2012 EDUCATIONAL BOOK - American Society of Clinical Oncology

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available data comes from an era when taxane adjuvant use was not yet standard, and even anthracycline-based regimens were not always used. These data may not apply to our current MBC patient population. Available trials have produced the following conclusions: for taxane-naive and anthracycline-naive/minimally exposed patients, single-agent anthracycline or single-agent taxane yield similar results; for taxane-naive and anthracycline-resistant/refractory patients, single-agent taxane led to better outcomes than single-agent anthracyclines; combinations of anthracyclines plus taxanes in the metastatic setting consistently led to higher response rates, sometimes higher time to progression or PFS, higher toxicity, but not better OS. Because of this, sequential single agent therapy is not only appropriate, but preferred for most patients. A 2008 meta-analysis of individual patient data concludes that taxanes do not improve survival when compared with anthracyclines, either as single agents or in anthracycline combinations and that taxanes in combination with anthracyclines modestly improve response rate (RR) and PFS but not OS. 13 For patients pretreated with both anthracyclines and taxanes, the most consistent data concerns capecitabine use. Vinorelbine has been compared head-to-head with docetaxel and yielded similar efficacy and significantly less toxicity. Given that both these agents are available as oral formulations and are associated with much less toxicity including alopecia, they are attractive options. Although there is also some data supporting rechallenging with taxanes as firstline therapy, the wealth of other available options and toxicity concerns make this a less appealing option. A common question relates to the use of combination of cytotoxic agents compared with their sequential use as monotherapy. Available evidence 14 suggests monotherapy as the preferred option (even in the presence of visceral metastases) in all cases except those with a rapid progressive or highly symptomatic disease. It is important to know that there are no data to support an optimal sequence of therapies and that only eribulin led to an OS benefit. Therefore, treatment decisions must be individualized, taking into account many other factors beyond efficacy. Chemotherapy: Optimal Duration and Number of Lines of Therapy Many studies have looked into the question of optimal duration of systemic therapy, mainly chemotherapy, for which the balance between efficacy and toxicity is perhaps more difficult to achieve. Recently, a meta-analysis of published trials 15 has looked into this issue and concluded that longer first-line chemotherapy duration is associated with marginally longer OS and a substantially longer PFS, and treatment should be prescribed until progression or unacceptable toxicity. Treatment Present: Metastatic Breast Cancer in 2012 Today’s systemic treatment decisions are guided by a range of factors: 1) the subtype of the breast cancer (defined by ER status and HER2) 2) sites of disease 3) disease tempo 4) presence and extent of symptoms 5) prior therapy 6) availability of effective local therapy and 7) patient preferences. 30 Hormone Receptor-Positive MBC Hormone therapy is the preferred first-line treatment for most. Several options are available, including the AIs tamoxifen and fulvestrant (not U.S. Food and Drug Administration (FDA)-approved for first-line use). In postmenopausal patients who present de novo with metastatic disease or those who have only received tamoxifen in the adjuvant setting, treatment with an AI is standard of care. 16 A substantial number of these patients remain on an AI with disease control for prolonged periods. In a minimally symptomatic patient without an extensive disease burden, it is reasonable to try a second-line agent, even if there has been no or little benefit with the initial treatment. Among patients who develop disease progression after an objective response or prolonged disease stabilization on first-line treatment, another endocrine agent is generally preferred. Treatment with fulvestrant, a steroidal AI (assuming a nonsteroidal agent was used initially) or tamoxifen (unless there had been prior progression on tamoxifen) are reasonable. 17 Unfortunately, clinical benefit from second-line therapy in the metastatic setting is less impressive than with first-line treatment. Some patients will continue to derive benefit from hormone therapy and can go on to receive thirdand fourth-line therapy. Many patients with a new diagnosis of MBC will have already progressed on an adjuvant aromatase inhibitor. For these, options are more limited. In general, fulvestrant is used as the first-line metastatic treatment in such patients. A recent study conducted by the Southwest Oncology Group that compared anastrozole alone with anastrozole plus fulvestrant in the first-line setting 18 suggested an advantage both in terms of PFS and OS for the combination. In premenopausal women with MBC, tamoxifen remains the standard treatment, often administered in conjunction with a luteinizing hormone releasing hormone (LHRH) agonist. 19 For premenopausal women who develop metastatic disease while on tamoxifen, the usual approach is a combination of an LHRH agonist and an AI. AIs are ineffective in women with functioning ovaries. Ultimately, women with hormone receptor-positive disease become refractory to endocrine therapy. At that point, chemotherapy is administered. A wide variety of choices are available, and treatment options are similar to those that are available for women with triple-negative disease. Both the taxanes and capecitabine are commonly given in the first-line setting. Although capecitabine does not have FDA approval for first-line therapy, several small studies comparing capecitabine with other agents have suggested that capecitabine is a reasonable initial approach. 20 Triple-Negative Breast Cancer SLEDGE, CARDOSO, WINER, AND PICCART Options are limited to chemotherapy in patients with triple-negative breast cancer. Most patients have received adjuvant chemotherapy, often with a short disease-free interval. For these reasons, chemotherapy options in the metastatic setting are often limited. Survival from the time of metastatic disease tends to be relatively short, with a median of approximately 1 year. 21 Treatment options for metastatic triple-negative disease include all of the available chemotherapeutic agents and regimens. Given the widespread use of anthracyclines in the adjuvant setting, these agents are not commonly used in the
TREATMENT OF ADVANCED BREAST CANCER Table 1. Targeting Breast Cancer Cells Compound HER2 Molecular Target Clinical Trials Pharmaceutical Pertuzumab HER2 -Phase I pertuzumab, T-DM1 and paclitaxel in HER2� MBC (NCT00951665) -Phase I/II T-DM1 with pertuzumab in trastuzumab pretreated HER2� MBC (NCT00875979) -Phase II Pertuzumab, trastuzuman and weekly paclitaxel in HER2� MBC (NCT01276041) -Phase III pertuzumab � T-DM1 versus T-DM1�placebo versus trastuzumab � taxane in HER2� MBC (MARIANNE) (NCT01120184) -Phase II trastuzumab � capecitabine � pertuzumab in HER2� MBC (PHEREXA) (NCT01026142) -Phase II pertuzumab with trastuzumab and AI in HR�HER2� MBC (NCT01491737) -Phase II of pertuzumab and trastuzuman with neoadjuvant chemotherapy in HER2� BC (NCT00976989) -Phase III, trastuzumab � chemotherapy � pertuzumab in early stage HER2� BC (APHINITY) (NCT01358877) Genentech Trastuzumab-DM1 HER Family HER2 -Phase I pertuzumab, T-DM1 and paclitaxel in HER2� MBC (NCT00951665) -Phase I T-DM1 monotherapy in HER2� MBC in patients with normal or reduced hepatic function (NCT01513083) -Phase I with T-DM1 � GDC0941 versus trastuzumab � GDC0941 in trastuzumab pretreated HER2� MBC (NCT00928330) -Phase I T-DM1 � docetaxel in HER2�MBC (NCT00934856) -Phase I/II T-DM1 with pertuzumab in trastuzumab pretreated HER2� MBC (NCT00875979) -Phase II T-DM1 sequentially with anthracycline-based chemotherapy, as adjuvant or neoadjuvant therapy in HER2� BC (NCT01196052) -Phase III pertuzumab � T-DM1 versus T-DM1 � placebo versus trastuzumab � taxane in HER2� MBC (MARIANNE) (NCT01120184) -Phase III T-DM1 versus lapatinib � capecitabine in HER2� MBC (EMILIA) (NCT00829166) Genentech MM-111 HER2/HER3 bispecific -Phase I with cisplatin, capecitabine, trastuzumab or lapatinib, trastuzumab or paclitaxel, Merrimack moAb trastuzumab in HER2� MBC (NCT01304784) -Phase I with trastuzumab in HER2� MBC (NCT01097460) -Phase I monotherapy in HER2� MBC (NCT00911898) MM-121 HER3 -Phase II of MM121� exemestane in HER2- MBC (NCT01151046) -Phase II with paclitaxel in HER2- MBC (NCT01421472) -Phase I with paclitaxel in HER2- MBC (NCT01209195) -Phase I with XL147 (SAR245408) in advanced solid tumors (NCT01436565) Merrimack Neratinib EGFR, HER2 and HER4 TKI -Phase I neratinib with trastuzumab and weekly paclitaxel in HER2� MBC (NCT01423123) Pfizer -Phase I/II neratinib with temsirolimus in HER2� or TN MBC (NCT01111825) -Phase II neratinib with paclitaxel in HER2� MBC (NCT00445458) -Phase I/II neratinib with trastuzumab in HER2� MBC (NCT00398567) -Phase I/II neratinib with vinorelbine in HER2� MBC (NCT00706030) -Phase II neratinib with capecitabine in HER2� MBC (NCT00741260) -Phase II neratinib versus lapatinib with capecitabine in HER2� MBC -Phase II monotherapy in HER2� MBC pts with CNS mets (NCT01494662) -Phase II of neoadjuvant chemotherapy with neratinib or trastuzumab followed by postoperative trastuzumab in HER2� BC (NCT01008150) -Phase II of neratinib plus paclitaxel versus trastuzumab plus paclitaxel in HER2� MBC (NEFERTT) (NCT00915018) -Phase III of neratinib after adjuvant trastuzumab in HER2� BC (ExteNET) (NCT00878709) Afatinib HGF/cMET EGFR, HER2 TKI -Phase I afatinib with vinorelbine in EGFR and/or HER2 overexpressing advanced solid tumors (NCT00906698) -Phase II afatinib or afatinib with chemotherapy (paclitaxel or vinorelbine weekly) in HER2� MBC (LUX-Breast 2) (NCT01271725) -Phase II Afatinib in HER2� inflammatory breast cancer (NCT01325428) -Phase II afatinib alone or in combination with vinorelbine in HER2� MBC with CNS mets (Lux-Breast 3) (NCT01441596) -Phase III afatinib plus vinorelbine versus trastuzumab plus vinorelbine in HER2� MBC after trastuzumab failure (Lux-Breast 1) (NCT01125566) Boehringer Ingelheim Foretinib VEGFR2/cMET -Phase I/II with lapatinib in HER2�MBC (NCT01138384) -Phase II monotherapy in met TNBC (NCT01147484) GSK Cabozantinib c-Met/VEGFR2/AXL/ KIT/TIE2/FLT3/RET -Phase II monotherapy in HR� MBC (NCT01441947) Exelixis Onartuzumab (MetMAb) c-Met -Phase II of onartuzumab and/or bevacizumab in combination with paclitaxel in met TNBC (NCT01186991) Genentech IGFR Ganitumab (AMG 479) IGF-1R -Phase I/II with trastuzumab in HER2� MBC ( NCT01479179) Takeda with Amgen -Phase II with exemestane or fulvestrant in HR� MBC (NCT00626106) BMS-754807 IGF-1R and InsR dual Inhibition -Phase II � letrozole in HR� MBC (NCT01225172) Bristol Myers Squibb -Phase I/II with trastuzumab in HER2�MBC (NCT00788333) OSI-906 IGF-1R -Phase II with OSI-906 � letrozole/goserelin � erlotinib in HR� MBC (NCT01205685) Astellas Cixutumumab (IMC-A12) IGF-1R -Phase I/II with temsirolimus in advanced or MBC (NCT00699491) -capecitabine and lapatinib � Cixutumumab in HER2� locally advanced or MBC (stages IIIB– IV) (NCT00684983) -Phase II cixutumumab � antiestrogens in HR� MBC (NCT00728949) Lilly Dalotuzumab IGF1R -Phase I monotherapy in the neoadjuvant setting (NCT00759785) -Phase II dalotuzumab � ridaforolimus (MK-8669) in HR� MBC (NCT01234857) Merck 31
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AMERICAN SOCIETY OF CLINICAL ONCOLO
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American Society of Clinical Oncolo
Page 5 and 6: American Society of Clinical Oncolo
Page 7 and 8: New Looks and Challenges for Cooper
Page 9 and 10: Genitourinary Cancer Best Use of Im
Page 11 and 12: Research and Standard of Care: Lung
Page 13 and 14: Practice Management and Information
Page 15 and 16: 2012 ASCO Annual Meeting Disclosure
Page 17 and 18: Matti S. Aapro, MD Clinique De Geno
Page 19 and 20: Hedy Lee Kindler, MD The University
Page 21 and 22: Douglas E. Wood, MD University of W
Page 23 and 24: Mary Lou Smith, JD, MBA Research Ad
Page 25 and 26: ASCO and Conquer Cancer Foundation
Page 27 and 28: Letter from the Editor The theme of
Page 29 and 30: Adjuvant Therapy for Older Women wi
Page 31 and 32: TREATMENT FOR OLDER WOMEN WITH BREA
Page 37 and 38: MANAGEMENT OF T1 BREAST CANCERS the
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Page 43 and 44: MANAGEMENT OF T1 BREAST CANCERS 93.
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Page 47 and 48: ADJUVANT ENDOCRINE THERAPY reductio
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Page 53 and 54: A DICKENS TALE OF THE TREATMENT OF
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Page 65 and 66: A FRESH LOOK AT DUCTAL CARCINOMA IN
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Page 71 and 72: Ductal Carcinoma In Situ, and the I
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Page 75 and 76: KEY QUESTIONS IN THE LOCO-REGIONAL
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Page 85 and 86: Clinical and Imaging Surveillance F
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Page 91 and 92: Advanced Imaging Techniques for the
Page 93 and 94: IMAGING TECHNIQUES FOR BREAST CANCE
Page 95 and 96: IMAGING TECHNIQUES FOR BREAST CANCE
Page 97 and 98: Update of the Oxford Overview: New
Page 99 and 100: UPDATE OF THE OXFORD OVERVIEW Fig.
Page 105 and 106: 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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PROSTATE CANCER RISK REDUCTION Auth
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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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PERSPECTIVES ON HEADLINE-MAKING NEW
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TTF THERAPY IN GLIOBLASTOMA Fig. 1.
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TTF THERAPY IN GLIOBLASTOMA istics.
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TTF THERAPY IN GLIOBLASTOMA because
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Limitations of Adaptive Clinical Tr
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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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T-DM1 AND THERAPEUTIC ANTIBODIES ag
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TARGETING CD30 IN HODGKIN LYMPHOMA
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TARGETING CD30 IN HODGKIN LYMPHOMA
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EARLY DRUG DEVELOPMENT: CASTING A W
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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.
Page 557 and 558:
MOLECULAR TESTING AND NSCLC logic d
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THYMOMA AND THYMIC CARCINOMA: UPDAT
Page 561 and 562:
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
Page 583 and 584:
TREATMENT OPTIONS IN INDOLENT LYMPH
Page 585 and 586:
Page 587 and 588:
Page 589 and 590:
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
Page 607 and 608:
CURRENT STATUS OF MYELOMA THERAPY T
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Maintenance Therapy for Myeloma: Ho
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MAINTENANCE THERAPY FOR MULTIPLE MY
Page 613 and 614:
Page 615 and 616:
Page 617 and 618:
NEW OPTIONS, NEW QUESTIONS: HOW TO
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THERAPIES FOR PATIENTS WITH METASTA
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Page 623 and 624:
Page 625 and 626:
ANTIEMETICS: CURRENT STANDARDS, EME
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ANTIEMETICS: ASCO GUIDELINE UPDATE
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Page 631 and 632:
Page 633 and 634:
Page 635 and 636:
Chemotherapy-Induced Nausea and Vom
Page 637 and 638:
INCIDENCE AND PREVALENCE OF CHEMOTH
Page 639 and 640:
New Frontiers in Mucositis By Dougl
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MUCOSAL INJURY CAUSED BY CANCER THE
Page 643 and 644:
Page 645 and 646:
Page 647 and 648:
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
Page 655 and 656:
The Oncologist as the Patient with
Page 657 and 658:
THE ONCOLOGIST AS THE PATIENT OR RE
Page 659 and 660:
Prolonged Febrile Neutropenia in th
Page 661 and 662:
FEBRILE NEUTROPENIA IN PEDIATRIC CA
Page 663 and 664:
FEBRILE NEUTROPENIA IN PEDIATRIC CA
Page 665 and 666:
TREATMENT APPROACHES IN CHILDREN wh
Page 667 and 668:
TREATMENT APPROACHES IN CHILDREN th
Page 669 and 670:
GENETIC COUNSELING OF THE PATIENT W
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CANCER PREDISPOSITION IN CHILDHOOD
Page 673 and 674:
Page 675 and 676:
Page 677 and 678:
Page 679 and 680:
HOW TO MANAGE VERY RARE PEDIATRIC C
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RARE CANCER IN CHILDREN Registries
Page 683 and 684:
Genetic Alterations in Childhood Me
Page 685 and 686:
GENETIC ALTERATIONS IN CHILDHOOD ME
Page 687 and 688:
Desmoid-Type Fibromatosis in Childr
Page 689 and 690:
CHEMOTHERAPY FOR DESMOID TUMOR Tabl
Page 691 and 692:
CHEMOTHERAPY FOR DESMOID TUMOR 14.
Page 693 and 694:
Targeting the Insulin-Like Growth F
Page 695 and 696:
TARGETING THE IGF SYSTEM Fig. 1. Th
Page 697 and 698:
TARGETING THE IGF SYSTEM malignanci
Page 699 and 700:
Hedgehog Pathway in Pediatric Cance
Page 701 and 702:
HEDGEHOG PATHWAY IN PEDIATRIC CANCE
Page 703 and 704:
HEDGEHOG PATHWAY IN PEDIATRIC CANCE
Page 705 and 706:
Development and Refinement of Augme
Page 707 and 708:
ABFM THERAPY FOR PEDIATRIC ALL than
Page 709 and 710:
ABFM THERAPY FOR PEDIATRIC ALL Auth
Page 711 and 712:
RADIOTHERAPY FOR PEDIATRIC HODGKIN
Page 713 and 714:
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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