevacizumab infusion may not necessarily reflect a cytotoxic tumor effect. Relying on the change in contrast enhancement alone can thus misrepresent treatment response, a phenomenon known as “pseudoresponse.” 9,10 Although the RANO criteria include FLAIR or T2 hyperintensity changes as potentially indicative of nonenhancing tumor progression, no quantification of nonenhancing tumor is performed. This is because of difficulties in determining the borders of T2 abnormal regions as well as differentiating gliosis and other treatment effects from tumor. This has spurred interest in physiologic imaging as a way of obtaining quantitative data on tumor burden, although to date, this goal has not been fully realized. From Dana-Farber Cancer Institute and Brigham and Women’s Hospital, Boston, MA; David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA; University of California, San Francisco, Department of Neurological Surgery, San Francisco, CA. Authors’ disclosures of potential conflicts of interest are found at the end of this article. Address reprint requests to Susan M. Chang, MD, University of California, San Francisco, Department of Neurological Surgery, 400 Parnassus Ave., A808, San Francisco, CA 94143-0372; email: changs@neurosurg.ucsf.edu. © 2012 by American Society of Clinical Oncology. 1092-9118/10/1-10 119
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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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DCIS: OPPORTUNITIES AND UNCHARTED W
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DCIS: OPPORTUNITIES AND UNCHARTED W
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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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Page 97 and 98: Update of the Oxford Overview: New
Page 99 and 100: UPDATE OF THE OXFORD OVERVIEW Fig.
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Page 107 and 108: Gene Patents and Personalized Medic
Page 109 and 110: GENE PATENTS AND EFFECTS ON PERSONA
Page 111 and 112: Chemoprevention for Breast Cancer:
Page 113 and 114: CHEMOPREVENTION FOR BREAST CANCER T
Page 115 and 116: CHEMOPREVENTION FOR BREAST CANCER C
Page 117 and 118: CONTROVERSIES IN PROSTATE CANCER: P
Page 119 and 120: PROSTATE CANCER RISK REDUCTION men
Page 121 and 122: PROSTATE CANCER RISK REDUCTION Auth
Page 123 and 124: PSA SCREENING: HARMS WITHOUT CLEAR
Page 125 and 126: PSA SCREENING: HARMS WITHOUT CLEAR
Page 127 and 128: GLIOBLASTOMA: TAKING THE STANDARD O
Page 129 and 130: GLIOBLASTOMA: BIOLOGY, GENETICS AND
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Page 137 and 138: FUTURE DIRECTIONS IN GBM THERAPY Ch
Page 139 and 140: ESTABLISHING TREATMENTS FOR GLIOBLA
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Page 147 and 148: CONCEPTS IN BRAIN TUMOR IMAGING tum
Page 149 and 150: CONCEPTS IN BRAIN TUMOR IMAGING Aut
Page 151 and 152: PERSPECTIVES ON HEADLINE-MAKING NEW
Page 153 and 154: TTF THERAPY IN GLIOBLASTOMA Fig. 1.
Page 155 and 156: TTF THERAPY IN GLIOBLASTOMA istics.
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Page 159 and 160: Limitations of Adaptive Clinical Tr
Page 161 and 162: LIMITATIONS OF ADAPTIVE CLINICAL TR
Page 163 and 164: LIMITATIONS OF ADAPTIVE CLINICAL TR
Page 165 and 166: Capturing the Patient Perspective:
Page 167 and 168: PATIENT-REPORTED OUTCOMES AS TRIAL
Page 169 and 170: PATIENT-REPORTED OUTCOMES AS TRIAL
Page 171 and 172: NEW LOOKS AND CHALLENGES FOR COOPER
Page 173 and 174: NCI NATIONAL CLINICAL TRIALS NETWOR
Page 175 and 176: Successful Integration of Cooperati
Page 177 and 178: COG: GIVING NEW MEANING TO COOPERAT
Page 179 and 180: A Critical Review of the Enrollment
Page 181 and 182: BLACK PATIENTS AND CANCER CLINICAL
Page 183 and 184: BLACK PATIENTS AND CANCER CLINICAL
Page 185 and 186: Trastuzumab Emtansine (T-DM1): Hitc
Page 187 and 188: T-DM1 AND THERAPEUTIC ANTIBODIES ag
Page 189 and 190: 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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the anterior pituitary axis is invo
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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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vanced solid tumors, even if they a
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Targeting Molecular Aberrations in
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date. With the advent of gene expre
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consortium to facilitate the testin
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ETHICAL CHALLENGES OF HEALTH CARE R
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HEALTH CARE REFORM AND ONCOLOGY dev
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HEALTH CARE REFORM AND ONCOLOGY aut
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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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stances (e.g., stage of career, fam
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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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mately 40% of patients with colorec
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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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is irrelevant if it is already rese
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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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outcomes; local, wound-site, and di
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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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Table 1. Comparison of Fluoropyrimi
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tients with stages II and III color
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ized by high fruit, vegetable, poul
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Exercise Change trial: a randomized
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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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an OS benefit with radiation therap
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a dose of 50.4 Gy to 59.4 Gy of rad
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more commonly given for APC, specia
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subcutaneous bolus or infusion. Hal
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patients are cared for completely w
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Varying Lymphadenectomies for Gastr
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Table 1. Regional Lymph Nodes of th
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Conclusion There are clear differen
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Will Disease Heterogeneity Help Def
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prematurely due to poor accrual. 18
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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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ated with unique dose distributions
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HCC, with encouraging outcomes in e
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tion. Advanced computer-based image
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a 5-year survival rate of 70% follo
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THE MANAGEMENT OF LESS COMMON BUT C
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Fig 1. PubMed publications and clin
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of therapeutic options, patient sel
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less informative than the GRETCH an
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Table 3. New Agents/Regimens under
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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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Fig. 1. FDA regulatory approvals in
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Prognostic, Predictive, and Surroga
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adhesion molecule and further chara
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and treatment options are expanding
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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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New Developments in Urothelial Canc
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Novel Approaches in Advanced Urothe
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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 LUNG CANCER Fig
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OLDER PATIENTS WITH LUNG CANCER adj
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Considerations and Controversies in
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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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ESGO EDUCATIONAL AND RESEARCH ACTIV
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UPFRONT TREATMENT OF OVARIAN CANCER
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ANTIANGIOGENICS AND PARP INHIBITORS
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ANTIANGIOGENICS AND PARP INHIBITORS
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Intraperitoneal Treatment in Ovaria
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INTRAPERITONEAL TREATMENT IN OVARIA
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Dose-Dense Chemotherapy and Neoadju
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CHEMOTHERAPY FOR OVARIAN CANCER Fig
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CHEMOTHERAPY FOR OVARIAN CANCER whi
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UTERINE SARCOMA: CHALLENGING CASES
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HISTOLOGIC FEATURES AND MANAGEMENT
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SURGICAL OPTIONS FOR UTERINE SARCOM
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SURGICAL OPTIONS FOR UTERINE SARCOM
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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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Important Early Advances in Squamou
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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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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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Table 1. Prevalence of Prostate Can
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Table 3. Potential Risks and Benefi
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Overdiagnosis and Overtreatment of
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een reached by other modeling effor
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east cancer community have FDA-appr
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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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tigators should develop prospective
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MANAGEMENT OF CHRONIC LYMPHOCYTIC L
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PREDICTIVE PARAMETERS IN CLL Table
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PREDICTIVE PARAMETERS IN CLL patien
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Transplant in Chronic Lymphocytic L
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WHEN TO OFFER TRANSPLANTATION IN CL
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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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LUNG CANCER IN ROMANIA reimbursemen
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A New Model: Physician-Patient Coll
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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 Study
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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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ROLE OF HCT FOR INDOLENT LYMPHOMA T
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ROLE OF HCT FOR INDOLENT LYMPHOMA e
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CONTROVERSIES IN MYELOMA: INDUCTION
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TRANSPLANTATION FOR MYELOMA Alterna
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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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CURRENT STATUS OF MYELOMA THERAPY F
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CURRENT STATUS OF MYELOMA THERAPY T
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Maintenance Therapy for Myeloma: Ho
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MAINTENANCE THERAPY FOR MULTIPLE MY
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NEW OPTIONS, NEW QUESTIONS: HOW TO
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THERAPIES FOR PATIENTS WITH METASTA
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ANTIEMETICS: CURRENT STANDARDS, EME
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ANTIEMETICS: ASCO GUIDELINE UPDATE
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Chemotherapy-Induced Nausea and Vom
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INCIDENCE AND PREVALENCE OF CHEMOTH
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New Frontiers in Mucositis By Dougl
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MUCOSAL INJURY CAUSED BY CANCER THE
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Short- and Long-term Cardiovascular
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Recent Advances in Cardiotoxicity o
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CARDIOTOXICITY OF ANTICANCER THERAP
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CARDIOTOXICITY OF ANTICANCER THERAP
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The Oncologist as the Patient with
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THE ONCOLOGIST AS THE PATIENT OR RE
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Prolonged Febrile Neutropenia in th
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FEBRILE NEUTROPENIA IN PEDIATRIC CA
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FEBRILE NEUTROPENIA IN PEDIATRIC CA
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TREATMENT APPROACHES IN CHILDREN wh
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TREATMENT APPROACHES IN CHILDREN th
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GENETIC COUNSELING OF THE PATIENT W
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CANCER PREDISPOSITION IN CHILDHOOD
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HOW TO MANAGE VERY RARE PEDIATRIC C
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RARE CANCER IN CHILDREN Registries
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Genetic Alterations in Childhood Me
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GENETIC ALTERATIONS IN CHILDHOOD ME
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Desmoid-Type Fibromatosis in Childr
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CHEMOTHERAPY FOR DESMOID TUMOR Tabl
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CHEMOTHERAPY FOR DESMOID TUMOR 14.
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Targeting the Insulin-Like Growth F
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TARGETING THE IGF SYSTEM Fig. 1. Th
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TARGETING THE IGF SYSTEM malignanci
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Hedgehog Pathway in Pediatric Cance
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HEDGEHOG PATHWAY IN PEDIATRIC CANCE
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HEDGEHOG PATHWAY IN PEDIATRIC CANCE
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Development and Refinement of Augme
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ABFM THERAPY FOR PEDIATRIC ALL than
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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
Page 715 and 716:
Role of Doxorubicin in Rhabdomyosar
Page 717 and 718:
DOXORUBICIN IN RHABDOMYOSARCOMA 8.
Page 719 and 720:
Identification of Novel Biologic Ta
Page 721 and 722:
NOVEL TARGETS IN THE TREATMENT OF D
Page 723 and 724:
Is Biopsy Safe in Children with New
Page 725 and 726:
SAFETY OF DIPG BIOPSY IN CHILDREN F
Page 727 and 728:
SAFETY OF DIPG BIOPSY IN CHILDREN 1
Page 729 and 730:
CHILDREN WITH DIFFUSE INTRINSIC PON
Page 731 and 732:
Communication and Decision Support
Page 733 and 734:
COMMUNICATION AND DECISION SUPPORT
Page 735 and 736:
Page 737 and 738:
Page 739 and 740:
Planning for the Future: The Role o
Page 741 and 742:
present in the office suite but doe
Page 743 and 744:
Summary and Care Plan are provided.
Page 745 and 746:
DOING IT RIGHT, AND FOR LESS: IMPLE
Page 747 and 748:
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
Page 759 and 760:
Page 761 and 762:
Page 763 and 764:
PHYSICIAN WELLNESS: COPING WITH REP
Page 765 and 766:
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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