tbuckley/cabot-search huggingface dataset:
TGF-β Mediates Renal Fibrosis via the Smad3-Erbb4-IR Long Noncoding RNA Axis
Authors: Min Feng, Patrick Ming-Kuen Tang, Xiao-Ru Huang, Si-Fan Sun, Yong-Ke You, Jun Xiao, Lin-Li Lv, An-Ping Xu, Hui-Yao Lan
Journal: Molecular Therapy (2017)

Transforming growth factor β (TGF-β)/Smad3 signaling plays a role in tissue fibrosis. We report here that Erbb4-IR is a novel long non-coding RNA (lncRNA) responsible for TGF-β/Smad3-mediated renal fibrosis and is a specific therapeutic target for chronic kidney disease. Erbb4-IR was induced by TGF-β1 via a Smad3-dependent mechanism and was highly upregulated in the fibrotic kidney of mouse unilateral ureteral obstructive nephropathy (UUO). Silencing Erbb4-IR blocked TGF-β1-induced collagen I and alpha-smooth muscle actin (α-SMA) expressions in vitro and effectively attenuated renal fibrosis in the UUO kidney by blocking TGF-β/Smad3 signaling. Mechanistic studies revealed that Smad7, a downstream negative regulator of TGF-β/Smad signaling, is a target gene of Erbb4-IR because a binding site of Erbb4-IR was found on the 3′ UTR of Smad7 gene. Mutation of this binding site prevented the suppressive effect of Erbb4-IR on the Smad7 reporter activity; in contrast, overexpression of Erbb4-IR largely inhibited Smad7 but increased collagen I and α-SMA transcriptions. Thus, kidney-specific silencing of Erbb4-IR upregulated renal Smad7 and thus blocked TGF-β/Smad3-mediated renal fibrosis in vivo and in vitro. In conclusion, the present study identified that Erbb4-IR is a novel lncRNA responsible for TGF-β/Smad3-mediated renal fibrosis by downregulating Smad7. Targeting Erbb4-IR may represent a precise therapeutic strategy for progressive renal fibrosis. Transforming growth factor β (TGF-β)/Smad3 signaling plays a role in tissue fibrosis. We report here that Erbb4-IR is a novel long non-coding RNA (lncRNA) responsible for TGF-β/Smad3-mediated renal fibrosis and is a specific therapeutic target for chronic kidney disease. Erbb4-IR was induced by TGF-β1 via a Smad3-dependent mechanism and was highly upregulated in the fibrotic kidney of mouse unilateral ureteral obstructive nephropathy (UUO). Silencing Erbb4-IR blocked TGF-β1-induced collagen I and alpha-smooth muscle actin (α-SMA) expressions in vitro and effectively attenuated renal fibrosis in the UUO kidney by blocking TGF-β/Smad3 signaling. Mechanistic studies revealed that Smad7, a downstream negative regulator of TGF-β/Smad signaling, is a target gene of Erbb4-IR because a binding site of Erbb4-IR was found on the 3′ UTR of Smad7 gene. Mutation of this binding site prevented the suppressive effect of Erbb4-IR on the Smad7 reporter activity; in contrast, overexpression of Erbb4-IR largely inhibited Smad7 but increased collagen I and α-SMA transcriptions. Thus, kidney-specific silencing of Erbb4-IR upregulated renal Smad7 and thus blocked TGF-β/Smad3-mediated renal fibrosis in vivo and in vitro. In conclusion, the present study identified that Erbb4-IR is a novel lncRNA responsible for TGF-β/Smad3-mediated renal fibrosis by downregulating Smad7. Targeting Erbb4-IR may represent a precise therapeutic strategy for progressive renal fibrosis.
Loss of USP28 drives resistance to BRAF targeted therapy in melanoma
Authors: A. Saei, M. Palafox, T. Benoukraf, N. Kumari, P.W. Jaynes, P.V. Iyengar, J.L. Charles Richard, Z.F. Isa, B. Pang, M. Guzman, H. Yang, W.L. Tam, V. Serra, P.J.A. Eichhorn
Journal: Annals of Oncology (2017)
L’impact socio-économique des infections nosocomiales
Authors: R Plowman
Journal: Eurosurveillance (2000)

D’apres un rapport publie recemment, les patients adultes hospitalises dans des services specialises communs qui developpent une infection nosocomiale sejournent a l’hopital en moyenne 2,5 fois plus longtemps que les patients non infectes et representent un cout d’hospitalisation trois fois superieur(1). De meme, apres leur sortie de l’hopital, ces patients generent un surcout pour les medecins generalistes, les infirmieres locales et les hopitaux. L’etude, realisee par le PHLS (Public Health Laboratory Service) et la London School of Hygiene and Tropical Medicine sous la responsabilite du Departement de la Sante au Royaume-Uni, a egalement montre que ces patients generaient un surcout personnel et ne reprenaient leurs activites quotidiennes ou leur travail qu’apres une periode plus longue que les patients non infectes (1).
GW28-e1202 Advanced glycation end-products induced electrical remodeling in atrial myocytes in the type 2 diabetic mellitus
Authors: Yang Hui, Kuang Su-juan, Rao Fang, Liu Xiao-ying, Shan Zhixin, Lin Qiuxiong, Li Xiaohong, Zhu Jiening, Wu Shulin, Deng Chunyu
Journal: Journal of the American College of Cardiology (2017)
GW28-e0466 THE EFFECT OF COENZYME Q10 ON THE CONTENT OF PROINFLAMMATORY MARKERS AND THE REALIZATION OF THE MITOCHONDRIAL MECHANISM OF APOPTOSIS IN CHRONIC HEART FAILURE
Authors: Galina Kukharchik, Olga Lobanova, Lana Sichinava, Larisa Gaikovaya, Alexey Ermakov
Journal: Journal of the American College of Cardiology (2017)
GW28-e0754 High Cl- promotes VCAM-1 expression via NKCC-1-mediated PI3K/ AKT/ GSK3β/ IκBα/ NFκB pathway in high Nacl-exposed endothelial cells
Authors: Zhenjie Gu, Yongbiao Fang, Shaohua Wang, Yangxin Chen
Journal: Journal of the American College of Cardiology (2017)
Frequency of actionable somatic alterations with genomic profiling: the Columbia University experience.
Authors: Adam J. Widman, Meghna S. Trivedi, Kimberly Mayumi Komatsubara, Anthony Sireci, Mahesh Mansukhani, Andrew T Turk, Susan Jean Hsiao, Katherine D. Crew, Richard D. Carvajal
Journal: Journal of Clinical Oncology (2016)

e23132 Background: Personalized medicine in oncology is increasingly available due to the development of more targeted therapies as well as the decreasing expense and rapid results of next generation sequencing (NGS). At Columbia University Medical Center, patients undergo genomic profiling with a NGS assay called the Columbia Combined Cancer Panel (CCCP). We sought to assess the frequency of actionable alterations identified across tumor types. Methods: The CCCP can detect alterations in 467 tumor-specific genes and exons. The results are categorized into 4 tiers: tier 1 variants are actionable alterations associated with tumor type and tier 2 variants are alterations in targeted pathways, actionable alterations in other tumor types, or alterations in well-established cancer genes. Tier 3 and 4 variants do not currently have potential to be targeted. We retrospectively reviewed 219 consecutive adult oncology patients who underwent CCCP testing between 07/10/2014 and 12/15/2015. We examined clinical characteristics, such as tumor type, age, gender, smoking status, and frequency of actionable alterations. We defined 53 gene alterations as actionable based on the potential to be targeted with a currently available approved therapy or an investigational therapy as part of a clinical trial. Results: Of the 219 patients, median age was 61 (range 18-88), 51% were male, and 43% had a documented history of smoking (6% unknown smoking status). The most common tumor types were non-small cell lung cancer (13%), melanoma (9%), and pancreas cancer (7%). The CCCP detected a median of 6 genomic alterations per patient (range 0-63), with 97% having at least one alteration. Sixty-four percent of patients had an alteration defined as actionable and 4.6% had tier 1 variants. The tumor types most likely to have an actionable alteration were colorectal (92%) and melanoma (90%), and their most common alterations were APC and GNA11/GNAQ (reflecting local referral patterns), respectively. Across all tumor types, PIK3CA was the most frequent actionable alteration (9.1%). Conclusions: CCCP testing detected actionable tumor mutations in a majority of cases and can identify candidates who may benefit from personalized cancer care.
Vaccination with PSA146-154 peptide for advanced prostate cancer: A 10-year follow-up.
Authors: Vivek Upadhyay, David J Peace
Journal: Journal of Clinical Oncology (2014)

e14024 Background: Prostate cancer is the second leading cause of cancer-related death among men in the United States. Although localized disease may be definitively treated with prostatectomy or radiotherapy, advanced metastatic disease can only be managed transiently with androgen-deprivation therapy (ADT) and other systemic therapies. Given the prevalence and lack of curative options for advanced disease, novel treatments warrant investigation. Methods: A study begun in 2002 at UIC examined whether vaccination against PSA146-154 peptide elicited specific T cell immunity in 28 patients with advanced disease. In order to measure immune responses, three distinct readouts were used: induction of responses to DTH skin testing for PSA146-154 peptide, detection of CD8+ PSA146-154 peptide-tetramer +T cells, and via PSA146-154 peptide-induced release of IFN-γ in pre versus post-vaccine peripheral blood mononuclear cell samples. All three assays were completed by 26 and 52 weeks following vaccination. The current study examines the long-term effects of the vaccine ten years post immunization and determines survival differences between immune responders and non-responders. Results: Individuals who demonstrated a DTH response against PSA146-154 peptide have improved survival compared to individuals who did not develop a DTH response against the peptide (80.154 months ± 7.849 v. 72.69 months ± 10.358, p = .12). By contrast, specific responses to the PSA peptide detected by IFN gamma production or tetramer staining did not correlate with improved survival. Analysis of mRNA from peripheral blood mononuclear cells of DTH responders revealed increased expression of genes involved in plasmacytoid dendritic cell function (7 genes, with .5 fold to 4.25 fold increased expression in DTH responders). Conclusions: Together, these findings suggest that vaccination against the PSA146-154 peptide may lead to improved survival in patients who effectively mount a peptide-specific DTH response. Furthermore, the RNA expression profile of responders implicates an antitumor role for plasmacytoid dendritic cells.
Dual catenin loss in murine liver causes tight junctional deregulation and progressive intrahepatic cholestasis
Authors: Tirthadipa Pradhan‐Sundd, Lili Zhou, Ravi Vats, An Jiang, Laura Molina, Sucha Singh, Minakshi Poddar, Jacquelyn Russell, Donna B Stolz, Michael Oertel, Udayan Apte, Simon Watkins, Sarangarajan Ranganathan, Kari N. Nejak‐Bowen, Prithu Sundd, Satdarshan Pal Monga
Journal: Hepatology (2017)

β‐Catenin, the downstream effector of the Wnt signaling, plays important roles in hepatic development, regeneration, and tumorigenesis. However, its role at hepatocyte adherens junctions (AJ) is relatively poorly understood, chiefly due to spontaneous compensation by γ‐catenin. We simultaneously ablated β‐ and γ‐catenin expression in mouse liver by interbreeding β‐catenin–γ‐catenin double‐floxed mice and Alb‐Cre transgenic mice. Double knockout mice show failure to thrive, impaired hepatocyte differentiation, cholemia, ductular reaction, progressive cholestasis, inflammation, fibrosis, and tumorigenesis, which was associated with deregulation of tight junctions (TJ) and bile acid transporters, leading to early morbidity and mortality, a phenotype reminiscent of progressive familial intrahepatic cholestasis (PFIC). To address the mechanism, we specifically and temporally eliminated both catenins from hepatocytes using adeno‐associated virus 8 carrying Cre‐recombinase under the thyroid‐binding globulin promoter (AAV8‐TBG‐Cre). This led to a time‐dependent breach of the blood–biliary barrier associated with sequential disruption of AJ and TJ verified by ultrastructural imaging and intravital microscopy, which revealed unique paracellular leaks around individual hepatocytes, allowing mixing of blood and bile and leakage of blood from one sinusoid to another. Molecular analysis identified sequential losses of E‐cadherin, occludin, claudin‐3, and claudin‐5 due to enhanced proteasomal degradation, and of claudin‐2, a β‐catenin transcriptional target, which was also validated in vitro. Conclusion: We report partially redundant function of catenins at AJ in regulating TJ and contributing to the blood–biliary barrier. Furthermore, concomitant hepatic loss of β‐ and γ‐catenin disrupts structural and functional integrity of AJ and TJ via transcriptional and posttranslational mechanisms. Mice with dual catenin loss develop progressive intrahepatic cholestasis, providing a unique model to study diseases such as PFIC. (H epatology 2018;67:2320‐2337).
Detectability of RET fusions by amplicon-based next generation sequencing in nationwide lung cancer genomic screening project: LC-SCRUM-Japan
Authors: Y. Usui, K. Kirita, S. Matsumoto, Y. Ohe, M. Nishio, T. Seto, M. Kodani, K. Taima, Y. Hattori, T. Kohno, K. Yoh, K. Goto
Journal: Annals of Oncology (2017)
Intrinsic tumor features underlying clinical subtype discordance in early breast cancer
Authors: V. Kotoula, E. Giannoulatou, K. Papadopoulou, I. Tikas, K. Manousou, M. Bobos, S. Lakis, G. Lazaridis, I. Efstratiou, F. Zagouri, G. Pentheroudakis, H. Gogas, C. Christodoulou, A. Koutras, A. Psyrri, C. Papandreou, P. Papakostas, D. Bafaloukos, D. Pectasides, G. Fountzilas
Journal: Annals of Oncology (2017)
Potential drug interactions in older patients with cancer: Updated data from the ELCAPA cohort survey
Authors: G. Beinse, D. Reitter, L. Segaux, M. Carvalho-Verlinde, C. Tournigand, B. Rousseau, T. Cudennec, E. Paillaud, F. Canouï-Poitrine, P. Caillet
Journal: Annals of Oncology (2017)
Practice patterns in metastatic castration-resistant prostate cancer (mCRPC): Evidence from the veterans health administration
Authors: A. Halwani, Z. Burningham, K.M. Rasmussen, V. Patil, S. Narayanan, S-W. Lin, S. Carroll, L-I. Hsu, J. Graff, R. Dreicer, S. Gupta, C. Low, B.C. Sauer
Journal: Annals of Oncology (2017)
Multimodal imaging approach to examine biodistribution kinetics of Cabotegravir (GSK1265744) long acting parenteral formulation in rat
Authors: Beat M. Jucker, Hasan Alsaid, Mary Rambo, Stephen C. Lenhard, Bao Hoang, Fang Xie, M. Reid Groseclose, Stephen Castellino, Valeriu Damian, Gary Bowers, Manish Gupta
Journal: Journal of Controlled Release (2017)
Astrocyte-Secreted Glypican 4 Regulates Release of Neuronal Pentraxin 1 from Axons to Induce Functional Synapse Formation
Authors: Isabella Farhy-Tselnicker, Adriana C.M. van Casteren, Aletheia Lee, Veronica T. Chang, A. Radu Aricescu, Nicola J. Allen
Journal: Neuron (2017)

The generation of precise synaptic connections between developing neurons is critical to the formation of functional neural circuits. Astrocyte-secreted glypican 4 induces formation of active excitatory synapses by recruiting AMPA glutamate receptors to the postsynaptic cell surface. We now identify the molecular mechanism of how glypican 4 exerts its effect. Glypican 4 induces release of the AMPA receptor clustering factor neuronal pentraxin 1 from presynaptic terminals by signaling through presynaptic protein tyrosine phosphatase receptor δ. Pentraxin then accumulates AMPA receptors on the postsynaptic terminal forming functional synapses. Our findings reveal a signaling pathway that regulates synaptic activity during central nervous system development and demonstrates a role for astrocytes as organizers of active synaptic connections by coordinating both pre and post synaptic neurons. As mutations in glypicans are associated with neurological disorders, such as autism and schizophrenia, this signaling cascade offers new avenues to modulate synaptic function in disease.
Recovery of humoral immunity in patients with durable complete responses following chimeric antigen receptor modified t cells directed against CD19 (CTL019).
Authors: Stephen J. Schuster, Jakub Svoboda, Sunita Nasta, Elise A. Chong, David L. Porter, Daniel Jeffrey Landsburg, Anthony R. Mato, Vijay G. Bhoj, Michael Milone, Simon F. Lacey, Lauren E. Strelec, Alice Y. Zhou, Jan J. Melenhorst, Anne Chew, Jens Hasskarl, Mariusz A. Wasik, Katherine Marcucci, Zhaohui Zheng, Bruce Levine, Carl H. June
Journal: Journal of Clinical Oncology (2016)

7564 Background: Autologous T cells genetically modified to express a chimeric antigen receptor with an external anti-CD19 antibody domain, and CD3ζ and 4-1BB signaling domains (CTL019) can achieve remissions in patients (pts) with relapsed/refractory (r/r) CD19+ non-Hodgkin lymphomas (NHL). We studied the effect of this therapy on humoral immunity. Methods: Serial immunoglobulin (Ig) levels were measured in pts with complete response (CR) to CTL019 on a phase II trial. Pts had r/r CD19+ follicular lymphoma (FL), diffuse large B cell lymphoma (DLBCL), or mantle cell lymphoma (MCL). After collection of lymphocytes, pts received lymphodepleting chemotherapy followed 1 - 4 days later by 1 - 5 x 108CTL019 cells intravenously. Response was assessed every 3 months (mo) for 24 mo. Enrollment is reported from Feb 2014 – Nov 2015, survival analyses through Jan 2016. Results: 43 pts enrolled: median age 56 years (range 25-77); female: male ratio 17:26; median prior therapies 4 (range 1-19); prior ASCT 14 (33%). 30 pts received CTL019; 29 are evaluable for response (15 DLBCL; 13 FL; 1 MCL). Best overall response rate is 59% (17/29); CR 52% (15/29); DLBCL CR 40% (6/15); FL CR 69% (9/13). To date, no pt in CR has relapsed (median follow up 14 mo). 2 pts were receiving IV Ig before CTL019; 2 pts started IV Ig after CTL019 for hypogammaglobulinemia with frequent infections. 10 pts (6 DLBCL; 4 FL) in CR > 5 mo (median 17 mo; range 5-21) did not received IV Ig and had no > grade 2 or recurrent infections. Baseline IgG levels were decreased in all 10 pts (median 514 mg/dL; range 200-639; normal > 650), IgA in 6/10 pts (median 46 mg/dL; range 34-134; normal > 50), and IgM in 8/10 pts (median 28 mg/dL; range 8-74; normal > 40). 4/10 pts had IgG recovery to their baseline level (1 pt at 21 mo) or to normal levels at 6, 9, and 15 mo (total % IgG increases: 10%, 19%, 29%, respectively). 2/10 pts had IgA recovery to > baseline levels (total % IgA increases 3% and 17% at 18 mo). 5/10 pts had total % IgM increases: 6% at 18 mo, 13% at 12 mo, 21% at 12 mo, 46% at 9 mo, and 441% at 15 mo. Conclusions: In adult r/r NHL pts, CTL019 cells can induce a sustained CR during which Ig levels may improve. Most pts do not need Ig replacement after CTL019 therapy. Clinical trial information: NCT02030834.
Utility of Pit-1 Immunostaining in Distinguishing Pituitary Adenomas of Primitive Differentiation from Null Cell Adenomas
Authors: Julieann C. Lee, Melike Pekmezci, Jonathan L. Lavezo, Hannes Vogel, Laurence Katznelson, Merav Fraenkel, Griffith Harsh, Mohanpal Dulai, Arie Perry, Tarik Tihan
Journal: Endocrine Pathology (2017)
Investigation of an outbreak of amœbiasis in Georgia
Authors: P Kreidl, P Imnadze, L Baidoshvili, D Greco
Journal: Eurosurveillance (1999)

Entamoeba histolytica, a protozoan parasite, occurs worldwide and 12% of the world's population are estimated to be infected. The prevalence of infection varies between 1% in industrialised countries to between 50% and 80% in tropical countries, where tra
Combining functional imaging with circulating biomarker analysis to improve prognostication of metastatic castration-resistant prostate cancer (mCRPC)
Authors: V. Conteduca, S. Salvi, P. Caroli, E. Scarpi, G. Schepisi, C. Lolli, D. Wetterskog, S.L. Burgio, C. Menna, V. Casadio, F. Matteucci, G. Paganelli, G. Attard, U. De Giorgi
Journal: Annals of Oncology (2017)
Long term survival in patients responding to an Anti-PD-1/PD-L1 therapy and disease outcome upon treatment discontinuation
Authors: M-L. Gauci, E. Lanoy, S. Champiat, J-M. Michot, A. Varga, R. Bahleda, E. Angevin, A. Gazzah, L. Verlingue, F. Bigot, S. Aspeslagh, E. Castanon, C. Baldini, S. Postel-Vinay, C. Massard, A. Hollebecque, J-C. Soria, A. Marabelle
Journal: Annals of Oncology (2017)
The stem cell factor SALL4 is an essential transcriptional regulator in mixed lineage leukemia-rearranged leukemogenesis
Authors: Lina Yang, Li Liu, Hong Gao, Jaya Pratap Pinnamaneni, Deepthi Sanagasetti, Vivek P. Singh, Kai Wang, Megumi Mathison, Qianzi Zhang, Fengju Chen, Qianxing Mo, Todd Rosengart, Jianchang Yang
Journal: Journal of Hematology & Oncology (2017)

The stem cell factor spalt-like transcription factor 4 (SALL4) plays important roles in normal hematopoiesis and also in leukemogenesis. We previously reported that SALL4 exerts its effect by recruiting important epigenetic factors such as DNA methyltransferases DNMT1 and lysine-specific demethylase 1 (LSD1/KDM1A). Both of these proteins are critically involved in mixed lineage leukemia (MLL)-rearranged (MLL-r) leukemia, which has a very poor clinical prognosis. Recently, SALL4 has been further linked to the functions of MLL and its target gene homeobox A9 (HOXA9). However, it remains unclear whether SALL4 is indeed a key player in MLL-r leukemia pathogenesis. Using a mouse bone marrow retroviral transduction/ transplantation approach combined with tamoxifen-inducible, CreERT2-mediated Sall4 gene deletion, we studied SALL4 functions in leukemic transformation that was induced by MLL-AF9—one of the most common MLL-r oncoproteins found in patients. In addition, the underlying transcriptional and epigenetic mechanisms were explored using chromatin immunoprecipitation (ChIP) sequencing (ChIP-Seq), mRNA microarray, qRT-PCR, histone modification, co-immunoprecipitation (co-IP), cell cycle, and apoptosis assays. The effects of SALL4 loss on normal hematopoiesis in mice were also investigated. In vitro and in vivo studies revealed that SALL4 expression is critically required for MLL-AF9-induced leukemic transformation and disease progression in mice. Loss of SALL4 in MLL-AF9-transformed cells induced apoptosis and cell cycle arrest at G1. ChIP-Seq assay identified that Sall4 binds to key MLL-AF9 target genes and important MLL-r or non-MLL-r leukemia-related genes. ChIP-PCR assays indicated that SALL4 affects the levels of the histone modification markers H3K79me2/3 and H3K4me3 at MLL-AF9 target gene promoters by physically interacting with DOT1-like histone H3K79 methyltransferase (DOT1l) and LSD1/KDM1A, and thereby regulates transcript expression. Surprisingly, normal Sall4 f/f /CreERT2 mice treated with tamoxifen or vav-Cre-mediated (hematopoietic-specific) Sall4 −/− mice were healthy and displayed no significant hematopoietic defects. Our findings indicate that SALL4 critically contributes to MLL-AF9-induced leukemia, unraveling the underlying transcriptional and epigenetic mechanisms in this disease and suggesting that selectively targeting the SALL4 pathway may be a promising approach for managing human MLL-r leukemia.
A phase 1b/2 trial of lenvatinib plus pembrolizumab in patients with renal cell carcinoma
Authors: C-H. Lee, V. Makker, D. Rasco, M. Taylor, C. Dutcus, R. Shumaker, E.V. Schmidt, D. Stepan, D. Li, R.J. Motzer
Journal: Annals of Oncology (2017)
Demographic and health care service utilization by 4417 patients with hidradenitis suppurativa
Authors: Guy Shalom, Meir Babaev, Tamar Freud, Shmuel Tiosano, Nadav Pam, Amir Horev, Jacob Dreiher, Daniel A. Vardy, Doron Comaneshter, Arnon D. Cohen
Journal: Journal of the American Academy of Dermatology (2017)
Safety and immunobiological activity of intratumoral (IT) double-stranded RNA (dsRNA) BO-112 in solid malignancies: First in human clinical trial
Authors: I. Marquez Rodas, M.E. Rodriguez Ruiz, S. Lopez-Tarruella Cobo, J.L. Perez Gracia, M. Ponz Sarvise, R. Alvarez, E. de Miguel, Y. Jerez, A. Calvo Ferrandiz, M. Blanco Codesido, J. Gayarre, R. Ramos Medina, A. Calles, M.A. Aznar, L. Planelles, M. Quintero, S. Martin Algarra, M. Martin Jimenez, I. Melero
Journal: Annals of Oncology (2017)
EORTC experience with advanced/metastatic epithelioid sarcoma patients treated in prospective trials: Clinical profile and response to systemic therapy
Authors: N. Touati, P. Schoffski, S. Litière, I. Judson, S. Sleijfer, W.T.A. van der Graaf, A. Italiano, N. Isambert, T. Gil, J.-Y. Blay, D. Stark, T. Brodowicz, S. Marreaud, A. Gronchi
Journal: Annals of Oncology (2017)