2012 EDUCATIONAL BOOK - American Society of Clinical Oncology

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motherapy with or without concurrent cediranib and also the effect of maintenance cediranib in platinum-sensitive relapsed ovarian cancer. Reasons for Adding a New Treatment There are many unresolved questions as to the optimal use of bevacizumab in patients with ovarian cancer. It is a very expensive therapy, so it is important to consider the questions in Table 2 and the issues that follow when deciding whether to use this new drug. Improved Survival Survival curves from the GOG-0218 and ICON7 trials are still falling, so it seems unlikely that there will be more long-term survivors or cures than with cytotoxic chemotherapy alone. Results from the ICON7 trial show that there is no improved survival for low-risk patients, but an almost 8-months-longer median survival for patients at high risk for relapse. If the survival benefit from first-line use is unclear and OCEANS shows improved survival in patients after first relapse, a case could be made for reserving it for relapse therapy. Increased Response Rate ICON7 and OCEANS both demonstrated an increased response rate. A tumor response is likely to lead to resolution of cancer-related symptoms. This is of most relevance to patients who have experienced relapse because most patients receiving first-line treatment will have minimal symptoms from their cancer after surgery. Patients who do have cancer-related symptoms are usually candidates now for neoadjuvant therapy. However, administering bevacizumab in this setting might raise concerns regarding impaired wound healing after subsequent surgery. Delaying Relapse It is debatable whether the 2- to 4-month delay in PFS justifies the ongoing treatment with 3-weekly infusions, especially in view of the results from OCEANS showing that the addition of bevacizumab to second-line treatment seems to also delay PFS. Less Toxic than Standard Therapy Table 2. Unresolved Questions Regarding the Use of Bevacizumab in Ovarian Cancer Unresolved Question Option 1/Comment Option 2/Comment What dose? 15 mg/kg 3 weekly licensed 7.5 mg/kg 3 weekly probably as effective and cheaper In combination or alone? With chemotherapy as improves response rate Only as maintenance (only addition of maintenance improved PFS in GOG218) For what duration? Until progression For defined period-22 cycles Should evidence of progression be sought? CA-125 every 6 weeks, and or CT every 3 months will shorten therapy Bevacizumab has been shown to add to toxicity of standard chemotherapy, especially hypertension, bleeding, thromboembolic events, and gastric perforations. Administering bevacizumab as maintenance therapy reduces time without therapy. Rationale for PARP Inhibitors Poly (ADP-ribose) polymerase (PARP), an enzyme discovered almost 50 years ago, 11 is crucial for the repair of single-strand DNA breaks (SSBs) via the base excision repair (BER) pathway. Although it has no direct effect on double-strand DNA breaks (DSBs), 12 when a DNA replication fork comes across a persistent SSB (i.e., if PARP was inhibited), the fork could collapse or form a DSB. 13 Tumor cells deficient in BRCA1/2 are unable to repair these DSBs as a result of defects in homologous recombination. The concept of two genetic mutations, that individually have little effect but when combined are lethal, is known as synthetic lethality 14 and such an interaction exists between BRCA1/2 and PARP. PARP inhibitors lead to selective death of tumor cells that have hereditary or acquired BRCA1/2 (homozygous) mutations but have no selective effect on the normal cells of BRCA carriers (heterozygous). Homologous recombination defects are thought to occur in up to 50% of high-grade serous carcinomas, 15 not only through BRCA1/2 mutations but interestingly, via a “BRCAness” phenotype. Recent microarray studies have identified a BRCAness gene expression profile in patients with sporadic ovarian cancer that corresponds with responsiveness to platinum-based chemotherapy and to PARP inhibitors. 16 Clinical Trials No CA-125 or scans will prolong bevacizumab and delay next line of therapy Which first-line patients? All stage 4 and stage 3 with suboptimal surgery Try to select those likely to have short remission Which line of therapy? First line Relapse Abbreviations: CA, cancer antigen; CT, computed tomography; GOG, Gynecologic Oncology Group; PFS, progression-free survival. 342 ROUX, ZWEIFEL, AND RUSTIN A phase I trial investigated olaparib (AZD2281) in patients with solid tumors refractory to conventional chemotherapy and enriched for patients with BRCA1/2 mutations. Partial responses were noted in 63% of patients (12 of 19) including eight patients with ovarian cancer. 17 Durable responses (median, 28 weeks; range, 10 to 86) correlating with an increased platinum-free interval were reported in an expanded cohort of 50 patients from this trial. The overall response rate (RR) was 69% in platinum-sensitive disease, 50% in platinum-resistant disease, and 27% in platinumrefractory disease. Dose-limiting toxicity was seen at 400 mg and 600 mg twice daily, so the dose-expansion cohort received 200 mg twice daily with minimal toxicity—mainly fatigue and GI symptoms. These encouraging results led to several phase II trials; a single-arm, open-label sequential dosing trial in patients with BRCA1/2 mutations reported clinical efficacy in both dosing cohorts, but higher response rates were seen in those receiving olaparib 400 mg twice daily compared with 100 mg twice daily (RR, 33% and 12.5%, respectively). 18 The toxicities were fatigue, sickness, and anemia but mostly grades 1 and 2. A randomized phase II trial comparing the efficacy of olaparib at two dose levels with pegylated liposomal doxo-
ANTIANGIOGENICS AND PARP INHIBITORS IN OVARIAN CANCER rubicin (PLD) in patients with BRCA1/2-mutated ovarian cancer did not show a significant PFS advantage for either olaparib dosing schedule (200 mg twice daily, 6.5 months; 400 mg twice daily, 8.8 months) compared with PLD (7.1 months; HR � 0.88; p � 0.66). 19 Nonetheless, with comparable efficacy, replacing PLD with a tablet is an attractive option. The concept of BRCAness as described earlier herein led to the investigation of whether PARP inhibitors were clinically active in patients with sporadic serous ovarian cancers. A phase II trial of olaparib 400 mg twice daily in patients with (n � 17) and without (n � 47) BRCA1/2 mutations reported a response rate of 41% and 24%, respectively. The better responses were again seen mostly in patients with platinum-sensitive disease. 20 A phase II randomized placebo-controlled trial of olaparib monotherapy as maintenance treatment for patients with relapsed platinum-sensitive serous ovarian cancer was reported at ASCO in 2011. 21 PFS by Response Evaluation Criteria in Solid Tumors (RECIST) criteria was significantly longer in the olaparib group (n � 136) compared with the placebo group (n � 129;8.4 vs. 4.8 months; HR � 0.35; p � 0.00001; Fig. 1). The PFS did not translate into an OS benefit, which has led AstraZeneca (Wilmington, DE) to stop pursuing this indication. Besides those evaluating olaparib, clinical trials are underway with several other PARP inhibitors as monotherapy in ovarian cancer and include MK4827 (Merck; Whitehouse Station, NY), CEP-9722 (Cephalon, Frazer, PA), ABT-888 (Abbott Laboratories, Abbott Park, IL) and rucaparib (previously PF-01367338 or AG014699). Preliminary phase I results for MK4827 have shown efficacy comparable with olaparib 22 and certainly warrant further investigation in this setting. BMN-673 (BioMarin Pharmaceutical Inc., Novato, CA) is the most selective and potent PARP inhibitor reported to date, and phase I data are awaited with interest. Authors’ Disclosures of Potential Conflicts of Interest Employment or Leadership Positions Consultant or Advisory Role Author Rene Roux* Martin Zweifel* Gordon J. S. Rustin AstraZeneca; Roche *No relevant relationships to disclose. 1. Campos SM, Ghosh S. A current review of targeted therapeutics for ovarian cancer. J Clin Oncol. 2010;28:149362. 2. Mukherjee L, Rustin G. Antivascular therapy in gynaecological cancers. In Kehoe S, Edmondson RJ, Gore M, et al (eds): Gynaecological Cancers: Biology and Therapeutics. London: RCOG Press, 2011;121-137. 3. Burger RA, Sill MW, Monk BJ, et al. Phase II trial of bevacizumab in persistent or recurrent epithelial ovarian cancer or primary peritoneal cancer: a Gynecologic Oncology Group Study. J Clin Oncol. 2007;25:5165- 5171. 4. Cannistra SA, Matulonis UA, Penson RT, et al. Phase II study of bevacizumab in patients with platinum-resistant ovarian cancer or peritoneal serous cancer. J Clin Oncol. 2007;25:5180-5186. 5. Perren TJ, Swart AM, Pfisterer J, et al. A phase 3 trial of bevacizumab in ovarian cancer. N Engl J Med. 2011;365:2484-2496. 6. Burger RA, Brady MF, Bookman MA, et al. Incorporation of bevacizumab in the primary treatment of ovarian cancer. N Engl J Med. 2011;365: 2473-2483. Conclusion Bevacizumab 7.5 mg/kg 3-weekly, should be considered for patients who are at high risk of having a short PFS because the bevacizumab might delay time to symptomatic relapse, and it is this group of patients who seem to achieve a substantial survival gain. For patients with optimally debulked disease, the greatest benefit from bevacizumab is more likely to be part of relapse therapy. The greatest benefit from PARP inhibitors will be in patients with BRCA mutations, but they are also likely to have a role in patients with high-grade serous ovarian cancers. Myelosuppression is likely to prevent PARP inhibitor administration in combination with chemotherapy. Because they have shown single-agent activity and can delay progression, they have the potential to be used as another line of relapse therapy or as maintenance therapy after chemotherapy for relapse. Stock Ownership Honoraria REFERENCES Fig 1. Progression-free survival of patients in a phase II randomized placebo-controlled trial of olaparib monotherapy as maintenance treatment for patients with relapsed platinum-sensitive serous ovarian cancer. Reprinted with permission. © American Society of Clinical Oncology. All rights reserved. 21 Boehringer Ingelheim Research Funding Expert Testimony Other Remuneration 7. Katsumata N, Yasuda M, Takahashi F, et al. Dose-dense paclitaxel once a week in combination with carboplatin every 3 weeks for advanced ovarian cancer: a phase 3, open-label, randomised controlled trial. Lancet. 2009;374: 1331-1338. 8. Gonzalez-Martin A, Gladieff L, Stroyakovskiy D, et al. Front-line bevacizumab (BEV) combined with weekly paclitaxel (wPAC) and carboplatin (C) for ovarian cancer (OC): safety results from the concurrent chemotherapy (CT) phase of the OCTAVIa study. Presented at: European Multidisciplinary Cancer Congress; 2011; Stockholm, Sweden (abstr 8002). 9. Aghajanian C, Finkler NJ, Rutherford T, et al. OCEANS: A randomized, double-blinded, placebo-controlled phase III trial of chemotherapy with or without bevacizumab (BEV) in patients with platinum-sensitive recurrent epithelial ovarian (EOC), primary peritoneal (PPC), or fallopian tube cancer (FTC). J Clin Oncol. 2011;29:45S (suppl; abstr LBA5007). 10. Coleman RL. Making of a phase III study in recurrent ovarian cancer: the odyssey of GOG 213. Clin Ovarian Cancer. 2008;1:78-80. 11. Chambon P, Weill JD, Mandel P. Nicotinamide mononucleotide activa- 343
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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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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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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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Page 363 and 364: Prognostic Factors in Advanced RCC
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Page 377 and 378: ADJUVANT THERAPY FOR OLDER PATIENTS
Page 379 and 380: Adjuvant Systemic Therapy Adjuvant
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Page 399 and 400: RECENT CLINICAL HIGHLIGHTS IN GYNEC
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Page 409 and 410: UPFRONT TREATMENT OF OVARIAN CANCER
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Page 425 and 426: UTERINE SARCOMA: CHALLENGING CASES
Page 427 and 428: HISTOLOGIC FEATURES AND MANAGEMENT
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Page 437 and 438: PATIENTS WITH HPV-POSITIVE OROPHARY
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Page 449 and 450: GENOMIC AND PROTEOMIC TECHNOLOGIES
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Page 453 and 454: TREATMENT OF THYROID CANCERS: NEW I
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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
Page 591 and 592:
ROLE OF HCT FOR INDOLENT LYMPHOMA T
Page 593 and 594:
ROLE OF HCT FOR INDOLENT LYMPHOMA e
Page 595 and 596:
CONTROVERSIES IN MYELOMA: INDUCTION
Page 597 and 598:
TRANSPLANTATION FOR MYELOMA Alterna
Page 599 and 600:
TRANSPLANTATION FOR MYELOMA compare
Page 601 and 602:
TRANSPLANTATION FOR MYELOMA autolog
Page 603 and 604:
CURRENT STATUS OF MYELOMA THERAPY K
Page 605 and 606:
CURRENT STATUS OF MYELOMA THERAPY F
Page 607 and 608:
CURRENT STATUS OF MYELOMA THERAPY T
Page 609 and 610:
Maintenance Therapy for Myeloma: Ho
Page 611 and 612:
MAINTENANCE THERAPY FOR MULTIPLE MY
Page 613 and 614:
Page 615 and 616:
Page 617 and 618:
NEW OPTIONS, NEW QUESTIONS: HOW TO
Page 619 and 620:
THERAPIES FOR PATIENTS WITH METASTA
Page 621 and 622:
Page 623 and 624:
Page 625 and 626:
ANTIEMETICS: CURRENT STANDARDS, EME
Page 627 and 628:
ANTIEMETICS: ASCO GUIDELINE UPDATE
Page 629 and 630:
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
Page 641 and 642:
MUCOSAL INJURY CAUSED BY CANCER THE
Page 643 and 644:
Page 645 and 646:
Page 647 and 648:
Short- and Long-term Cardiovascular
Page 649 and 650:
Recent Advances in Cardiotoxicity o
Page 651 and 652:
CARDIOTOXICITY OF ANTICANCER THERAP
Page 653 and 654:
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
Page 671 and 672:
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
Page 681 and 682:
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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