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RECENT UPDATES IN MDS AND MDS/MPNS INCLUDING HEMATOPOIETIC CELL TRANSPLANTATION TABLE 2. Frequency of Recurrent Mutations among WHO-defined MDS/MPNs 4,136,139,144 Mutation CMML JMML aCML MDS/MPN-U RARS-T Clinical Significance ASXL1 40 0 69 Unknown 15 Adverse CALR 0 0 0 0 1 Unknown CBL 10* 15** 0 Unknown 4 Adverse/Favorable CSF3R 0 0 Variable 0 0 Predictive DNMT3A 2 0 Unknown Unknown 15 Unknown ETV6 1 0 Unknown Unknown 3 Unknown EZH2 5 0 Unknown 10 Unknown Unknown IDH1/2 6 0 Unknown Unknown Unknown Unknown JAK2 8 0 7 19 57* Favorable JAK3 Unknown 12 Unknown Unknown Unknown Neutral K/N RAS 19 39 35 14 Unknown Neutral NF1 13 Unknown Unknown Unknown Neutral PTPN11 44 Unknown Unknown Unknown Neutral RUNX1 15 0 Unknown 14 Unknown Neutral SETBP1 15* 8 48 10 1 Adverse SF3B1 6 0 Unknown Unknown 93 Favorable SRSF2 46 0 Unknown Unknown 7 Adverse TET2 58 0 Unknown 30 25 Neutral TP53 1 0 Unknown Unknown Unknown Unknown U2AF1 5 0 Unknown Unknown 5 Unknown ZRSF2 8 0 Unknown Unknown 3 Unknown Abbreviations: WHO, World Health Organization; MDS/MPNs, myelodysplastic syndromes/myeloproliferative neoplasms; CMML, chronic myelomonocytic leukemia; JMML, juvenile myelomonocytic leukemia; aCML, atypical chronic myeloid leukemia; MDS/MPN-U, myelodysplastic syndromes/myeloproliferative neoplasms–unclassifiable; RARS-T, refractory anemia with ring sideroblost and thrombocytosis. and TET2 is highly specifıc for patients with CMML, which aids in the diagnosis of the treated CMML patient when historic monocytosis may be unclear and current monocytosis may be suppressed by HMAs or cytoreductive agents. 31 The prognostic signifıcance of recurrent mutations in CMML also has been tested. Interrogation of the most common mutations in CMML has identifıed ASXL1 to be independently prognostic. 48,73 This has led to its incorporation into two independent prognostic scoring systems. However, larger data sets will be required to fully annotate the prognostic signifıcance of single and combination mutations in CMML. Juvenile Myelomonocytic Leukemia Although the monocytic phenotype of juvenile myelomonocytic leukemia (JMML) is similar to that of CMML, the genetic fıngerprint of JMML is distinct. 128 Greater than 90% of recurrently mutated genes in JMML cluster on RAS pathway activation. 129 These gene mutations include NF1, N-RAS, K-RAS, PTPN-11, and CBL. 130,131 Both somatic and germline mutations of these genes have been identifıed, with the latter most associated with congenital genetic syndromes such as Noonan syndrome (PTPN11) and Neurofıbromatosis type 1 (NF1). 132-134 Secondary events in JAK3 and SETBP1 also have been described and suggest a poor prognosis. 135,136 This genetic landscape, along with its characteristic GM-CSF hypersensitivity, has resulted in major advances in the molecular understanding of JMML. 128 Further, the presence of these mutations can alter treatment decisions and management. Patients with CBL mutations and its associated congenital syndrome can manifest a JMML phenotype that is self-limited. 131 Therefore, a watchful waiting strategy is often employed in these children, as opposed to allogeneic transplant in other RAS-mutated JMML cases. 137 Atypical Chronic Myeloid Leukemia Atypical chronic myeloid leukemia (aCML)Atypi is a disease characterized by severe neutrophil dysplasia and cytopenias in the absence of the BCR:ABL fusion protein. This disease has historically been diffıcult to diagnose given the pathologic overlap between it and other MDS/MPNs, particularly MDS/MPN-Unclassifıable. Further, the diagnostic diffıculty present in discerning aCML from chronic neutrophil leukemia (CNL) has made the annotation of aCML-specifıc mutations challenging. 138 Gene mutations identifıed in aCML/ CNL include JAK2, SETBP1, NRAS, and CSF3R. Analysis of these genes can identify a clonal event in over 50% of these diseases. 139-141 CSF3R mutations are notable because they represent a potential predictive marker for targeted therapy. Preclinical data suggest that truncating CSF3R mutations predict sensitivity to SRC inhibition and CSF3R mutations affecting the membrane proximal portion for the receptor asco.org/edbook | 2015 ASCO EDUCATIONAL BOOK e405
ODENIKE, ONIDA, AND PADRON predicts sensitivity to JAK2 inhibition. 139 The latter has been validated in clinical case reports with ruxolitinib therapy in aCML. 142 However, two separate reports have failed to identify CSF3R mutations in a stringently defıned aCML cohort and were exclusively seen in CNL. 143,144 Nonetheless, mutational analysis for CSF3R should be performed if aCML is suspected, given the potential therapeutic implications. Myelodysplastic Syndromes/Myeloproliferative Neoplasms–Unclassifiable The genetic study of MDS/MPN-Unclassifıable (U) has been limited by diffıculties in the diagnostic standardization of this entity. MDS/MPN-U is defıned by having clinicopathologic features of myeloproliferation, dysplasia, and cytopenias but not meeting criteria for other well-defıned MDS/MPNs. It is hypothesized that many MDS/MPN-U cases may be reclassifıced into other WHO-defıned MDS/MPNs with mutational profıling. To this end, a recent retrospective study identifıed a clinical and genetic signature that could identify aCML among those cases initially identifıed as MDS/MPN-U. 144 More investigation is needed to better annotate disease-specifıc genetic fıngerprints to confıdently allow for reclassifıcation of MDS/MPN cases. Refractory Anemia with Ring Sideroblast and Thrombocytosis Refractory anemia with ring sideroblost and thrombocytosis RARS-T) is defıned by the presence of ringed sideroblasts and a platelet count of greater than 450 x 10 8 /dL and is included as a provisional category within the group of MDS/ MPN-U by WHO. 8,14 Similar to cases of MDS with ringed sideroblasts (RARS), the genetic landscape of RARS-T is dominated by the presence of mutations in SF3B1 that occur at a frequency reported between approximately 60 to 90%. 28,29,145 Other recurrent mutations identifıed in both RARS and RARS-T include TET2, ASXL1, and EZH2. 146 However, RARS-T has been demonstrated to additionally harbor mutations in JAK2 at rates approximating 50% and, less frequently, mutations in other signaling mutations such as CBL and CALR, which are rarely seen in RARS. 28,146-149 This raises the possibility that mutations in JAK2 mayberesponsible for the thrombocytosis uniquely seen in RARS-T. Although conventional wisdom states that the natural history of RARS-T is relatively benign, emerging data suggest that annotation of mutations in RARS-T may reveal a more aggressive subtype. A recent report identifıed SF3B1 and JAK2 mutations as favorably prognostic and associated with improved survival compared to their mutated counterpart. For example, SF3B1 wild-type cases of RARS-T had a median survival of 3.3 years compared to 6.9 years in mutated cases. THERAPIES IN ADULT MYELODYSPLASTIC SYNDROMES/MYELOPROLIFERATIVE NEOPLASMS No pharmacologic agents have been demonstrated to alter the natural history of MDS/MPNs. As such, the general approach for the treatment of these groups of diseases is to focus on therapeutic strategies tailored to symptomatology with individual patients. There is little evidence to suggest that patients with asymptomatic MDS/MPN benefıt from current standard treatment. However, it is strongly recommended that all patients with MDS/MPN be considered for clinical trial when available. Allogeneic stem cell transplant has the most robust data suggesting a disease modifying effect in MDS/MPNs 94,150-152 and should therefore be considered in higher-risk patients with MDS/MPN. Although there has been substantial progress in the prognostication of CMML cases, challenges remain in adequately risk-stratifying other MDS/MPNs for clinical transplant decision making. 48,153,154 Below is a summary of treatment options and their disease-specifıc supporting data. Hypomethylating Agents Very limited data are available for the use of HMAs for the treatment of aCML, MDS/MPN-U, or RARS-T. 155 However, robust data exist that demonstrate the activity of HMAs in CMML. Several phase II studies have demonstrated that azacitadine is active in CMML and associated with acceptable therapy-associated toxicity. 156,157 Oral azacitadine more recently has been tested for the treatment of CMML with clinical responses seen in 35% of patients previously treated with HMA for MDS and CMML, and in 73% of patients receiving azacitadine as fırst-line therapy. 158 Decitabine also has been examined in multiple phase II trials, with response rates ranging from 10 to 58% in patients with CMML. 159 However, despite well-documented activity, no evidence exists that HMAs increase overall survival or decrease progression to AML. Therefore, we reserve this therapy for patients with CMML in which cytopenias are the predominant symptom. We would not favor HMAs in rapidly proliferative patients with CMML, given the relatively long median time to HMA response. There is no CMML-specifıc evidence to favor one HMA over another. Lenalidomide and Interferon There has been limited data testing the activity of lenalidomide in CMML and RARS-T. In CMML, lenalidomide has been tested in combination with metronomic doses of melphalan. Although the study was small in number, a 25 and 33% response rate was identifıed in patients with myelodysplastic and myeloproliferative CMML, respectively. 160 A case study also has reported a proliferative of CMML cases with isolated del(5q) treated with lenalidomide that achieved blast clearance and cytoreduction. In RARS-T, three case reports have demonstrated clinical activity with respect to hematologic and splenomegaly improvement irrespective of cytogenetic abnormalities. 161-163 Interferon has been tested in aCML in a limited number of cases with modest activity. 164,165 Cytoreductive Agents Patients with MDS/MPN with rapid and severe myeloproliferative or constitutional symptoms should be considered for treatment with cytoreductive agents. These therapies range e406 2015 ASCO EDUCATIONAL BOOK | asco.org/edbook
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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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Managing Ovarian Cancer in the Olde
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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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GYNECOLOGIC CANCER Cervical Cancer
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GYNECOLOGIC CANCER Managing Ovarian
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GYNECOLOGIC CANCER Treatment of the
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CHEMOTHERAPY FOR PATIENTS WITH BMOC
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INDUSTRY AND ONCOLOGY KEY POINTS F
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TREATMENT OF PHILADELPHIA CHROMOSOM
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CD19 CAR THERAPY FOR ALL FIGURE 1.
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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 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
Page 650 and 651:
DAVID W. SCOTT FIGURE 3. The Lymph2
Page 652 and 653:
DAVID W. SCOTT 10. Shaffer AL 3rd,
Page 654 and 655:
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
Page 680 and 681:
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
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BHUTANI, LANDGREN, AND USMANI 15. K
Page 690 and 691:
MOREAU AND TOUZEAU Multiple Myeloma
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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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