bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 6461: HER2 positive DCIS increases short term risk of ipsilateral invasive ductal carcinoma in breast conserving surgery patients
Authors: O'Keefe Thomas , Blair Sarah , Hosseini Ava , Harismendy Olivier , Wallace Anne 
Published: September 2020

Abstract
Purpose: The impact of HER2 status in ductal carcinoma in situ (DCIS) lesions on the risk of progression to invasive ductal carcinoma (IDC) has been debated with reports of both increased and decreased risk of development of invasive breast cancer in HER2 positive patients. We aim to use a large national database to elucidate the effect of HER2 positivity on ipsilateral IDC (iIDC) development.
Methods: We performed survival analyses on patient-level data using the US National Cancer Institute's Surveillance, Epidemiology, and End Results program to identify patients diagnosed with DCIS who underwent lumpectomy and had known HER2, estrogen and progesterone receptor statuses, grade, comedonecrosis, age, tumor size, and radiation therapy (RT). Competing risks analysis was performed.
Results: 1,540 patients meeting inclusion criteria were identified. Median age at diagnosis was 60 with median follow-up time of 44.5 months. 22 (1.4%) patients developed iIDC and 27 (1.8%) developed ipsilateral in situ or contralateral disease. 1,035 (67.2%) patients were HER2 negative and 417 (27.1%) were HER2 positive. The estimated cumulative incidence of iIDC at 5 years was 1.9% for all patients, 1.2% (95% CI 0.6-2.1%) for HER2 negative patients, and 4.0% (95% CI 2.9-5.4%) for HER2 positive patients. On competing risks regression, two factors were significant for iIDC: RT within 20 months (HR=0.02, p=0.0002) and HER2 positivity (HR=2.81, p=0.046).
Conclusions: HER2 may serve as a prognostic factor for consideration in decision making in patients for whom it is available, and in our analysis was the only lesion-related factor to significantly relate to iIDC development.
Citation Format: Thomas O'Keefe, Sarah Blair, Ava Hosseini, Olivier Harismendy, Anne Wallace. HER2 positive DCIS increases short term risk of ipsilateral invasive ductal carcinoma in breast conserving surgery patients [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 6461.
Abstract 6472: Clonal lineage and somatic hypermutation analysis of chronic lymphocytic leukemia by long-amplicon IGH chain sequencing
Authors: Chang Jayde , Davis Zadie , Quest Graeme , Feilloter Harriet , Toro Michelle , Lowman Geoffrey , Pickle Loni , Hyland Fiona , Looney Timothy 
Published: September 2020

Abstract
Background: Current next-generation sequencing (NGS) approaches for analyzing SHM commonly rely on multiplex primers targeting the framework 1 (FR1) or leader region of the IGH variable gene in combination with joining gene primers to amplify rearranged IGH chains from gDNA template. Limitations include the potential for joining gene mutations to interfere with primer binding and an inability to evaluate isotype. Here we present a method for translational research investigations of IGH chain SHM employing multiplex FR1 and isotype (constant gene) specific primers (Oncomine IGH-LR assay primers) to amplify IGH chains from RNA template. We evaluated performance by comparing SHM values obtained from NGS of RNA from 54 CLL samples amplified using Oncomine IGH-LR primers to values obtained by Sanger sequencing or NGS of RNA amplified using FR1 or leader region/J gene primers.
Methods: IGH chains from 54 CLL samples derived from two separate sequencing sites (Site 1: 24 samples, Site 2: 30 samples) were amplified from peripheral blood using Oncomine IGH-LR assay followed by sequencing via the Ion Gene Studio S5. Clonotyping, clonal lineage identification and somatic hypermutation analysis was performed by Ion Reporter via comparison to the IMGT reference database. Oncomine IGH-LR assay SHM values were compared to those obtained via NGS-based sequencing utilizing FR1/J gene primers (Site 1) or Sanger sequencing utilizing IGH-leader or FR1 and joining gene primers (Site 2).
Results: IGHV SHM values were highly concordant between NGS approaches (Spearman cor =.957, Site 1) and between Sanger sequencing and NGS approaches (Spearman cor = .849, Site 2). Sequence data obtained using Oncomine IGH-LR assay enables more in-depth clonal lineage analysis, including evaluation of isotype representation and subclonal evolution.
Conclusions: These results support the robustness and reliability of multiplex FR1 and constant gene based IGH chain amplification for the translational research characterization of somatic hypermutation in CLL and other B cell neoplasms.
Citation Format: Jayde Chang, Zadie Davis, Graeme Quest, Harriet Feilloter, Michelle Toro, Geoffrey Lowman, Loni Pickle, Fiona Hyland, Timothy Looney. Clonal lineage and somatic hypermutation analysis of chronic lymphocytic leukemia by long-amplicon IGH chain sequencing [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 6472.
Abstract 659: Synergistic antitumor activity of futibatinib (TAS-120), a FGFR1-4 inhibitor, and PI3K pathway inhibitors
Authors: Miura Akihiro , Sootome Hiroshi , Komori Toshiharu , Ochiiwa Hiroaki , Hirai Hiroshi 
Published: September 2020

Abstract
Background: Futibatinib, a selective irreversible small-molecule fibroblast growth factor receptor (FGFR) 1–4 inhibitor is currently being investigated in phase 2 studies in patients with various FGFR-deregulated cancers. FGFRs use the PI3K pathway to promote cell growth and survival, suggesting that a combination of futibatinib with PI3K pathway inhibitors may result in synergistic activity. Therefore, we investigated the antitumor effects of futibatinib plus PI3K pathway inhibitors, everolimus (mTOR inhibitor) or MK2206 (AKT inhibitor).
Methods: Human endometrial FGFR2-N549K-mutated AN3CA cancer cells were treated with futibatinib plus either everolimus or MK2206 or with each agent alone. AKT, ERK, mTOR, and S6 phosphorylation, cell viability, and apoptosis (via caspase-3/7 activity) were assessed. Cell growth inhibition was measured and combination indices (CIs) determined using CalcuSyn software; a CI&lt;0.9 indicates synergy. Antitumor activity of futibatinib plus everolimus in ANC3A xenografts was evaluated by assessing relative tumor volume (RTV).
Results: In ANC3A cells, the combination of futibatinib with MK2206 inhibited AKT phosphorylation; futibatinib plus either MK2206 or everolimus inhibited mTOR phosphorylation to a greater degree than monotherapy. Apoptosis induction by caspase-3/7 was readily detected with futibatinib plus MK2206, but low to no activity was observed with either agent alone. A synergistic effect on cell growth inhibition was observed for futibatinib plus everolimus (CI=0.26) or MK2206 (CI=0.14). In AN3CA xenografts, there was a significant (P&lt;0.05) decrease in RTV with futibatinib plus everolimus vs monotherapy (Table).
Table.Relative tumor volume in AN3CA mouse xenografts treated with futibatinib or everolimus or combination therapyTreatment (mg/kg/d)Relative tumor volumeDay 0Day 3Day 6Day 10Day 15Control14.657.8116.4937.77Futibatinib (15)a13.084.516.8412.59Futibatinib (50)a12.292.703.154.76Everolimus (2)a12.664.046.3410.24Futibatinib + Everolimus (15 + 2)b11.841.921.681.91Futibatinib + Everolimus (50 + 2)b11.501.310.840.72aDays 1–14 (oral);bDays 1–14 + Days 1–14 (both oral).
Conclusions: The combination of futibatinib plus a PI3K pathway inhibitor resulted in synergistic antitumor effects. These data are encouraging and can serve as a basis for investigating the combination of PI3K pathway inhibitors with futibatinib.
Citation Format: Akihiro Miura, Hiroshi Sootome, Toshiharu Komori, Hiroaki Ochiiwa, Hiroshi Hirai. Synergistic antitumor activity of futibatinib (TAS-120), a FGFR1-4 inhibitor, and PI3K pathway inhibitors [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 659.
Abstract 6636: Therapy with BXCL701 (B), a DPP8, DPP9, DPPIV and FAP inhibitor, in combination with anti-PD1 antibody (PD1) in a syngeneic murine pancreatic ductal adenocarcinoma (PDAC) model improves treatment outcomes and induces intratumoral NK cell infiltrates and a marked reduction in tumor stromal fibrosis
Authors: Wang Shangzi , Fitzgerald Allison , Ajina Reham , Jablonsk Sandra A. , Weiner Louis M. , MacDougall John , Agarwal Veena , O'Neill Vince J. 
Published: September 2020

Abstract
PDAC is typically resistant to chemotherapy and immunotherapy; therefore, novel strategies are needed to enhance therapeutic response. BXCL701 is a well-studied inhibitor of dipeptidyl peptidases 4, 8, 9, and Fibroblast Activation Protein, and has been postulated to work through cytokine induction and macrophage pyroptosis. We examined the effects of BXCL701 and/or PD1 therapy in murine models of PDAC. In the mT3-2D PDAC model, combination therapy of established (~75mm3) sc tumors reduced tumor growth to a greater extent (PBS: 1349±230 mm3 on day 42 vs B + PD1: 355±161mm3, p&lt;0.0001) following a 28-day treatment program of PBS, B (1mg/kg by daily oral gavage), PD1 (10mg/kg ip weekly) or the combination of B + PD1. Treatment with either B or PD1 alone had minimal anti-tumor effects. B + PD1 therapy was accompanied by significant tumor infiltration of NK cells by IHC, flow cytometry and Nanostring analysis. A dramatic reduction of tumor stromal fibrosis by Masson's trichrome staining was found in tumors treated with B alone or B + PD1. These findings suggest that the combination of BXCL701 with anti-PD1 antibody therapy can exert anti-tumor effects associated with increased intratumoral NK cell content and the loss of fibrosis that may facilitate immunotherapy efficacy.
Citation Format: Shangzi Wang, Allison Fitzgerald, Reham Ajina, Sandra A. Jablonsk, Louis M. Weiner, John MacDougall, Veena Agarwal, Vince J. O'Neill. Therapy with BXCL701 (B), a DPP8, DPP9, DPPIV and FAP inhibitor, in combination with anti-PD1 antibody (PD1) in a syngeneic murine pancreatic ductal adenocarcinoma (PDAC) model improves treatment outcomes and induces intratumoral NK cell infiltrates and a marked reduction in tumor stromal fibrosis [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 6636.
Abstract 6697: DT095895, a selective EP4 receptor antagonist with monotherapy efficacy in syngeneic mouse model(s) and best-in-class properties
Authors: Blayo Anne-Laure , Deshons Laurène , Dumont Alexia , Franchet Christel , Halter Célia , Herbin Ludovic , Hommet Gaël , Mayer Stanislas , Bessede Alban , Nafia Imane , Sidhoum Marjorie , Leroy Xavier , Schann Stephan 
Published: September 2020

Abstract
Elevated levels of Prostaglandin E2 (PGE2), an eicosanoid notably synthesized by the cyclooxygenase-2 (COX-2), exert strong immunosuppressive effects in the tumor microenvironment. COX-2-positive solid tumors have the ability to use this pathway as a resistance mechanism, especially to escape from the host immune system, thus limiting the anti-tumor effects of immune checkpoint inhibitors (ICI). These immunosuppressive effects are largely mediated by the EP4 receptor, expressed on multiple immune cells. A novel series of EP4 receptor antagonists has been developed, with improved pharmacokinetic properties when compared to the EP4 receptor antagonists currently being evaluated in clinical trials. An intensive lead optimization program led to the identification of DT095895, a small molecule development candidate with a “best-in class” potential. Its preclinical package will be presented in the poster. DT095895 was assessed in multiple syngeneic mouse tumor models selected for their COX-2 expression profile. Efficacy was seen both in a monotherapy setting, as well as in combination with ICI. Additionally, a specific biomarker program was implemented and validated in order to show target engagement. A phospho-flow murine whole blood assay was set up to assess the ability of DT095895 to inhibit CREB phosphorylation induced by a selective EP4 receptor agonist in CD3+ cells. This biomarker was further developed for human whole blood to support Phase 1 and clinical trials studies. In conclusion, DT095895 is a selective EP4 receptor antagonist and demonstrates strong anti-tumor effects in multiple syngeneic mouse tumor models, both as a monotherapy and in combination with ICI, through the inhibition of the PGE2-induced immunosuppression. DT095895 progresses in regulatory development.
Citation Format: Anne-Laure Blayo, Laurène Deshons, Alexia Dumont, Christel Franchet, Célia Halter, Ludovic Herbin, Gaël Hommet, Stanislas Mayer, Alban Bessede, Imane Nafia, Marjorie Sidhoum, Xavier Leroy, Stephan Schann. DT095895, a selective EP4 receptor antagonist with monotherapy efficacy in syngeneic mouse model(s) and best-in-class properties [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 6697.
Abstract CT231: Clinical study of the safety and tolerability of laser interstitial thermal therapy and avelumab for recurrent glioblastoma
Authors: Hormigo Adilia , Mandeli John , Ghatan Saadi , Hadjipanayis Constantinos , Yong Raymond , Kim-Schulze Seunghee , Gnjatic Sacha 
Published: September 2020

Abstract
Background: Glioblastoma (GBM) is a fatal disease with no standard care for disease progression and as other cancers is known to evade the immune system. Avelumab is a human IgG1 antibody that binds PD-L1 and blocks the interaction between PD-L1 and its receptors PD-1 and B7-1. Consequently, the suppressive effect on T cell function is inhibited and anti-tumor CD8+ T cells cytotoxicity is restored.Laser Interstitial Thermal Therapy (LITT) is a minimally invasive technique that allows the delivery of light energy causing disruption of the blood-brain barrier and hyperthermia of a brain lesion, initiating a cascade of events leading to coagulative necrosis and potentially triggering immunogenic death of cancer cells. It is hypothesized that avelumab combined with MRI-guided LITT has acceptable safety, tolerability and will generate robust immunomodulation and clinical activity to treat brain cancer. Methods: This phase 1 study is enrolling adult patients with first recurrence of GBM. The study follows a 3+3 design exploring safety and tolerability in part A, Avelumab alone and part B, Avelumab combined with LITT (NCT03341806). Objective response will be determined by iRANO criteria and secondary objectives include PFS and OS. Avelumab is administered intravenously within a week of LITT and every two weeks thereafter until disease progression or intolerable toxicity. Tissue immune biomarkers, signature of plasma analytes, and circulating cellular signature profiling are assessed. Part A and B completed enrollment with no serious infusion or immune-related adverse events. The study will proceed with an expansion cohort on January 2020. A Simon minimax two-stage design will be used for efficacy. The first stage consists of the 6 subjects evaluable from the safety cohorts in Part 1B together with the first 8 subjects in the expansion cohort (total of 14 subjects).
Citation Format: Adilia Hormigo, John Mandeli, Saadi Ghatan, Constantinos Hadjipanayis, Raymond Yong, Seunghee Kim-Schulze, Sacha Gnjatic. Clinical study of the safety and tolerability of laser interstitial thermal therapy and avelumab for recurrent glioblastoma [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr CT231.
Abstract CT284: Phase 3 KEYNOTE-937: Adjuvant pembrolizumab versus placebo in patients with hepatocellular carcinoma and complete radiologic response after surgical resection or local ablation
Authors: Zhu Andrew , Kudo Masatoshi , Vogel Arndt , Yau Thomas , Zhou Jian , Kim Eunhee , Malhotra Usha , Siegel Abby B. , Cheng Ann-Lii 
Published: September 2020

Abstract
Background: For patients with hepatocellular carcinoma (HCC) who are undergoing potentially curative surgical resection or local ablation, 5-year recurrence rates are up to 50%-80%; there is no standard of care for adjuvant treatment. The programmed death 1 inhibitor pembrolizumab is approved for the treatment of patients with HCC previously treated with sorafenib. There is no direct evidence of benefit with pembrolizumab in the HCC adjuvant setting, but a favorable benefit/risk profile is anticipated based on data from other indications. KEYNOTE-937 (NCT03867084) is a randomized, double-blind, phase 3 trial to examine the safety and efficacy of adjuvant pembrolizumab versus placebo in patients with complete radiologic response after surgical resection or local ablation of HCC. Methods: Eligible patients are aged ≥18 years and have confirmed HCC, complete radiologic response after complete resection or local ablation, Eastern Cooperative Oncology Group performance status of 0, and class A Child-Pugh score. Patients with past or ongoing HCV or controlled HBV are eligible if they meet certain criteria. Patients (N~950) will be randomly assigned 1:1 to receive pembrolizumab 200 mg or placebo every 3 weeks and stratified by geographic region, prior local therapy (resection vs ablation), recurrence risk, and alpha-fetoprotein level at diagnosis. Treatment will continue for up to 17 cycles (~1 year) or until documented disease recurrence, unacceptable toxicity, or investigator/patient decision to withdraw. Dual primary end points are recurrence free survival (RFS) and overall survival. Secondary end points are safety, tolerability, and quality of life. Exploratory end points include distant metastases-free survival (DMFS); time to recurrence (TTR); and genomic, metabolic, and/or proteomic biomarkers. RFS, DMFS, and TTR will be assessed radiographically by the investigator and/or by subsequent biopsy and confirmed by blinded independent central review. Adverse events (AEs), graded per National Cancer Institute Common Terminology Criteria for Adverse Events version 4.0, will be recorded up to 30 days after last dose (90 days for serious AEs).
Citation Format: Andrew Zhu, Masatoshi Kudo, Arndt Vogel, Thomas Yau, Jian Zhou, Eunhee Kim, Usha Malhotra, Abby B. Siegel, Ann-Lii Cheng. Phase 3 KEYNOTE-937: Adjuvant pembrolizumab versus placebo in patients with hepatocellular carcinoma and complete radiologic response after surgical resection or local ablation [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr CT284.
Abstract CT406: Patients with cancer appear more vulnerable to SARS-COV-2: A multi-center study during the COVID-19 outbreak
Authors: Dai Meng-Yuan , Liu Dian-bo , Liu Miao , Zhou Fu-Xiang , Li Gui-Ling , Chen Zhen , Zhang Zhi-An , Md Hua-You , Wu Meng , Zheng Qi-Chao , Xiong Yong , Xiong Hui-Hua , Wang Chun , Chen Chang-Chun , Xiong Fei , Zhang Yan , Peng Ya-Qin , Ge Si-Ping , Zhen Bo , Yu Ting-Ting , Wang Ling , Wang Hua , Liu Yu , Chen Ye-Shan , Mei Jun-Hua , Gao Xiao-Jia , Li Zhu-Yan , Gan Li-Juan , He Can , Li Zhen , Shi Yu-Ying , Qi Yu-Wen , Yang Jing , Tenen Daniel G. , Chai Li , Mucci Lorelei Ann , Santillana Mauricio , Cai Hongbing 
Published: September 2020

Abstract
The novel COVID-19 outbreak has affected more than 200 countries and territories as of March 2020. Given that patients with cancer are generally more vulnerable to infections, systematic analysis of diverse cohorts of patients with cancer affected by COVID-19 are needed. We performed a multi-center study including 105 cancer patients and 536 age-matched non-cancer patients confirmed with COVID-19. Our results showed COVID-19 patients with cancer had higher risks in all severe outcomes. Patients with hematological cancer, lung cancer, or with metastatic cancer (stage IV) had the highest frequency of severe events. Non-metastatic cancer patients experienced similar frequencies of severe conditions to those observed in patients without cancer. Patients who received surgery had higher risks of having severe events, while patients with only radiotherapy did not demonstrate significant differences in severe events when compared to patients without cancer. These findings indicate that cancer patients appear more vulnerable to SARS-COV-2 outbreak. Since this is the first large cohort study on this topic, our report will provide the much-needed information that will benefit global cancer patients. As such, we believe it is extremely important that our study be disseminated widely to alert clinicians and patients.
Citation Format: Meng-Yuan Dai, Dian-bo Liu, Miao Liu, Fu-Xiang Zhou, Gui-Ling Li, Zhen Chen, Zhi-An Zhang, Hua-You Md, Meng Wu, Qi-Chao Zheng, Yong Xiong, Hui-Hua Xiong, Chun Wang, Chang-Chun Chen, Fei Xiong, Yan Zhang, Ya-Qin Peng, Si-Ping Ge, Bo Zhen, Ting-Ting Yu, Ling Wang, Hua Wang, Yu Liu, Ye-Shan Chen, Jun-Hua Mei, Xiao-Jia Gao, Zhu-Yan Li, Li-Juan Gan, Can He, Zhen Li, Yu-Ying Shi, Yu-Wen Qi, Jing Yang, Daniel G. Tenen, Li Chai, Lorelei Ann Mucci, Mauricio Santillana, Hongbing Cai. Patients with cancer appear more vulnerable to SARS-COV-2: A multi-center study during the COVID-19 outbreak [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr CT406.
Abstract LB-080: USP18 modulates the ISGylome, immune signaling and sensitizes tumor cells to irradiation and CTL recognition
Authors: Pinto-Fernandez Adan , Greenwood Helene , Salio Mariolina , Chen Jianzhou , Partridge Thomas , Vere George , Scott Hannah C. , Damianou Andreas , Borrow Persephone , Muschel Ruth , Cerundolo Vincenzo , Kessler Benedikt M. 
Published: September 2020

Abstract
The innate immune response plays a critical role in modulating the efficacy of and mechanisms conferring resistance to immune checkpoint blockade (ICB) therapies in humans. A major negative regulator of the Interferon (IFN) stimulated gene (ISG) pathway, is the ubiquitin-specific protease 18 (USP18). USP18 is the predominant human deubiquitylating enzyme that processes Interferon Stimulated Gene 15 ISG15, a ubiquitin-like protein that covalently modifies protein substrates, a tightly regulated process in the context of innate immunity. In this study, using advanced mass spectrometry and chemical biology tools, we defined the USP18 Interactome and ISG15ylome in chronic myeloid leukemia (CML)-derived cells (HAP1) treated with Interferon alpha (IFNα). Novel ISG15ylation targets were characterized that reduce the sensing of innate ligands and secretion of cytokines. In addition, we show that USP18 deletion leads to enhanced ISG15ylation profiles. Furthermore, we demonstrate that CML USP18-/- cells are more antigenic, leading to increased activation of cytotoxic T lymphocytes (CTLs), and are more susceptible to irradiation. Our results reinforce the role of USP18 as a key “brake” for inflammatory signals in tumor cells. As USP18 expression is upregulated in lung, breast and colon cancers, USP18 pharmacological inhibition may reflect a target opportunity in cancer immunotherapy.
Citation Format: Adan Pinto-Fernandez, Helene Greenwood, Mariolina Salio, Jianzhou Chen, Thomas Partridge, George Vere, Hannah C. Scott, Andreas Damianou, Persephone Borrow, Ruth Muschel, Vincenzo Cerundolo, Benedikt M. Kessler. USP18 modulates the ISGylome, immune signaling and sensitizes tumor cells to irradiation and CTL recognition [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr LB-080.