Hepatocellular carcinoma (HCC) is the second leading cause of cancer-related deaths worldwide. β-catenin is widely thought to be a major oncogene in HCC based on the frequency of mutations associated with aberrant Wnt signaling in HCC patients. Challenging this model, our data reveal that β-catenin nuclear accumulation is restricted to the late stage of the disease. Until then, β-catenin is primarily located at the plasma membrane in complex with multiple cadherin family members where it drives tumor cell survival by enhancing the signaling of growth factor receptors such as EGFR. Therefore, our study reveals the evolving nature of β-catenin in HCC to establish it as a compound tumor promoter during the progression of the disease.

Introduction Effective therapies for R/R AML remain limited. MEK or MDM2 inhibition can downregulate MCL1, overcoming resistance to BCL2 inhibition. Preclinical synergy was seen when combining BCL2 inhibitor Ven with MEK inhibitor cobimetinib (cobi) or MDM2 inhibitor idasa (Han et al. ASH 2016; Pan et al. Cancer Cell 2017), supporting clinical evaluation in AML. Preliminary data in a Phase Ib dose-escalation study (NCT02670044) evaluating Ven+cobi/idasa in R/R AML suggested both combinations were tolerable (Daver et al. ASH 2017). However, Ven+cobi was closed due to limited clinical activity. Here we present data for additional pts, longer follow-up and biomarker analyses for Ven+idasa. Methods This ongoing, open-label, multicenter study evaluates safety, tolerability and efficacy of Ven+idasa in R/R AML or secondary AML previously treated for an antecedent hematologic disease. Pts >60 yrs of age and ineligible for cytotoxic therapy/allogeneic stem cell transplant were enrolled. A 2-dimensional dose escalation was used to establish the maximum tolerated dose: pts received doses of Ven orally (PO) daily (400mg or 600mg) + idasa PO daily on Days 1-5 (150mg, 200mg, or 400mg) in 28-day cycles. Plasma samples were taken for PK analysis at Cycles 1 and 2 Days 1 and 5, and Cycle 4 Day 1. BCL2, BCLxL and MCL1 status and minimal residual disease (MRD) were assayed centrally at Covance Laboratories using multicolor flow cytometry. Mutation (mut) sequencing was performed by Foundation Medicine using FoundationOne Heme at screening and from last bone marrow collected on study. Results As of April 6 2018, 34 pts received Ven+idasa across all dose cohorts (Table 1). Median age: 74 (range 64-93) yrs; median prior therapies: 1 (range 1-4); ECOG performance status 2: 18%; refractory: 56%; secondary AML: 53%; adverse cytogenetics: 27%. Pre-therapy mut data were available for 32 pts; most common muts were RUNX1 14 (41%), ASXL1 11 (32%), SRSF2 11 (32%). Other significant pre-therapy muts: TP53 6 (18%), IDH2 7 (21%), IDH1 1 (3%), FLT3 4 (13%). The most common adverse events (AEs) were diarrhea (88%) and nausea (71%); the most common grade (Gr) ≥3 AEs were neutropenia (32%), febrile neutropenia (32%), thrombocytopenia (29%; Table 2). After 2 cases of Gr 3 diarrhea in the Ven 600mg cohorts, mandatory prophylaxis was implemented; no further cases of Gr ≥3 diarrhea were seen in the following 10 pts. Laboratory tumor lysis syndrome occurred in 3 pts (9%); none required treatment discontinuation. There was no apparent PK drug-drug interaction between Ven and idasa. PK was dose-proportional over the ranges tested for Ven and idasa. The recommended Phase II dose (RP2D) has not been identified yet. Across all dose cohorts, 30/34 pts were response-evaluable; the remaining 4 were still on study treatment without post-baseline response assessment. The anti-leukemic response rate (CR+CRp+CRi+MLFS+PR) was 37% (11/30). Across the 2 Ven 600mg cohorts, which are being considered for RP2D, the anti-leukemic response rate was 9/18 (50%) (Table 1, Figure 1). MRD negativity (<0.1%) was achieved in 43% (3/7) of pts with CR+CRp+CRi (Table 3). The median time to CR+CRp+CRi+PR (all pts) was 1.8 mo (range 0.8-2.7), with median response duration of 8.1 mo (range 0.3-9.7). Median overall survival in all pts and in the Ven 600mg cohorts was 3.9 mo and 5.3 mo (range 0.2-17.6), respectively; median follow-up was 2.9 mo (range 0-18). The anti-leukemic response rate was 86% in pts with IDH2 mut and 57% in pts with a RUNX1 mut, but only 20% in pts with a TP53 mut (Table 4). 8/20 pts with end-of-treatment mut data had either new TP53 muts or an increase in mut TP53 allele frequency (Figure 2). In 14 evaluable pts, those with AML blasts with a high ratio of BCL2:BCLxL or BCL2:MCL1 had a response rate of 100% (5/5) versus 11% (1/9) in pts with low ratios (Table 4). Conclusion Ven+idasa has a tolerable safety profile with appropriate prophylaxis in this R/R AML population. An anti-leukemic response rate of 50% was seen at dose levels being considered for RP2D (Ven 600mg + idasa 150/200mg). Overall, responses appeared deep and durable. Preliminary biomarker data indicate that the relative ratio of BCL2 to BCLxL and MCL1 may be important for Ven+idasa activity, whereas pts with baseline TP53 muts had lower response rates. To confirm the clinical benefit and safety of Ven+idasa, the combination will be further evaluated in an expansion arm, after confirmation of the RP2D. Disclosures Daver: Kiromic: Research Funding; ImmunoGen: Consultancy; Sunesis: Research Funding; Pfizer: Research Funding; Novartis: Research Funding; Novartis: Consultancy; Incyte: Research Funding; Daiichi-Sankyo: Research Funding; Sunesis: Consultancy; Karyopharm: Research Funding; Alexion: Consultancy; Pfizer: Consultancy; ARIAD: Research Funding; BMS: Research Funding; Otsuka: Consultancy; Incyte: Consultancy; Karyopharm: Consultancy. Pollyea:Karyopharm: Membership on an entity's Board of Directors or advisory committees; Curis: Membership on an entity's Board of Directors or advisory committees; Argenx: Consultancy, Membership on an entity's Board of Directors or advisory committees; Agios: Consultancy, Membership on an entity's Board of Directors or advisory committees, Research Funding; Celgene: Membership on an entity's Board of Directors or advisory committees; Pfizer: Consultancy, Membership on an entity's Board of Directors or advisory committees, Research Funding; AbbVie: Consultancy, Research Funding; Gilead: Consultancy; Celyad: Consultancy, Membership on an entity's Board of Directors or advisory committees. Garcia:Celgene: Consultancy. Jonas:Genentech/Roche: Research Funding; AbbVie: Consultancy, Research Funding; Amgen: Consultancy; Glycomimetics: Research Funding; Esanex: Research Funding; Pharmacyclics: Research Funding; Incyte: Research Funding; LP Therapeutics: Research Funding; Tolero: Consultancy; Forma: Research Funding; Celgene: Consultancy, Research Funding; Accelerated Medical Diagnostics: Research Funding; Kalobios: Research Funding; Daiichi Sankyo: Research Funding. Yee:Agensys, Astex, GSK, Onconova, Genentech/Roche: Research Funding; Celgene, Novartis, Otsuka: Membership on an entity's Board of Directors or advisory committees. Fenaux:Otsuka: Honoraria, Research Funding; Roche: Honoraria; Jazz: Honoraria, Research Funding; Janssen: Honoraria, Research Funding; Celgene: Honoraria, Research Funding. Assouline:Roche: Honoraria, Research Funding, Speakers Bureau; Janssen: Honoraria, Membership on an entity's Board of Directors or advisory committees, Research Funding; BMS: Honoraria, Research Funding, Speakers Bureau; Pfizer: Honoraria, Research Funding, Speakers Bureau; Novartis: Research Funding. Olin:Daiichi Sankyo, Astellas, Genentech: Research Funding. Roboz:Cellectis: Research Funding; Janssen Pharmaceuticals: Consultancy; Janssen Pharmaceuticals: Consultancy; Daiichi Sankyo: Consultancy; Roche/Genentech: Consultancy; Novartis: Consultancy; Astex Pharmaceuticals: Consultancy; Bayer: Consultancy; Orsenix: Consultancy; Pfizer: Consultancy; Argenx: Consultancy; Otsuka: Consultancy; Bayer: Consultancy; Aphivena Therapeutics: Consultancy; Roche/Genentech: Consultancy; Celgene Corporation: Consultancy; Jazz Pharmaceuticals: Consultancy; Otsuka: Consultancy; Jazz Pharmaceuticals: Consultancy; AbbVie: Consultancy; Novartis: Consultancy; Sandoz: Consultancy; Argenx: Consultancy; Eisai: Consultancy; Aphivena Therapeutics: Consultancy; Celgene Corporation: Consultancy; Orsenix: Consultancy; AbbVie: Consultancy; Astex Pharmaceuticals: Consultancy; Pfizer: Consultancy; Daiichi Sankyo: Consultancy; Eisai: Consultancy; Celltrion: Consultancy; Cellectis: Research Funding; Celltrion: Consultancy; Sandoz: Consultancy. Kirschbrown:Roche: Other: Ownership interests PLC; Genentech: Employment. Green:Genentech: Employment. Ma:Genentech: Employment. Dail:Genentech: Employment, Equity Ownership. Wang:Genentech Inc: Employment; F. Hoffmann-La Roche Ltd: Equity Ownership. Ott:Roche: Other: Ownership interests PLC. Mobasher:Genentech Inc: Employment; F. Hoffmann-La Roche Ltd: Other: Ownership interests non-PLC. Phuong:Genentech Inc: Employment, Equity Ownership, Other: Ownership interests PLC. Hong:Genentech Inc/Roche: Employment, Other: Ownership interests PLC. Konopleva:Stemline Therapeutics: Research Funding. Andreeff:Aptose: Equity Ownership, Membership on an entity's Board of Directors or advisory committees; Oncoceutics: Equity Ownership, Membership on an entity's Board of Directors or advisory committees; Celgene: Consultancy; Eutropics: Equity Ownership, Membership on an entity's Board of Directors or advisory committees; Oncolyze: Equity Ownership; United Therapeutics: Patents & Royalties: GD2 inhibition in breast cancer ; SentiBio: Equity Ownership; Daiichi-Sankyo: Consultancy, Patents & Royalties: MDM2 inhibitor activity patent, Research Funding; Astra Zeneca: Research Funding; Reata: Equity Ownership; Amgen: Consultancy, Research Funding; Jazz Pharma: Consultancy.

Introduction: Patients (pts) with higher-risk myelodysplastic syndrome (HR-MDS) and those who fail to respond to or relapse/progress after treatment with hypomethylating agents (HMA) have limited therapeutic options and poor prognosis. PD-L1 expression is upregulated in HR-MDS pts (compared with lower-risk MDS pts) and in those who fail HMA therapy. Combining inhibition of the PD-L1/PD-1 pathway with azacitidine may improve outcomes in MDS. Methods: We conducted a Phase Ib trial of the anti-PD-L1 monoclonal antibody atezolizumab, with or without azacitidine, in HMA-failure and HMA-naive MDS pts (NCT02508870). The primary objective was to determine the safety and tolerability of atezolizumab as a single agent or in combination with azacitidine. An initial safety evaluation was performed in three cohorts. Cohort A1 (10 pts) consisted of HMA-failure HR-MDS pts treated with atezolizumab alone (1200mg IV q3w). Cohort B1 (11 pts) consisted of HMA-failure HR-MDS pts treated with atezolizumab (840mg IV q2w) in combination with azacitidine (75mg/m2 qd for 7 days q4w) for 6 cycles, followed by atezolizumab maintenance alone (1200mg IV q3w). Cohort C1 (6 pts) consisted of HMA-naive HR-MDS pts treated with atezolizumab (840mg IV q2w) in combination with azacitidine (75mg/m2 qd for 7 days q4w). If atezolizumab alone or in combination with azacitidine was deemed safe and tolerable in Cohorts A1 and B1, an additional 1:1 randomization into two cohorts of 30 pts each (Cohorts A2 and B2) was planned. If the combination of atezolizumab and azacitidine was found to be safe and tolerable in Cohort C1, an additional expansion cohort (Cohort C2) of 14 pts with HMA-naive HR-MDS was planned. Primary endpoints included determining the safety and tolerability of atezolizumab-based regimens in HR-MDS and defining the recommended Phase II dose for the combination. Results: As of January 2018, 42 HR-MDS pts had been treated with atezolizumab-based regimens: Cohort A, 10 pts; Cohort B, 11 pts; Cohort C, 21 pts. Median age for the entire pt cohort was 76 years (range: 63−89). Median treatment duration for Cohorts A, B, and C was 4.2, 5.5, and 5.8 months, respectively. The overall response rate for Cohorts A, B, and C was 0%, 9% (hematologic improvement [HI]: 9%), and 62% (CR, 14%; mCR, 19%; mCR + HI, 10%; HI, 19%), respectively. All pts in Cohorts A and B have discontinued therapy, with a median overall survival (OS) of 5.9 months and 10.7 months, respectively. For pts in Cohort C, 8/21 pts remain on therapy, and median OS has not been reached. Grade 3−5 adverse events (AEs) in >10% of pts were primarily hematologic; grade 3−5 febrile neutropenia occurred in 29% of all pts and was particularly common in pts receiving the atezolizumab-azacitidine combination (Cohorts B [36%] and C [33%] compared with Cohort A [10%]; Table 1). In Cohort A, 70% (7/10) of pts died, as did 64% (7/11) of pts in Cohort B and 29% (6/21) of pts in Cohort C. Median time to death was 160 days (Cohort A), 299 days (Cohort B), and 53 days (Cohort C). Timing and causes of death were different in the three cohorts. Causes of death were more commonly from disease progression in Cohorts A and B, while serious AEs accounted for all deaths in Cohort C (Table 2). In addition, deaths within 3 months occurred in 10%, 18%, and 29% of pts in Cohorts A, B, and C, respectively. The high early death rate compared with historical controls observed in HMA-naive HR-MDS patients (Cohort C) led to early termination of the study prior to completing recruitment. Biomarker assessment demonstrated PD-L1 expression on variable proportions of AML blasts in samples from all pts analyzed. However, PD-L1 expression was not associated with clinical response (Figure). Conclusions: Combination of atezolizumab plus azacitidine in HMA-naive HR-MDS pts had an unfavorable safety profile, which led to early termination. Limited responses were observed with atezo-based regimens (with or without azacitidine) in HMA-failure HR-MDS pts, without excessive or unexpected toxicity. Better understanding of the reasons associated with the differential toxicity profile observed between HMA-naive versus HMA-failure HR-MDS pts will be crucial for potential future developments of this combination. Disclosures Gerds: Incyte: Consultancy; Celgene: Consultancy; CTI Biopharma: Consultancy; Apexx Oncology: Consultancy. Khaled:Daiichi: Consultancy; Alexion: Consultancy, Speakers Bureau; Juno: Other: Travel Funding. Lin:Jazz Pharmaceuticals: Honoraria. Pollyea:AbbVie: Consultancy, Research Funding; Karyopharm: Membership on an entity's Board of Directors or advisory committees; Curis: Membership on an entity's Board of Directors or advisory committees; Gilead: Consultancy; Agios: Consultancy, Membership on an entity's Board of Directors or advisory committees, Research Funding; Argenx: Consultancy, Membership on an entity's Board of Directors or advisory committees; Celgene: Membership on an entity's Board of Directors or advisory committees; Pfizer: Consultancy, Membership on an entity's Board of Directors or advisory committees, Research Funding; Celyad: Consultancy, Membership on an entity's Board of Directors or advisory committees. Dail:Genentech: Employment, Equity Ownership. Green:Genentech: Employment. Ma:Genentech: Employment. Medeiros:Genentech: Employment, Equity Ownership. Phuong:Genentech Inc: Employment, Equity Ownership, Other: Ownership interests PLC. Wenger:F. Hoffmann-La Roche Ltd: Employment, Equity Ownership, Other: Ownership interests PLC. Yan:Roche: Employment.

Introduction:Programmed death-ligand 1 (PD-L1) contributes to tumor escape from immune surveillance by binding to programmed death-1 (PD-1), a negative regulator of T-cell responses. PD-L1 is expressed by both tumor cells and immune cells in the tumor microenvironment. In contrast, the role of PD-L2 in tumor immunity is unclear. To better understand the contribution of PD-L1/L2 to immune escape in marrow-based hematologic malignancies, we used multi-color flow cytometry and immunohistochemistry (IHC) to characterize cell-specific PD-L1/PD-L2 expression in patients with multiple myeloma (MM), myelodysplastic syndrome (MDS) and acute myelogenous leukemia (AML). Results:PD-L1 was detectable (> 2% positive cells) in 100% of patients, with distinct disease-specific patterns. PD-L1 was expressed most widely in MM, predominantly by malignant plasma cells (median, 95% of plasma cells; n = 5) and lymphocytes (median, 12% of marrow lymphocytes; n = 5). In contrast, in MDS and AML, PD-L1 was more commonly expressed by non-tumor hematopoietic cells: MDS median, 36% of CD34− myeloid precursors and 47% of lymphocytes (n = 13) vs 12% of CD34+ myeloid blasts; AML median, 19% of CD34− myeloid precursors and 26% of lymphocytes (n = 7) vs 16% of CD34+ myeloid blasts were PD-L1+. A higher proportion of CD8+ T cells expressed PD-L1 compared with CD4+ T cells in all 3 malignancies: the CD8:CD4 ratio for PD-L1+ T cells was 3.02 in MM (n = 11), 1.92 in MDS (n = 10), and 1.29 in AML (n = 7). PD-L2 expression was largely absent in AML and MDS (< 2% of CD34+ blasts or lymphocytes expressed PD-L2 (n = 13 MDS and n = 7 AML) but was expressed in a subset of patients with MM on plasma cells (median, 18%; n = 5) but not lymphocytes (< 2%). Across all indications on both tumor cells and lymphocytes, PD-L1 was expressed by a larger fraction of cells than PD-L2 (AML: CD34+ blasts, P < .01 and lymphocytes, P = .005 [n = 7]; MDS: CD34+ blasts, P < .01 and lymphocytes, P = .0001 [n = 13]; MM: plasma cells, P = .03 and lymphocytes, P = .04 [n = 5]). These results were confirmed in a distinct set of 16 cases of primary AML analyzed independently, with detectable PD-L1 expression on myeloid blasts in 14 of 16 cases (88%) without co-expression of PD-L2 (0 of 16 cases). Comparisons of flow cytometry and IHC revealed that some IHC methods may underestimate the prevalence of PD-L1/PD-L2 in marrow-based hematologic malignancies, and results comparing different methods for detecting PD-L1/PD-L2 in the bone marrow will be presented. Conclusions:PD-L1 is highly prevalent in MM, MDS and AML, with significant expression by non-tumor hematopoietic cells, particularly CD8+ T cells. PD-L2 expression was largely absent in myeloid diseases but detectable in MM. Interestingly, PD-L1 expression was most common on tumor cells in MM and on non-tumor hematopoietic cells in MDS, whereas expression on non-tumor and tumor cells in AML was comparable. These data support clinical development of anti-PD-L1/PD-1 therapies in MM, MDS and AML. Future analyses will determine whether different patterns of PD-L1 expression are associated with clinical efficacy. Authors M Dail, L Yang, S Rodig, and J Venstrom contributed equally to this work. Disclosures Dail: Genentech, Inc.: Employment. Green:Genentech, Inc.: Employment. Ma:Genentech, Inc.: Employment. Robert:Genentech, Inc.: Employment. Kadel:Genentech, Inc.: Employment. Koeppen:Roche: Employment, Equity Ownership. Adamkewicz:Genentech, Inc.: Employment. Byon:Genentech, Inc.: Employment. Woodard:Genentech, Inc.: Employment. Rodig:Bristol-Myers Squibb: Honoraria, Research Funding; Perkin Elmer: Membership on an entity's Board of Directors or advisory committees. Venstrom:Genentech: Employment.

he nose is the keystone and first fixation point on looking at the face. 1 Its delicate scroll-like curves and creases vary with shadows and light, and the skin covering the nose transitions from thin and pliable on the proximal two-thirds to thick and sebaceous on the distal third. 2 Functionally, it serves as a conduit to breathe and smell, is intimately involved with taste, and acts as a barrier for large airborne particles and dust. Its prominence as the facial centerpiece makes it highly susceptible to sun damage, making it the most common site of head and neck skin cancers. 3 Skin cancers found in the H-zone are traditionally treated with Mohs excision and repaired by a reconstructive surgeon. 4 The nose provides a unique challenge for the reconstructive surgeon, as defects can consist of missing skin, cartilaginous framework, and/or mucosal lining

The mechanisms regulating the homeostasis of HSCs remain poorly understood. Here, Kim et al. identify the Rb/E2f module as a central molecular hub in the regulation of cell cycle and homeostasis in HSCs. This mechanism drives the enforced differentiation of proliferative HSCs to avoid their unnecessary accumulation.

Introduction:TIGIT (T-cell immunoglobulin and immunoreceptor tyrosine-based inhibitory motif [ITIM] domain) is an inhibitory immunoreceptor expressed by T and natural killer (NK) cells that is an important regulator of anti-tumor and anti-viral immunity. TIGIT shares its high-affinity ligand PVR (CD155) with the activating receptor CD226 (DNAM-1). We have recently shown that TIGIT blockade, together with PD-L1/PD-1 blockade, provides robust efficacy in syngeneic tumor and chronic viral infection models. Importantly, CD226 blockade abrogates the benefit of TIGIT blockade, suggesting additional benefit of TIGIT blockade through elaboration of CD226-mediated anti-tumor immunity, analogous to CTLA-4/CD28 regulation of T-cell immunity. Whether TIGIT and CD226 are expressed in patients with multiple myeloma (MM) and how TIGIT expression relates to PD-L1/PD-1 expression is unknown. Here we evaluate expression of TIGIT, CD226, PD-1 and PD-L1 in patients with MM to inform novel immunotherapy combinations. Methods:We performed multi-color flow cytometry (n = 25 patients), and multiplex qRT-PCR (n = 7) on bone marrow specimens from patients with MM to assess expression of TIGIT, CD226, PD-1, and PD-L1 on tumor and immune cells. Cells were stained with fluorescently conjugated monoclonal antibodies to label T cells (CD3, CD4, CD8), NK cells (CD56, CD3), plasma cells (CD38, CD45, CD319, CD56), inhibitory/activating receptors (PD-1, TIGIT, PD-L1, CD226), and an amine-reactive viability dye (7-AAD). Stained and fixed cells were analyzed by flow cytometry using BD FACSCanto™ and BD LSRFortessa™. Results:TIGIT, CD226 and PD-L1/PD-1 were detectable by flow cytometry in all patients with MM who were tested, with some overlapping and distinct expression patterns. TIGIT was commonly expressed by marrow-infiltrating CD8+ T cells (median, 65% of cells), CD4+ T cells (median, 12%) and NK cells. In contrast, CD226 was more commonly expressed by marrow-infiltrating CD4+ T cells (median, 74%) compared with CD8+ T cells (median, 38%). PD-1 was expressed by marrow-infiltrating CD8+ T cells (median 38%) and CD4+ T cells (median, 16%). TIGIT was co-expressed with PD-1 on CD8+ T cells (67%-97% TIGIT+ among PD-1+), although many PD-1-negative CD8+ T cells also expressed TIGIT (39%-78% of PD-1-negative). PD-L1 was also expressed by CD8+ (median, 23%) and CD4+ (median, 8%) T cells in addition to MM plasma cells (median, 95%), albeit with significantly lower intensity on T cells compared with plasma cells. The expression of TIGIT and PD-L1 mRNA was highly correlated (R2 = 0.80). Analysis of PVR expression will also be presented. Conclusions: TIGIT, CD226, PD-1, and PD-L1 were commonly expressed in MM bone marrow, but with different patterns. Among CD8+ T cells, the frequency of TIGIT+ T cells was almost twice that of PD-1+ T cells, whereas the majority of CD4+ T cells expressed CD226. TIGIT blockade may complement anti-PD-L1/PD-1 immunotherapy by activating distinct T-cell/NK-cell subsets with synergistic clinical benefit. These results provide new insight into the immune microenvironment of MM and rationale for targeting both the PD-L1/PD-1 interaction and TIGIT in MM. Disclosures Yadav: Genentech, Inc.: Employment. Green:Genentech, Inc.: Employment. Ma:Genentech, Inc.: Employment. Robert:Genentech, Inc.: Employment. Glibicky:Makro Technologies Inc.: Employment; Genentech, Inc.: Consultancy. Nakamura:Genentech, Inc.: Employment. Sumiyoshi:Genentech, Inc.: Employment. Meng:Genentech, Inc.: Employment, Equity Ownership. Chu:Genentech Inc.: Employment. Wu:Genentech: Employment. Byon:Genentech, Inc.: Employment. Woodard:Genentech, Inc.: Employment. Adamkewicz:Genentech, Inc.: Employment. Grogan:Genentech, Inc.: Employment. Venstrom:Roche-Genentech: Employment.

Background Feeding and eating disorders present with a variety of medical complications, some of which may be life-threatening. Emergency Medicine (EM) physicians may interact with patients with eating disorders, however, EM physicians’ knowledge and perceptions of resources for treating patients with eating disorders have not been examined. The purpose of this study was to explore previous training/education, perceptions of available resources, and educational needs in treating eating disorders in practicing EM physicians. Methods An investigator-developed survey was used in this cross-sectional pilot study, distributed to EM Residency Program Coordinators in the United States to distribute to EM physicians and residents. The survey assessed EM physicians’ previous training and education in treating and diagnosing eating disorders. The primary outcomes assessed were participants’ previous training/education in eating disorders, knowledge of local resources for patients, and educational needs on a variety of topics related to adult and adolescent eating disorders. Data were described descriptively and SAS 9.4 was used to analyze data. Results Of the 162 participants, just 1.9% completed a rotation on eating disorders during residency. Ninety-three percent were unfamiliar with the American Psychiatric Association’s Practice Guideline for the Treatment of Patients with Eating Disorders; 95% were unfamiliar with the publication, “Emergency Department management of patients with eating disorders” by Trent et al. The majority were not aware of resources for patients with eating disorders including community and online support groups, the National Eating Disorders Association, and local treatment programs. At least 50% agreed additional education on 15 of the 19 topics examined would be useful; 85% agreed to wanting education on the assessment of patients with eating disorders in the Emergency Department. Conclusions Most EM physicians lack training in eating disorders and knowledge of resources available for patients post-Emergency Department discharge. EM physicians agree additional education on a number of topics would be beneficial, particularly assessment of eating disorders in the Emergency Department, medical complications of eating disorders, and hospital admission criteria for those with eating disorders.