tbuckley/cabot-search huggingface dataset:
Oncolytic VSV Primes Differential Responses to Immuno-oncology Therapy
Authors: Nicholas M. Durham, Kathy Mulgrew, Kelly McGlinchey, Noel R. Monks, Hong Ji, Ronald Herbst, JoAnn Suzich, Scott A. Hammond, Elizabeth J. Kelly
Journal: Molecular Therapy (2017)

Vesicular stomatitis virus encoding the IFNβ transgene (VSV-IFNβ) is a mediator of potent oncolytic activity and is undergoing clinical evaluation for the treatment of solid tumors. Emerging preclinical and clinical data suggest treatment of tumors with oncolytic viruses may sensitize tumors to checkpoint inhibitors and increase the anti-tumor immune response. New generations of immuno-oncology molecules including T cell agonists are entering clinical development and could be hypothesized to enhance the activity of oncolytic viruses, including VSV-IFNβ. Here, we show that VSV-IFNβ exhibits multiple mechanisms of action, including direct cell killing, stimulation of an innate immune response, recruitment of CD8 T cells, and depletion of T regulatory cells. Moreover, VSV-IFNβ promotes the establishment of a CD8 T cell response to endogenous tumor antigens. Our data demonstrate a significant enhancement of anti-tumor function for VSV-IFNβ when combined with checkpoint inhibitors, but not OX40 agonists. While the addition of checkpoint inhibitors to VSV-IFNβ generated robust tumor growth inhibition, it resulted in no increase in viral replication, transgene expression, or immunophenotypic changes beyond treatment with VSV-IFNβ alone. We hypothesize that tumor-specific T cells generated by VSV-IFNβ retain activity due to a lack of immune exhaustion when checkpoint inhibitors were used.
PERK induces resistance to cell death elicited by endoplasmic reticulum stress and chemotherapy
Authors: Iris C. Salaroglio, Elisa Panada, Enrico Moiso, Ilaria Buondonno, Paolo Provero, Menachem Rubinstein, Joanna Kopecka, Chiara Riganti
Journal: Molecular Cancer (2017)

Nutrient deprivation, hypoxia, radiotherapy and chemotherapy induce endoplasmic reticulum (ER) stress, which activates the so-called unfolded protein response (UPR). Extensive and acute ER stress directs the UPR towards activation of death-triggering pathways. Cancer cells are selected to resist mild and prolonged ER stress by activating pro-survival UPR. We recently found that drug-resistant tumor cells are simultaneously resistant to ER stress-triggered cell death. It is not known if cancer cells adapted to ER stressing conditions acquire a chemoresistant phenotype.To investigate this issue, we generated human cancer cells clones with acquired resistance to ER stress from ER stress-sensitive and chemosensitive cells.ER stress-resistant cells were cross-resistant to multiple chemotherapeutic drugs: such multidrug resistance (MDR) was due to the overexpression of the plasma-membrane transporter MDR related protein 1 (MRP1). Gene profiling analysis unveiled that cells with acquired resistance to ER stress and chemotherapy share higher expression of the UPR sensor protein kinase RNA-like endoplasmic reticulum kinase (PERK), which mediated the erythroid-derived 2-like 2 (Nrf2)-driven transcription of MRP1. Disrupting PERK/Nrf2 axis reversed at the same time resistance to ER stress and chemotherapy. The inducible silencing of PERK reduced tumor growth and restored chemosensitivity in resistant tumor xenografts.Our work demonstrates for the first time that the adaptation to ER stress in cancer cells produces a MDR phenotype. The PERK/Nrf2/MRP1 axis is responsible for the resistance to ER stress and chemotherapy, and may represent a good therapeutic target in aggressive and resistant tumors.
Leukotriene B <sub>4</sub> antagonism ameliorates experimental lymphedema
Authors: Wen Tian, Stanley G. Rockson, Xinguo Jiang, Jeanna Kim, Adrian Begaye, Eric M. Shuffle, Allen B. Tu, Matthew Cribb, Zhanna Nepiyushchikh, Abdullah H. Feroze, Roham T. Zamanian, Gundeep S. Dhillon, Norbert F. Voelkel, Marc Peters-Golden, Jan Kitajewski, J. Brandon Dixon, Mark R. Nicolls
Journal: Science Translational Medicine (2017)

Lymphedema is a common debilitating condition with very limited treatment options, and leukotriene B 4 may be a key pathogenic molecule and therapeutic target.
Abstract A28: Oxygen-dependent translatome remodeling is controlled by eIF2α dephosphorylation
Authors: J.J. David Ho, Nathan C. Balukoff, Grissel Cervantes, Ayalivis De La Rosa, Stephen Lee
Journal: Cancer Research (2017)

Abstract Introduction: Eukaryotic translation initiation factor 2α (eIF2α) is a core component of the cellular translation machinery. Alterations in eIF2α phosphorylation constitute a key adaptation during a variety of physiological stresses, including oxygen deprivation (hypoxia). We recently found that cancer cells respond to hypoxia through the systemic reprogramming of cap-dependent mRNA translation efficiencies by switching to the hypoxic eIF4F, eIF4FH. In the present study, we sought to elucidate the role(s) of eIF2α phosphorylation and dephosphorylation in this translatome remodeling process. In particular, the growth arrest and DNA damage-inducible protein GADD34 has been reported as an adaptive, stress-activated mediator of eIF2α dephosphorylation. We aimed to determine the role of GADD34 in the cellular hypoxic response. Findings: Our results indicate that hypoxia-induced eIF2α phosphorylation is a transient response with corresponding effects on translation efficiencies. Using next-generation mRNA sequencing (mRNA-seq), we reveal the dynamic profile of the translatome remodeling process during acute and chronic hypoxia. Our findings demonstrate that GADD34-mediated eIF2α dephosphorylation is required for hypoxic protein synthesis. GADD34 silencing results in high levels of eIF2α phosphorylation and severe global translational inhibition. Notably, GADD34 regulates the translation of hypoxia-inducible proteins in a hypoxia-inducible factor 2α (HIF-2α)-dependent manner. Finally, high throughput mass spectrometry (MS) analysis reveals several potential hypoxia-regulated GADD34 post-translational modifications (PTMs). Efforts are underway to validate and determine the effect(s) of these PTMs on GADD34 protein stability and/or activity. Conclusion: We demonstrate that GADD34-mediated eIF2α dephosphorylation regulates oxygen-dependent translatome reprogramming in cancer cells. This pathway represents an exciting potential target for cancer therapeutics. Citation Format: J.J. David Ho, Nathan C. Balukoff, Grissel Cervantes, Ayalivis De La Rosa, Stephen Lee. Oxygen-dependent translatome remodeling is controlled by eIF2α dephosphorylation. [abstract]. In: Proceedings of the AACR Special Conference on Translational Control of Cancer: A New Frontier in Cancer Biology and Therapy; 2016 Oct 27-30; San Francisco, CA. Philadelphia (PA): AACR; Cancer Res 2017;77(6 Suppl):Abstract nr A28.
Real-world use of elbasvir/grazoprevir and outcomes in patients with chronic hepatitis C: retrospective data analyses from the TRIO Network
Authors: B. Bacon, M. Curry, D. Dieterich, S. Flamm, K. Kowdley, S. Milligan, C. Nwankwo, N. Tsai, Z. Younossi, N. Afdhal
Journal: Journal of Hepatology (2017)
Immune Reconstitution after Umbilical Cord Blood Versus Peripheral Blood Progenitor Cell Transplantation in Adults Following Myeloablative Conditioning
Authors: Rohtesh S. Mehta, Nelli Bejanyan, Qing Cao, Xianghua Luo, Claudio Brunstein, Sarah Cooley, Bruce R. Blazar, Daniel J. Weisdorf, John E. Wagner, Jeffrey S. Miller, Michael R. Verneris
Journal: Blood (2016)
Ap-1 Family Members C-Jun, JunB and Fra-2 Mediate Apoptosis and Differentiation in AML through Activation of GADD45á and ADFP Following Non-Steroidal Anti-Inflammatory Drug Treatment.
Authors: Akos Czibere, Raminder Singh, Ingmar Bruns, Luiz Fernando Zerbini, Rainer Haas
Journal: Blood (2008)
Mining for osteogenic surface topographies: In silico design to in vivo osseo-integration
Authors: Frits F.B. Hulshof, Bernke Papenburg, Aliaksei Vasilevich, Marc Hulsman, Yiping Zhao, Marloes Levers, Natalie Fekete, Meint de Boer, Huipin Yuan, Shantanu Singh, Nick Beijer, Mark-Anthony Bray, David J. Logan, Marcel Reinders, Anne E. Carpenter, Clemens van Blitterswijk, Dimitrios Stamatialis, Jan de Boer
Journal: Biomaterials (2017)
“Can health status questionnaires be used as a measure of physical activity in COPD patients?” Heleen Demeyer, Ivan Dueñas-Espín, Corina De Jong, Zafeiris Louvaris, Miek Hornikx, Elena Gimeno-Santos, Matthias Loeckx, Ioannis Vogiatzis, Wim Janssens, Nicholas S. Hopkinson, Roberto A. Rabinovich, Niklas Karlsson, Judith Garcia-Aymerich and Thierry Troosters, on behalf of the PROactive consortium.<i>Eur Respir J</i>2016; 47: 1565–1568.
Authors: Heleen Demeyer, Ivan Dueñas-Espín, Corina De Jong, Zafeiris Louvaris, Miek Hornikx, Elena Gimeno-Santos, Matthias Loeckx, Ioannis Vogiatzis, Wim Janssens, Nicholas Hopkinson, Roberto Rabinovich, Niklas Karlsson
Journal: European Respiratory Journal (2017)

This article from the March 2015 issue of the European Respiratory Journal was published with an error in the author list. The third author, Corina De Jong, was incorrectly listed as Corina De Jongh. The article has been corrected and republished online.
Annexin A1 supplementation prevents the progression to fibrosis of nonalcoholic steatoepatitis (NASH)
Authors: S. Bruzzì, S. Sutti, A. Toscani, C. Bozzola, C. Reutelingsperger, D. Kusters, S. Mcarthur, M. Perretti, E. Albano
Journal: Journal of Hepatology (2017)
Methylation signatures in blood show accelerated epigenetic aging in patients with non-alcoholic steatohepatitis compared to healthy controls
Authors: R. Loomba, Y. Gindin, Z. Jiang, E. Lawitz, C.S. Djedjos, S. Caldwell, R. Xu, D. Gong, R.P. Myers, G.M. Subramanian, Z. Goodman, M. Charlton, N.H. Afdhal, A.M. Diehl
Journal: Journal of Hepatology (2017)
Effect of Family History, Body-Fat Distribution, and Reproductive Factors on the Risk of Postmenopausal Breast Cancer
Authors: Thomas A. Sellers, Lawrence H. Kushi, John D. Potter, Susan A. Kaye, Christine L. Nelson, Paul G. McGovern, Aaron R. Folsom
Journal: New England Journal of Medicine (1992)

A family history of breast cancer reflects shared cultural factors, genetic predisposition, or both. There is evidence that the estimated risk associated with a family history of breast cancer increases multiplicatively in combination with other risk factors. We examined the combined effect of family history and anthropometric and reproductive factors on the risk of breast cancer in postmenopausal women.Using data from a prospective cohort study, we studied 37,105 women 55 to 69 years of age to determine whether known risk factors for breast cancer are modified by a reported family history at the time of entry into the study.During the first 4 years of follow-up, 493 new breast cancers were diagnosed. The association of the waist-to-hip ratio (the circumference of the waist divided by that of the hips) with the risk of breast cancer was limited predominantly to women with a family history of breast cancer; the age-adjusted relative risk of breast cancer for the women above the fourth quintile for waist-to-hip ratio as compared with those below the first quintile was 3.2 in women with a family history of breast cancer and 1.2 for women without such a family history. An interaction was observed between a family history of breast cancer and the number of live-born children; the protective effect of higher parity was observed primarily among women with a family history of breast cancer. Similarly, the age-adjusted relative risk of breast cancer associated with a late age at first pregnancy (i.e., greater than or equal to 30 years) was 5.8 for women with a family history of breast cancer and 2.0 for women without such a family history.The increase in the risk of breast cancer associated with a high waist-to-hip ratio, low parity, or greater age at first pregnancy is more pronounced among women with a family history of breast cancer. These findings suggest etiologic differences between familial breast cancer and the sporadic form.
Ribavirin free versus Ribavirin containing therapy with all second generation direct acting antivirals for the treatment of hepatitis C virus genotype 1 infection; a pooled analysis of 4501 patients
Authors: H. Ahmed, A.I. Abushouk, A. Menshawy, A. Attia, A. Negida, S.A. Loutfy
Journal: Journal of Hepatology (2017)
Breast Cancer Working Group of the Cancer Intervention and Surveillance Modeling Network. Effects of mammography screening under different screening schedules: Model estimates of potential benefits and harms (Annals of Internal Medicine (2009) 151, (738-747))
Authors: J. S. Mandelblatt, K. A. Cronin, S. Bailey, Donald Berry, H. J. De Koning, G. Draisma
Journal: Annals of Internal Medicine (2010)
Non-invasive evaluation of clinically significant portal hypertension: validation of two novel algorithms combining liver and spleen stiffness using shear-wave elastography in a large independent cohort of patients with cirrhosis
Authors: L. Elkrief, P.-E. Rautou, M. Ronot, M. Zappa, M.Di. Burgio, O. Roux, J. Bissonnette, A. Payancé, D. Lebrec, C. Francoz, O. Soubrane, D. Valla, F. Durand, V. Vilgrain, L. Castéra
Journal: Journal of Hepatology (2017)
Prognostic Impact of ABCA3 Expression in Pediatric Acute Myeloid Leukemia
Authors: Antony Ceraulo, Aminetou Mint-Mohamed, Delphine Maucort-Boulch, Helene Lapillone, Guy Leverger, Etienne Paubelle, Lea Herpe, Catherine Koering, Christine Ragu, Yves Bertrand, Eric Wattel
Journal: Blood (2016)
Severity of liver disease rather than cirrhotic coagulopathy is associated with bleeding after endoscopic variceal band ligation
Authors: O. Seiz, C. Schramm, S. Groth, E. Vettorazzi, M. Wehmeyer, T. Goeser, T. Rösch, A.W. Lohse, J. Kluwe
Journal: Journal of Hepatology (2017)
Abstract IA27: A kinase inhibitor targeted to mTORC1 drives regression in glioblastoma
Authors: QiWen Fan, Ozlem Aksoy, Robyn Wong, Shirin Ilkhanizadeh, Chris Novotny, William Gustafson, Albert Tuong, Geraldine Cayanan, Erin Simonds, Daphne Haas-Kogan, Joanna Phillips, Theo Nicolaides, Theo Nicolaides, Masanori Okaniwa, Kevan Shokat, William A. Weiss
Journal: Cancer Research (2017)

Abstract San Francisco, San Francisco, CA. Glioblastoma (GBM), the most common primary brain tumor, numbers among the most aggressive of cancers. Although signaling from PI3K and AKT to mTOR is dysregulated prominently, we show here that blockade of these upstream targets affects mTOR activity minimally in glioma. Direct targeting using allosteric inhibitors (rapamycin) blocked mTORC1 incompletely, while we also show here that mTOR active site inhibitors (TORKi) have short residence times, limiting their efficacy preclinically. We therefore tested the third-generation mTOR inhbitior RapaLink-1 a TORKi to the mTORC1-specific binding domain of rapamycin, for activity in GBM. RapaLink-1 interacted with FKBP12, an abundant mTOR interacting protein, enabling accumulation of RapaLink-1 in tumor cells. RapaLink-1 showed better efficacy and durability than rapamycin or a TORKi, potently blocking cancer-derived, activating mutants of mTOR. RapaLink-1 drove regression of intracranial xenografts in-vivo, improving survival compared with earlier-generation inhibitors. Our studies re-establish mTOR as a central target in glioma, trace the failure of existing drugs to incomplete/nondurable inhibition of mTORC1, and offer a new class of mTORC1 inhibitors with improved potency and durability. Citation Format: QiWen Fan, Ozlem Aksoy, Robyn Wong, Shirin Ilkhanizadeh, Chris Novotny, William Gustafson, Albert Tuong, Geraldine Cayanan, Erin Simonds, Daphne Haas-Kogan, Joanna Phillips, Theo Nicolaides, Theo Nicolaides, Masanori Okaniwa, Kevan Shokat, William A. Weiss. A kinase inhibitor targeted to mTORC1 drives regression in glioblastoma. [abstract]. In: Proceedings of the AACR Special Conference on Translational Control of Cancer: A New Frontier in Cancer Biology and Therapy; 2016 Oct 27-30; San Francisco, CA. Philadelphia (PA): AACR; Cancer Res 2017;77(6 Suppl):Abstract nr IA27.
Dynamic risk prediction in Primary Biliary Cholangitis using the UK-PBC cohort
Authors: M. Carbone, A. Nardi, H. Ainsworth, M.A. Heneghan, G.M. Hirschfield, D. Thorburn, A. Bathgate, M. Aldersley, J.M. Neuberger, D. Stocken, H.J. Cordell, G.J. Alexander, R.N. Sandford, D.E. Jones, G.F. Mells
Journal: Journal of Hepatology (2017)
Membrane oxidative damage causes hemolitic anemia during ribavirin therapy for chronic hepatitis C
Authors: L. De Franceschi, F.Turrini Fturrini, C.Brugnara Cbrugnara, A. M. Stanzial, F.Manzato Fmanzato, F.Faccini Ffaccini, F.Noventa Fnoventa, R. Corrocher, G. Fattovich
Journal: Journal of Hepatology (1999)
Cooperating Commensals Restore Colonization Resistance to Vancomycin-Resistant Enterococcus faecium
Authors: Silvia Caballero, Sohn Kim, Rebecca A. Carter, Ingrid M. Leiner, Bože Sušac, Liza Miller, Grace J. Kim, Lilan Ling, Eric G. Pamer
Journal: Cell Host & Microbe (2017)
Higher rates of cirrhosis, decompensation, and hepatocellular carcinoma (HCC) in Asian and Hispanic patients with Hepatitis C (HCV) Infection compared to White and Black ethnicity regardless of gender differences: a single center study in the U.S.
Authors: P. Nguyen, A.K. Le, J. Hoang, L.A. Yasukawa, S.C. Weber, M. Stefanick, G. Garcia, M. Nguyen
Journal: Journal of Hepatology (2017)
Incidence of human cytomegalovirus infection and T-cell response in patients with psoriasis before and during antitumour necrosis factor-α therapy
Authors: L. Fornara, C. Fornara, R. Cananzi, D. Lilleri, M. Furione, V. Brazzelli
Journal: British Journal of Dermatology (2017)

psoriasis is a chronic inflammatory skin disease that affects approximately 2-3% of the world population.1 Among the cytokines produced by T cells, TNF-α has a crucial role in psoriasis.2 Thus, TNF-α blocking therapy is efficient in the treatment of psoriasis.

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A phase 2 dose-escalation study of lonafarnib plus ritonavir in patients with chronic hepatitis D: final results from the Lonafarnib with ritonavir in HDV-4 (LOWR HDV-4) study
Authors: H. Wedemeyer, K. Port, K. Deterding, A. Wranke, J. Kirschner, B. Bruno, B. Martins, J.S. Glenn, M. Kornberg, M.P. Manns
Journal: Journal of Hepatology (2017)
Do insurance status and neighborhood characteristics explain why minorities underutilize NCI cancer centers?
Authors: Lyen C. Huang, Yifei Ma, Justine V Ngo, Kim F Rhoads
Journal: Journal of Clinical Oncology (2012)

6010 Background: National Cancer-Institute (NCI) designated cancer centers provide some of the highest quality cancer care in the US, in part due to the availability of cutting edge technologies and access to cancer clinical trials. Racial/ethnic minorities suffer from persistent disparities in cancer outcomes, and these groups are typically under-represented in clinical trials. This may be due in part to under-utilization of NCI centers by these groups. Methods: A unique dataset linking the California Cancer Registry with California patient discharge abstracts was used to identify patients undergoing resection for a primary diagnosis of colorectal cancer (CRC) (1996-2006). Travel distance to treatment hospital was determined using GIS software. Chi-square analysis correlated patient demographics, clinical characteristics, insurance status, and neighborhood socioeconomics with NCI center use. Multivariable regression models were constructed to predict the likelihood of using an NCI center. Results: 95,994 CRC patients were identified. Median travel distance for care was &lt;5 miles. Only 12,659 (13%) lived within a 5 mile radius of an NCI center; and of those, fewer than 10% used the center for CRC care (n=1130). Black (OR 0.83 95%CI 0.72-0.95) and Hispanic (OR 0.72 95%CI 0.65-0.81) patients were less likely than white patients to use NCI centers. Neighborhood socioeconomics, but not insurance status, were significantly correlated with NCI under-utilization. Asian populations were more likely to use NCI centers than white patients (OR 1.40 95%CI 1.28-1.54). Conclusions: Black and Hispanic patients are less likely to use nearby NCI hospitals for CRC care. Outreach efforts in communities with low socioeconomic status and educational attainment may increase use of NCI centers, improve CRC outcomes, and increase minority enrollment in clinical trials.
Genomic Tumour Profiling with High-Density Oligonucleotide SNP Array in Sézary Syndrome.
Authors: Giandomenico Russo, Maria Grazia Narducci, Mauro Helmer Citterich, Maria Cristina Picchio, Cristina Critofoletti, Valeria Tocco, Enrico Scala, Francesca Sampogna, Marina Frontani, Diego Arcelli, Giuseppe Lombardo, Giannandrea Baliva, Elisabetta Caprini
Journal: Blood (2006)
Baseline and early on-treatment HBsAg level to predict HBsAg loss in nucleotide analog suppressed and HBeAg cleared chronic hepatitis B patients by switching to peginterferon alfa-2a: exploratory results of NEW SWITCH study
Authors: P. Hu, Q. Xie, Y. Li, X. Chen, X. Dou, J. Jiang, J. Shang, W. Zhang, G. Gong, Y. Sun, Y. Li, Y. Liu, G. Liu, D. Mao, X. Chi, H. Tang, X. Li, Y. Xie, X. Chen, J. Jiang, P. Zhao, J. Hou, Z. Gao, H. Fan, J. Ding, H. Ren
Journal: Journal of Hepatology (2017)
Galaxy-2 trial (NCT01798485): A randomized phase 3 study of ganetespib in combination with docetaxel versus docetaxel alone in patients with advanced lung adenocarcinoma.
Authors: Suresh S. Ramalingam, Bojan Zaric, Timur Ceric, Tudor E. Ciuleanu, James F. Spicer, Igor Bondarenko, Dmitry Komov, Enriqueta Felip, Enric Carcereny, Joachim Von Pawel, Miroslav Samarzija, Thierry Pieters, Michael Schenker, Manuel R. Modiano, Rodryg Ramlau, Marianna Koczywas, Florentina Teofilovici, Ilker Yalcin, Vojislav M. Vukovic, Dean Fennell
Journal: Journal of Clinical Oncology (2014)

TPS8118^ Background: Hsp90 is a molecular chaperone recognized as a key facilitator of cancer cell growth and survival. Ganetespib is a resorcinolic Hsp90 inhibitor that has shown single-agent activity in patients with lung, breast, and other cancers after progression on standard treatments. Ganetespib in combination with docetaxel induces synergistic efficacy in human non-small-cell lung carcinoma (NSCLC) tumor xenografts. Ganetespib is well tolerated and has not shown severe liver or common ocular toxicities reported for other Hsp90 inhibitors. Transient diarrhea is the most common adverse event, and is manageable with appropriate supportive care. A large randomized Phase 2 study of ganetespib in combination with docetaxel in advanced NSCLC patients (GALAXY-1 Trial) indicated good tolerability of the combination, and improvement in efficacy, including OS. Methods: GALAXY-2 is a randomized (1:1), international, open-label Phase 3 study enrolling patients who received and progressed on 1 prior systemic platinum-based combination therapy for advanced NSCLC of adenocarcinoma histology, were diagnosed ≥6 months before study entry, and whose tumors are negative for both EGFR mutations and ALK translocation (Target Patient Population [TPP]). Patients (N=700 TPP) are prospectively stratified for ECOG PS, total screening LDH, and geographic region (North America and Western Europe vs Rest of World). The primary endpoint is OS in the TPP. Key secondary endpoints include PFS, ORR, DCR, and DOR in the TPP. OS will also be analyzed in 3 subpopulations of the TPP: mKRAS, elevated LDH, and elevated LDH5. Patients in the control arm are treated with docetaxel 75 mg/m2 on Day 1 of a 3-week cycle. In the combination arm, ganetespib 150 mg/m2 is given on Day 1 with 75 mg/m2 docetaxel, and ganetespib 150 mg/m2 alone is given on Day 15 of each 3-week cycle. Two interim analyses for OS will be performed. Tumor tissue and blood samples will be collected for planned translational studies. Clinical trial information: NCT01798485.