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ESTEVA, MILLER, AND TEICHER TARGETS AND ANTIBODIES In selecting cell surface protein targets, whether on malignant cells, on malignant disease–associated cells (e.g., tumor endothelial cells), or in the tumor microenvironment, it is important that the antigen expression is abundant on the target cells or in the tumor region and is very limited on all other cells and normal tissues. 5-9 The patient whose tumor expresses high levels of the target antigen is most likely to benefıt from treatment. ADCs are targeted, potent cytotoxic agents. Most of the proteins being targeted with antibody conjugates are normal proteins, as opposed to mutant proteins; therefore, some antigen expression on normal cells is possible and even likely. Technologies for antibody discovery, development, and engineering are well established. Phage display libraries and humanized mice can produce fully human antibodies, and mouse antibody humanization can result in highly specifıc nonimmunogenic antibodies (Fig. 1). In most cases, the most appropriate antibody for ADC therapeutics requires that the antibodytarget complex internalize into the target cells where the drug is released. DRUGS The drugs most widely conjugated to form ADCs target tubulin or DNA and are uniformly highly potent cytotoxic agents with 50% inhibitory concentration (IC 50 ) values in the picomolar range in cell culture. Though ADCs are among the most tumor-selective anticancer therapeutics developed to date, only a small fraction of the drug reaches the intracellular target. The maytansinoids and dolastatin analogs target tubulin, and both suppress microtubule dynamics. 10 The duocarmycins and calicheamicins target the minor groove of DNA. The amatoxin analogs inhibit RNA polymerase II and III, and SN-38 targets toposiosmerase I, which results in DNA double-strand breaks. 11 These molecules have in KEY POINTS Most antibody-drug conjugate (ADC) targets are cell surface proteins that are much more abundant on tumor cells than on normal cells/tissues. ADCs selectively deliver targeted chemotherapy and could be important components of combination treatment regimens. ADCs are being targeted to solid tumors and to hematologic malignancies. The three components of ADCs, antibody, linker, and drug, must be stable in circulation for days or weeks. T-DM1 and brentuximab vedotin are the first two ADCs to gain regulatory approval for HER2-positive metastatic breast cancer and Hodgkin lymphoma, respectively. Patient selection and understanding about the toxicity profiles of these agents are critical for integration of ADCs into inpatient care. TABLE 1. ADCs in Clinical Development Conjugate Name Target Company Gemtuzumab ozogamicin, CD33 Pfizer Mylotarg Trastuzumab emtansine, T-DM1 HER2 Roche-Genentech Brentuximab vedotin, Adcetris CD30 Seattle Genetics- Takeda Inotuzumab ozogamicin, CD22 Pfizer CMC-544 CDX-011, Glembatumumab GPNMB Celldex Therapeutics vedotin SAR3419, huB4-DM4 CD19 Sanofi Lorvotuzumab mertansine, CD56 (NCAM) ImmunoGen IMGN901 Vorsetuzumab mafodotin; SGN-75 CD70 Seattle Genetics PSMA ADC PSMA Progenics Pinatuzumab vedotin; RG7593 CD22 Roche Polatuzumab vedotin; RG7596 CD79b Roche RG7450 STEAP1 Roche AGS-5ME AGS-5 (SLC44A4) Astellas AGS-22M6E Nectin-4 Astellas SAR566658, huDS6-DM4 CA6 (Muc1) Sanofi Indatuximab ravtansine; BT-062 CD138 (syndecan-1) Biotest Milatuzumab-DOX CD74 Immunomedics BAY 94-9343 Mesothelin Bayer Pharma IMGN529 CD37 ImmunoGen IMGN853 FOLR1 ImmunoGen Labetuzumab-SN-38; IMMU-130 CEACAM5 Immunomedics MLN0264 Guanylyl cyclase Millennium-Takeda IMMU-132 Trop-2 Immunomedics AMG-595 EGFR vIII Amgen AMG-172 CD70 Amgen AGS-15E SLITRK6 Astellas AGS-16C3F ENPP3 Astellas RG-7458 MUC16 Roche GSK2857916 BCMA GSK IMMU-132 Trop-2 Immunomedics HuMax-TF Tissue factor Genmab IMGN-242 CanAg ImmunoGen IMGN-289 EGFR ImmunoGen IMGN-388 Alpha v-integrin ImmunGen IMGN-633 CD33 ImmunoGen/Sanofi MEDI-547 EphA2 MedImmune MLN-0264 GCC Takeda MLN-2704 PSMA Takeda PF-06263507 5T4 Pfizer SAR-566658 huDS6 (Mucin 1) Sanofi SC16LD6.5 SC-16 Stem CentRx SGN-19A CD19 Seattle Genetics SGN-CD33A CD33 Seattle Genetics SGN-LIV1A LIV1 (ZIP6) Seattle Genetics Abbreviations: ADC, antibody-drug conjugate; DOX, doxorubicin; EGFR, epidermal growth factor receptor. e118 2015 ASCO EDUCATIONAL BOOK | asco.org/edbook
ANTIBODY-DRUG CONJUGATES AND T-DM1 FIGURE 1. Antibody-Drug Conjugate Schematic The drug is linked through the epsilon amino groups of lysine, through the intrastrand sulfhydryl linkages, and through genetically engineered unnatural amino acids to provide specific binding sites and, thus, a single chemical species. common an extreme potency and a lack of tumor selectivity, which limits the use of the parent compounds. Dolastatin 10, the parent molecule of the auristatins, was explored in clinical trials in the 1990s, but exploration was terminated in 1995 when the drug failed in a phase II trial in patients with prostate cancer. 12 The maytansinoids are exquisitely potent cytotoxic agents. Maytansine was assessed in early clinical trials in the early 1980s. The phase II clinical trials were disappointing, with very little evidence of response. 13 Duocarmycins are antibiotics that alkylate DNA in the A-T–rich regions of the double-helix minor groove. Several duocarmycins were evaluated in clinical trials, and dose-limiting toxicities occurred at doses too low to achieve antitumor activity. 14,15 Calicheamicins bind in the DNA minor grove and induce double-strand breaks, but they have narrow therapeutic indices and serious late toxicities. 16,17 SN-38, the active metabolite of irinotecan, is poorly bioavailable and has a narrow therapeutic index. 18 Amatoxins, cytotoxic cyclopeptides that target RNA polymerases, are produced by poison mushrooms. Normal tissue toxicities of the amantins precluded their clinical exploration. 19 ADCs are an effective method to increase the therapeutic index of these highly potent cytotoxic agents. The drugs used in ADCs must have suffıcient water solubility and prolonged stability in aqueous formulations and in plasma, and they must have a functional group that is suitable for conjugation with a linker and that must not be readily susceptible to lysosomal enzyme degradation. Consistent with the potent nature of the drug, ADCs are often scheduled like cytotoxic chemotherapy in clinical regimens, with dosing once every 3 weeks. 20-22 LINKERS Linkers are short spacers that covalently couple the drug to the antibody protein and must be stable in circulation (Fig. 1). Inside the cell, most linkers are labile; however, some are stable, requiring degradation of the antibody and linker to release the cytotoxic agent. 23,24 Many linkers react with lysine side chains throughout the antibody or with the sulfhydryls in the hinge regions of the antibody. Linkers in clinical use include acid-labile hydrazone linkers that are degraded under the low pH conditions found in lysosomes. Disulfıdebased linkers are selectively cleaved in the cytosol in the reductive intracellular milieu. Noncleavable thioether linkers release the drug after degradation of the antibody in the lysosome, and peptide linkers, such as citrulline-valine, are degraded by lysosomal proteases in cells. Linkers using L- and D-alanine and beta-glucuronide linkers are being explored. Linkers with polyethylene glycol spacers have been developed to increase the solubility of the conjugate. 25,26 Linkers can influence the circulating half-life and safety of conjugates by minimizing the release of the drug molecule in circulation and optimizing the delivery of the conjugate to the target tissue. Often, during drug development, investigators will test several linkers in safety and effıcacy assays to select the best candidate conjugate. ADCs Drug-loading stoichiometry and molecular homogeneity are important determinants of the safety and effıcacy of antibody conjugates (Fig. 1). The goal is to develop ADCs that are sin- asco.org/edbook | 2015 ASCO EDUCATIONAL BOOK e119
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AMERICAN SOCIETY OF CLINICAL ONCOLO
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American Society of Clinical Oncolo
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Controversies in Neoadjuvant Therap
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Clinical Trials of Precision Medici
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Managing Ovarian Cancer in the Olde
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Updates in the Multimodality Manage
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PEDIATRIC ONCOLOGY Real-Time Molecu
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2015 ASCO Annual Meeting Disclosure
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2015 Educational Book Expert Panel
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James Marshall, PhD Roswell Park Ca
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2015 Annual Meeting Supporters* MIS
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David Yurman Corporate Allies Conqu
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INVITED ARTICLES This year’s invi
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WONG, CAPASSO, AND ECKHARDT 3 3 sc
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WONG, CAPASSO, AND ECKHARDT terize
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WONG, CAPASSO, AND ECKHARDT for mul
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STEPHEN T. SONIS portantly, patient
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STEPHEN T. SONIS elements of a clus
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STEPHEN T. SONIS Defıning the clin
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STEPHEN T. SONIS predict oral mucos
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HUSSAIN AND DIPAOLA TABLE 1. U.S. F
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HUSSAIN AND DIPAOLA mizing use of p
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INVITED ARTICLES DIAGNOSTICS The Fu
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EDWARD S. KIM TABLE 1. Selected Umb
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EDWARD S. KIM platform that plans t
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INVITED ARTICLES HEAD AND NECK CANC
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GROSS AND COHEN treatments are poor
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GROSS AND COHEN 22. Ratner M. Pharm
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GILBERT ET AL tional scholars, lead
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GILBERT ET AL ment of physician com
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GILBERT ET AL greater understanding
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INVITED ARTICLES GASTROINTESTINAL C
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ENG ET AL colorectal cancer. Indeed
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INVITED ARTICLES BREAST CANCER I Wi
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WILLIAM M. SIKOV gational treatment
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DELUCHE, ONESTI, AND ANDRE Precisio
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DELUCHE, ONESTI, AND ANDRE the path
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DELUCHE, ONESTI, AND ANDRE combine
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SALAMA AND CHMURA Surgery or Ablati
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SALAMA AND CHMURA TABLE 1. Frequenc
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SALAMA AND CHMURA per patient was 8
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SALAMA AND CHMURA 4. Fisher B. Labo
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BREAST CANCER Controversies in Neoa
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WHITE AND DEMICHELE KEY POINTS
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WHITE AND DEMICHELE growing body of
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BREAST CANCER Individualizing the A
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OLDER WOMEN WITH EARLY-STAGE BREAST
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IMMUNITY IN TRIPLE-NEGATIVE BREAST
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MOLECULAR SUBTYPES AND NEW TARGETS
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ADJUVANT AND NEOADJUVANT THERAPY FO
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CANCER PREVENTION, GENETICS, AND EP
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ADDRESSING BARRIERS TO BREAST CANCE
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DECISION MAKING IN THE CONTEXT OF B
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SCHIFFMAN, FISHER, AND GIBBS econom
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SCHIFFMAN, FISHER, AND GIBBS High-r
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SCHIFFMAN, FISHER, AND GIBBS could
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SCHIFFMAN, FISHER, AND GIBBS due to
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CAN DIET AND LIFESTYLE PREVENT BREA
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REFORMING THE BUY-AND-BILL CHEMOTHE
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CHRISTINE M. LOVLY EGFR TKIs appear
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CHRISTINE M. LOVLY MAP2K1, which en
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CHRISTINE M. LOVLY patients with ad
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DEVELOPMENTAL THERAPEUTICS AND TRAN
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DAMODARAN, BERGER, AND ROYCHOWDHURY
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ZARDAVAS AND PICCART-GEBHART TABLE
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ZARDAVAS AND PICCART-GEBHART TABLE
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ZARDAVAS AND PICCART-GEBHART triple
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ZARDAVAS AND PICCART-GEBHART mutati
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MICHAEL A. POSTOW Managing Immune C
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MICHAEL A. POSTOW diarrhea symptoms
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MICHAEL A. POSTOW tion. One of thes
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MICHAEL A. POSTOW nitis during ipil
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GASTROINTESTINAL (COLORECTAL) CANCE
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PRECISION THERAPY FOR RECTAL CANCER
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PRECISION THERAPY FOR RECTAL CANCER
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GASTROINTESTINAL (COLORECTAL) CANCE
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MARWAN FAKIH was offset by a detrim
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MARWAN FAKIH TABLE 1. Biologicals i
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MARWAN FAKIH TABLE 3. EGFR Targetin
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MARWAN FAKIH TABLE 6. EGFR Targetin
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MARWAN FAKIH 5-fluorouracil (FOLFIR
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PUNT, SIMKENS, AND KOOPMAN 5-FU/LV
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PUNT, SIMKENS, AND KOOPMAN TABLE 1.
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PUNT, SIMKENS, AND KOOPMAN 35. Veno
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CERCEK, CUSACK, AND RYAN Treatment
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CERCEK, CUSACK, AND RYAN leagues pe
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GASTROINTESTINAL (NONCOLORECTAL) CA
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ABOU-ALFA ET AL sess liver function
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ABOU-ALFA ET AL tinuing liver injur
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ABOU-ALFA ET AL mors including HCC,
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ABOU-ALFA ET AL HCC (Anti-Programme
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AHN ET AL Making Sense of Current a
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AHN ET AL Pancreatic cancer has bee
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AHN ET AL Disclosures of Potential
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EGIDIO DEL FABBRO tion of precachex
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EGIDIO DEL FABBRO FIGURE 3. Mechani
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EGIDIO DEL FABBRO II RCT of ghrelin
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EGIDIO DEL FABBRO 22. Tan BH, Birds
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THE SPECTRUM OF NEUROENDOCRINE TUMO
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CHALLENGING THE TREATMENT PARADIGM
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STAGE I TESTICULAR GERM CELL CANCER
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STAGE I TESTICULAR GERM CELL CANCER
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GERM CELL TUMORS: LOOKING TO THE FU
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SALVAGE CHEMOTHERAPY Salvage Therap
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SALVAGE CHEMOTHERAPY References 1.
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EARLY CHEMOTHERAPY IN MEN WITH META
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RADIUM 223 AND METASTATIC CASTRATIO
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RADIUM 223 AND METASTATIC CASTRATIO
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IMMUNOTHERAPY FOR PROSTATE TUMORS I
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IMMUNOTHERAPY FOR PROSTATE TUMORS F
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IMMUNOTHERAPY FOR PROSTATE TUMORS T
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IMMUNOTHERAPY FOR PROSTATE TUMORS F
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IMMUNOTHERAPY FOR PROSTATE TUMORS a
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EVOLVING IMMUNOTHERAPY STRATEGIES I
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NOVEL IMMUNOTHERAPY AGENTS IN METAS
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PROMISING STRATEGIES IN BLADDER CAN
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GYNECOLOGIC CANCER Cervical Cancer
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MACKAY, WENZEL, AND MILESHKIN In th
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MACKAY, WENZEL, AND MILESHKIN admin
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MACKAY, WENZEL, AND MILESHKIN TABLE
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MACKAY, WENZEL, AND MILESHKIN ing s
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MACKAY, WENZEL, AND MILESHKIN 59. F
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GYNECOLOGIC CANCER Managing Ovarian
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DUSKA, TEW, AND MOORE KEY POINTS A
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DUSKA, TEW, AND MOORE FIGURE 2. Sur
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DUSKA, TEW, AND MOORE FIGURE 3. Che
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DUSKA, TEW, AND MOORE FIGURE 4. Ger
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DUSKA, TEW, AND MOORE 10. Griffıth
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GYNECOLOGIC CANCER Treatment of the
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CHEMOTHERAPY FOR PATIENTS WITH BMOC
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PROGRESS IN HEAD AND NECK SQUAMOUS
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HEAD AND NECK CANCER PI3-Kinase: Ge
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ISAACSSON VELHO, CASTRO JR, AND CHU
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SHARON H. GIORDANO Comparative Effe
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SHARON H. GIORDANO measured confoun
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SHARON H. GIORDANO These databases
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HEALTH SERVICES RESEARCH AND QUALIT
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INDUSTRY AND ONCOLOGY KEY POINTS F
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INDUSTRY AND ONCOLOGY has been “l
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INDUSTRY AND ONCOLOGY by (covered)
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INDUSTRY AND ONCOLOGY 42. World Hea
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CANCER CARE QUALITY: CURRENT STATE
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MANAGING OLDER PATIENTS WITH ALL Th
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MANAGING OLDER PATIENTS WITH ALL TA
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MANAGING OLDER PATIENTS WITH ALL FI
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MANAGING OLDER PATIENTS WITH ALL FI
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MANAGING OLDER PATIENTS WITH ALL ra
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TREATMENT OF PHILADELPHIA CHROMOSOM
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CD19 CAR THERAPY FOR ALL FIGURE 1.
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CD19 CAR THERAPY FOR ALL 5. Zhou G,
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NEW TARGETED THERAPIES FOR iNHL New
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NEW TARGETED THERAPIES FOR iNHL TAB
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NEW TARGETED THERAPIES FOR iNHL a P
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HEMATOPOIETIC CELL TRANSPLANTATION
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LEUKEMIA, MYELODYSPLASIA, AND TRANS
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MICHAEL W. DEININGER TABLE 1. Defin
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MICHAEL W. DEININGER the ATP-bindin
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MICHAEL W. DEININGER broad range ef
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MICHAEL W. DEININGER 30. Hughes T,
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PEMMARAJU AND MOLITERNO TABLE 1. Ac
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PEMMARAJU AND MOLITERNO drome (BCS)
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PEMMARAJU AND MOLITERNO 13. Xing S,
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THERAPIES AND INDICATIONS FOR PH-NE
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LEUKEMIA, MYELODYSPLASIA, AND TRANS
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RECENT UPDATES IN MDS AND MDS/MPNS
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LUNG CANCER Beyond Second-Line Trea
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BEYOND SECOND-LINE TREATMENT FOR LU
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BEYOND SECOND-LINE TREATMENT FOR LU
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LUNG CANCER New Therapies for Histo
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GERBER, PAIK, AND DOWLATI a tumor t
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GERBER, PAIK, AND DOWLATI squamous
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GERBER, PAIK, AND DOWLATI FIGURE 2.
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GERBER, PAIK, AND DOWLATI TABLE 1.
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GERBER, PAIK, AND DOWLATI gression
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GERBER, PAIK, AND DOWLATI Disclosur
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GERBER, PAIK, AND DOWLATI enzyme in
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GERBER, PAIK, AND DOWLATI receptor
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LILENBAUM, LEIGHL, AND NEUBAUER Exp
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LILENBAUM, LEIGHL, AND NEUBAUER tha
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LILENBAUM, LEIGHL, AND NEUBAUER Ref
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BERNARDO H.L. GOULART The Value of
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BERNARDO H.L. GOULART TABLE 1. Expe
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BERNARDO H.L. GOULART every 6 month
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BERNARDO H.L. GOULART lung-cancer/l
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LUNG CANCER Updates in the Multimod
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WOODARD AND JABLONS section, becaus
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WOODARD AND JABLONS mediastinum is
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WOODARD AND JABLONS FIGURE 1. Molec
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NASSER HANNA Current Standards and
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NASSER HANNA At the 2014 ASCO Annua
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NASSER HANNA culty of this task. Va
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LYMPHOMA AND PLASMA CELL DISORDERS
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NOWAKOWSKI AND CZUCZMAN sociated wi
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NOWAKOWSKI AND CZUCZMAN trial is in
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NOWAKOWSKI AND CZUCZMAN TABLE 2. DH
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NOWAKOWSKI AND CZUCZMAN 15. Aragon-
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DAVID W. SCOTT Cell-of-Origin in Di
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DAVID W. SCOTT FIGURE 1. The Origin
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DAVID W. SCOTT FIGURE 2. Immunohist
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DAVID W. SCOTT FIGURE 3. The Lymph2
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DAVID W. SCOTT 10. Shaffer AL 3rd,
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CHEAH, OKI, AND FANALE Novel Treatm
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CHEAH, OKI, AND FANALE an ongoing G
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CHEAH, OKI, AND FANALE a similar me
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CHEAH, OKI, AND FANALE TABLE 3. Sel
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CHEAH, OKI, AND FANALE eral T cell
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CHEAH, OKI, AND FANALE 77. Cairns R
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STEPHEN ANSELL associated with pati
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STEPHEN ANSELL Disclosures of Poten
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MATEOS AND SAN MIGUEL Smoldering Mu
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MATEOS AND SAN MIGUEL years. This f
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MATEOS AND SAN MIGUEL previously me
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MATEOS AND SAN MIGUEL TABLE 2. Risk
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MATEOS AND SAN MIGUEL 30. Rajkumar
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BHUTANI, LANDGREN, AND USMANI of th
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BHUTANI, LANDGREN, AND USMANI bette
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BHUTANI, LANDGREN, AND USMANI fıne
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BHUTANI, LANDGREN, AND USMANI FIGUR
Page 688 and 689:
BHUTANI, LANDGREN, AND USMANI 15. K
Page 690 and 691:
MOREAU AND TOUZEAU Multiple Myeloma
Page 692 and 693:
MOREAU AND TOUZEAU other effıcacy
Page 694 and 695:
MOREAU AND TOUZEAU was able to indu
Page 696 and 697:
MOREAU AND TOUZEAU Group consensus
Page 698 and 699:
LYMPHOMA AND PLASMA CELL DISORDERS
Page 700 and 701:
MANAGEMENT OF CLL Up-Front Manageme
Page 702 and 703:
MANAGEMENT OF CLL than 17p-/TP53mut
Page 704 and 705:
MANAGEMENT OF CLL could be associat
Page 706 and 707:
MANAGEMENT OF CLL tion by nonmalign
Page 708 and 709:
MANAGEMENT OF CLL fludarabine and c
Page 710 and 711:
MANAGEMENT OF CLL lymphocytic leuke
Page 712 and 713:
PROGNOSTIC FACTORS AND ADJUVANT RAD
Page 714 and 715:
Page 716 and 717:
Page 718 and 719:
MERKEL CELL CARCINOMA Merkel Cell C
Page 720 and 721:
MERKEL CELL CARCINOMA tions in PIK3
Page 722 and 723:
MERKEL CELL CARCINOMA treating MCC
Page 724 and 725:
MERKEL CELL CARCINOMA 32. Leonard J
Page 726 and 727:
MELANOMA/SKIN CANCERS Locoregional
Page 728 and 729:
PERFUSION AND INFUSION IN THE ERA O
Page 730 and 731:
Page 732 and 733:
Page 734 and 735:
NEOADJUVANT THERAPY OF MELANOMA Neo
Page 736 and 737:
NEOADJUVANT THERAPY OF MELANOMA TAB
Page 738 and 739:
NEOADJUVANT THERAPY OF MELANOMA ity
Page 740 and 741:
NEOADJUVANT THERAPY OF MELANOMA 4.
Page 742 and 743:
MELANOMA/SKIN CANCERS Targeted Mole
Page 744 and 745:
SULLIVAN ET AL FIGURE 1. Relevant S
Page 746 and 747:
SULLIVAN ET AL Resistance to BRAF i
Page 748 and 749:
SULLIVAN ET AL TABLE 1. Clinical Tr
Page 750 and 751:
SULLIVAN ET AL 17. Halait H, Demart
Page 752 and 753:
SULLIVAN ET AL NRAS-mutant melanoma
Page 754 and 755:
KLEPIN, RODIN, AND HURRIA Treating
Page 756 and 757:
KLEPIN, RODIN, AND HURRIA plication
Page 758 and 759:
KLEPIN, RODIN, AND HURRIA plan was
Page 760 and 761:
KLEPIN, RODIN, AND HURRIA patient-s
Page 762 and 763:
KLEPIN, RODIN, AND HURRIA 62. Blanc
Page 764 and 765:
PERIPHERAL NEUROTOXICITY IN CANCER
Page 766 and 767:
Page 768 and 769:
Page 770 and 771:
Page 772 and 773:
PARTRIDGE, JACOBSEN, AND ANDERSEN C
Page 774 and 775:
PARTRIDGE, JACOBSEN, AND ANDERSEN c
Page 776 and 777:
PARTRIDGE, JACOBSEN, AND ANDERSEN w
Page 778 and 779:
PARTRIDGE, JACOBSEN, AND ANDERSEN v
Page 780 and 781:
LESLIE R. SCHOVER Sexual Healing in
Page 782 and 783:
LESLIE R. SCHOVER tinuous ADT in pr
Page 784 and 785:
LESLIE R. SCHOVER 12. Potosky AL, H
Page 786 and 787:
CATHERINE H. VAN POZNAK TABLE 1. Wo
Page 788 and 789:
CATHERINE H. VAN POZNAK (tamoxifen,
Page 790 and 791:
CATHERINE H. VAN POZNAK TABLE 3. FD
Page 792 and 793:
CATHERINE H. VAN POZNAK premenopaus
Page 794 and 795:
SHARI GOLDFARB KEY POINTS Brea
Page 796 and 797:
SHARI GOLDFARB and friction with va
Page 798 and 799:
SHARI GOLDFARB importance both duri
Page 800 and 801:
PATIENT AND SURVIVOR CARE Moving Su
Page 802 and 803:
MAYER ET AL TABLE 1. Quality Metric
Page 804 and 805:
MAYER ET AL to enhance the quality
Page 806 and 807:
MAYER ET AL FIGURE 2. (A) Infertili
Page 808 and 809:
MAYER ET AL efıcial suggests that
Page 810 and 811:
PATIENT AND SURVIVOR CARE The Chall
Page 812 and 813:
BRUERA AND PAICE Choice of Opioid a
Page 814 and 815:
BRUERA AND PAICE toxicity and proce
Page 816 and 817:
BRUERA AND PAICE effective. Basic s
Page 818 and 819:
PEDIATRIC ONCOLOGY Real-Time Molecu
Page 820 and 821:
CARROLL, RAETZ, AND MEYER KEY POINT
Page 822 and 823:
CARROLL, RAETZ, AND MEYER most are
Page 824 and 825:
CARROLL, RAETZ, AND MEYER markers a
Page 826 and 827:
PEDIATRIC ONCOLOGY Translating Surv
Page 828 and 829:
REDUCING THE BURDEN OF LATE EFFECTS
Page 830 and 831:
Page 832 and 833:
Page 834 and 835:
Page 836 and 837:
PROFESSIONAL DEVELOPMENT The Challe
Page 838 and 839:
ADVANCES IN WEBSITE INFORMATION RES
Page 840 and 841:
Page 842 and 843:
Page 844 and 845:
Page 846 and 847:
COMMUNICATION AND TECHNOLOGY: IT’
Page 848 and 849:
Page 850 and 851:
Page 852 and 853:
PATIENT-REPORTED OUTCOMES IN ONCOLO
Page 854 and 855:
PATIENT-REPORTED OUTCOMES IN ONCOLO
Page 856 and 857:
PROFESSIONAL DEVELOPMENT Trends, An
Page 858 and 859:
CLINICAL ONCOLOGY PRACTICE 2015 FIG
Page 860 and 861:
CLINICAL ONCOLOGY PRACTICE 2015 (6.
Page 862 and 863:
CLINICAL ONCOLOGY PRACTICE 2015 Pro
Page 864 and 865:
ADJUVANT/NEOADJUVANT MEDICAL THERAP
Page 866 and 867:
Page 868 and 869:
Page 870 and 871:
INDICATIONS FOR ADJUVANT RADIATION
Page 872 and 873:
Page 874 and 875:
Page 876 and 877:
Page 878 and 879:
SARCOMA Latest Advances in Systemic
Page 880 and 881:
SYSTEMIC THERAPY FOR OSTEOSARCOMA A
Page 882 and 883:
SYSTEMIC THERAPY FOR OSTEOSARCOMA A
Page 884 and 885:
RETHINKING TREATMENT FOR CHONDROSAR
Page 886 and 887:
Page 888 and 889:
Page 890 and 891:
Page 892 and 893:
BONE SARCOMAS IN ADULTS local disea
Page 894 and 895:
BONE SARCOMAS IN ADULTS structure a
Page 896 and 897:
SARCOMA Well-Differentiated and Ded
Page 898 and 899:
ABBAS MANJI ET AL ticular region. 7
Page 900 and 901:
ABBAS MANJI ET AL MYXOID (ROUND CEL
Page 902 and 903:
ABBAS MANJI ET AL versus doxorubici
Page 904 and 905:
SHLUSH AND HERSHKOVITZ Clonal Evolu
Page 906 and 907:
SHLUSH AND HERSHKOVITZ FIGURE 1. Ti
Page 908 and 909:
TUMOR BIOLOGY New Strategies to Und
Page 910 and 911:
KNAPP, DHAWAN, AND OSTRANDER in dog
Page 912 and 913:
KNAPP, DHAWAN, AND OSTRANDER TABLE
Page 914 and 915:
KNAPP, DHAWAN, AND OSTRANDER 14. Fe
Page 916 and 917:
SOURBIER, SRINIVASAN, AND LINEHAN M
Page 918 and 919:
SOURBIER, SRINIVASAN, AND LINEHAN F
Page 920 and 921:
SOURBIER, SRINIVASAN, AND LINEHAN T
Page 922:
Author Index Abbas Manji, Gulam ...
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