tbuckley/cabot-search huggingface dataset:
Results of a feasibility study of I-124 girentuximab in metastatic clear cell renal cell carcinoma (m ccRCC).
Authors: Stephen Michael Keefe, Mark Alan Rosen, Janelle Robinson, Karen McGibney, Amy Marshall, Ronac Mamtani, David J. Vaughn, Peter J. O'Dwyer, Naomi B. Haas, Daniel A. Pryma
Journal: Journal of Clinical Oncology (2014)

406 Background: Carbonic anhydrase IX (CAIX), a transmembrane glycoprotein with an intracellular enzymatic domain, is overexpressed in ccRCC as a result of VHL loss. Chimeric antibody girentuximab is a monoclonal antibody that binds an extracellular epitope of CAIX. Iodine radiolabeled (I-124) girentuximab can be used as a PET radiotracer and has been shown to identify ccRCC primary tumors with high sensitivity and specificity. This study was designed to test the feasibility of using I-124 girentuximab PET/CT in the m ccRCC setting and to produce preliminary data regarding the operating characteristics of these scans in m ccRCC. Methods: Patients (pts) with ccRCC refractory to standard antiangiogenic therapy were treated with brivanib (Bristol-Myers Squibb, Co.), a tyrosine kinase inhibitor of VEGFR2 and FGFR. Baseline I-124 girentuximab scans were obtained. For 1 pt, a second scan was performed after 8 weeks. Clinical outcome was measured radiographically by RECIST 1.0 and standard cross-sectional imaging. Results: 5 pts had 6 I-124 girentuximab PET/CT scans. No adverse events occurred. 17 RECIST target lesions were identified at baseline. PET showed heterogeneous expression of CAIX in all scans: overall, 9 of 17 (53%) metastatic target lesions expressed CAIX. Progressive disease occurred in 5/6 pts within 4 months on treatment, and progression occurred in all 8 of the CAIX non-avid lesions (100%) in these pts. One pt achieved a RECIST partial response (PR) with treatment – the pt for whom paired studies were obtained. For this pt, a PET PR was observed 2 cycles earlier than with conventional imaging. Conclusions: I-124 girentuximab PET/CT was safe and feasible in m ccRCC. We found that metastases were detected. More importantly, for pts with ccRCC refractory to conventional antiangiogenic therapies, CAIX expression was heterogeneous, and progression occurred in CAIX non-avid lesions. Taken together, these data suggest that CAIX expression identified with this functional imaging modality represents a biological prerequisite for continued antiangiogenic therapeutic activity, and the heterogeneous CAIX expression observed helps to explain why brivanib was not useful in this setting. Clinical trial information: NCT01253668.
Lung endothelial monocyte-activating protein 2 is a mediator of cigarette smoke–induced emphysema in mice
Authors: Matthias Clauss, Robert Voswinckel, Gangaraju Rajashekhar, Ninotchka L. Sigua, Heinz Fehrenbach, Natalia I. Rush, Kelly S. Schweitzer, Ali Ö. Yildirim, Krzysztof Kamocki, Amanda J. Fisher, Yuan Gu, Bilal Safadi, Sandeep Nikam, Walter C. Hubbard, Rubin M. Tuder, Homer L. Twigg, Robert G. Presson, Sanjay Sethi, Irina Petrache
Journal: Journal of Clinical Investigation (2012)

During the preparation of Figure 2F, the label of the y axis was listed with incorrect units of measurement and without specifying the scale of 10 -2 .The y axis units should be ml/cm H 2 O.The correct figure is below.
SURG-40. INDICATIONS AND OUTCOMES OF BRAIN TUMOR SURGERY IN HIGH FIELD INTRA-OPERATIVE MRI
Authors: Ian F. Parney, Ryan Planchard
Journal: Neuro-Oncology (2016)

Intra-operative magnetic resonance imaging with a high field (≥ 1.5 Tesla) magnet is a powerful tool for neurosurgical image guidance. However, the indications and outcomes in brain tumor patients remain poorly defined. A prospective database of all brain tumor procedures performed by the senior author in a 1.5 T stationary intra-operative MRI (iMRI) was reviewed. All cases were performed with frameless stereotactic guidance using intra-operative imaging. Some cases were performed with motor and/or speech mapping using a bipolar stimulating electrode. A total of 270 iMRI procedures were performed for intracranial tumors. Craniotomy and resection of primary intra-axial tumors was the most common procedure (> 90%) with a minority of craniotomies for other tumors or stereotactic biopsy or laser-interstitial therapy procedures. Sixty-nine percent of tumors involved eloquent cortex directly or bordered on eloquent cortex. Electrophysiological stimulation of motor and/or speech function was performed in 136 cases. Sixty-four cases were performed awake. Most tumors (64%) were non-enhancing. Gross total resection was performed in 41%, extensive subtotal resection (>85%) in 30%, subtotal resection in 27%, and biopsy in 7%. Permanent new neurological deficits occurred in 6% and were major (reduced Karnofsky Performance Score by ≥10) in 4%. Regional / wound healing complications occurred in 5% and systemic complications in 4%. There were two deaths (0.7%) within 30 days of surgery, one due to tumor progression and one related to complications from infection. High field intra-operative MRI can be routinely incorporated into neurosurgical oncology and combined with electrophysiological stimulation mapping. This combination of optimal image-guidance and physiological guidance can facilitate safe, extensive resection even for challenging tumors in eloquent locations.
Evaluation of the Imatinib Treatment of Patients with Chronic Myeloid Leukemia (CML). a Retrospective Study from Algerian Working Group on CML (GAT-LMC)
Authors: K Djouadi, A Bouchakour, S Taoussi, MT Abad, Z Ouchenane, N Sidi Mansour, N Abdennebi, F Harieche, R Ahmed Nacer, RM Hamladji, Fz Touil, S Hamdi, B Entasoltane, M Brahimi, M Nachi, MA Bekadja, C Kerrar, L Allam, O Djidjik, N Boudjerra, M Belhani, S Bougherira, F Grifi, S Gherras, A Graine, H Ait Ali, Z Brahimi, L Touati, N Lakhdari, N Mehalhal, K Taibi, H Touhami, B Benzineb, N Mesli, D Saber Cherif, C Rahali, N Mansour, Y Meddour, S Chaib, Fz Ardjoun, F Maghraoui, S Hadjeb, M Zenori, M Benlazhar, Z Zouaoui, S Baghdad, A Bachiri, D Lamara, B Bendjabellah, M Benakli
Journal: Blood (2016)
CSIG-24. REGULATION OF Fn14 EXPRESSION BY EGFRvIII-STAT SIGNALING ENHANCES GLIOBLASTOMA CELL INVASION AND SURVIVAL
Authors: Alison Roos, Zachary Mayo, Heather Sonnemann, Gil Lambert, Harshil Dhruv, Jeffrey Winkles, Michael Berens, Nhan Tran, Marya Sabir
Journal: Neuro-Oncology (2016)

Glioblastoma Multiforme (GBM) is the most common malignant brain tumor in adults. Most GBM patients succumb to the disease less than one-year post diagnosis due to the highly invasive nature of the tumor, which prevents complete surgical resection and gives rise to tumor recurrence. The invasive phenotype also confers radio-and chemoresistant properties to the tumor cells; therefore, there is a need to develop new therapeutics that target drivers of GBM invasion. Amplification of EGFR is observed in over 50% of GBM tumors, of which half concurrently overexpress the variant EGFRvIII, and expression of both receptors confers a worse prognosis. EGFR and EGFRvIII cooperate to promote tumor progression and invasion, in part, through activation of the STAT-signaling pathway. Here we report that GBM cells expressing EGFRvIII show increased expression of a previously established mediator of glioma cell invasion and survival, fibroblast growth factor-inducible 14 (Fn14), at the mRNA and protein level. Treatment with STAT5 siRNA or Src inhibitors decreased Fn14 mRNA and protein expression. Finally, knockdown of Fn14 levels in the EGFRvIII-expressing glioma cells decreased both cell survival after temozolomide (TMZ) treatment and cell invasion, which suggests that Fn14, in part, mediates the oncogenic phenotypes conferred by EGFRvIII signaling. Since EGFR inhibitors display limited therapeutic efficacy in GBM patients, we hypothesize that Fn14-targeted therapies could potentially limit invasiveness and chemoresistance in EGFRvIII-dependent GBM tumors.
The role of indoleamine 2,3-dioxygenase expression in diffuse large B-cell lymphoma prognosis
Authors: I. Kryachok, T. Skrypets, O. Novosad, N. Khranovska, O. Skachkova, K. Ulianchenko, A.V. Martynchyk, I. Tytorenko, K. Filonenko, I. Stepanishyna, N. Svergun, O. Gorbach, O. Nevdakh
Journal: Annals of Oncology (2016)
The role of immune system on the efficacy of bevacizumab in patients with metastatic colorectal cancer (mCRC)
Authors: H. Akbulut, M. Ocal, G. Sonugur, B. Akay, C. Babahan, S. Abdi Abgarmi, A. Demirkazik, F. Icli
Journal: Annals of Oncology (2016)
Adherence to Iron Chelation Therapy and Associated Healthcare Resource Utilization and Costs in Medicaid Patients with Sickle Cell Disease
Authors: Francis Vekeman, Medha Sasane, Wendy Y Cheng, Agnihotram V Ramanakumar, Jonathan Fortier, Mei S. Duh, Carole Paley, Patricia Adams-Graves
Journal: Blood (2014)
Are the Myeloma Bone Microevironment Cells Tumoral or Not?.
Authors: Nicola Giuliani, Francesca Novara, Katia Todoerti, Nadia Zaffaroni, Raffaella Villa, Paola Storti, Maria Ester Bernardo, Cristina Manferdini, Elena Gabusi, Manuela Abeltino, Marina Bolzoni, Luca Agnelli, Alberto Rocci, Simona Colla, Gabriella Sammarelli, Vittorio Rizzoli, Orsetta Zuffardi, Antonino Neri, Gina Lisignoli
Journal: Blood (2009)
Harnessing the Properties of Natural Products
Authors: Asmaa Boufridi, Ronald J. Quinn
Journal: The Annual Review of Pharmacology and Toxicology (2017)

Natural products (NPs) have been used as traditional medicines since antiquity. With more than 1060 estimated compounds with molecular weights less than 500 Da representing chemical space, NPs occupy a very small percentage; however, they are significantly overrepresented in biologically relevant chemical space. The classical approach concentrates on identifying one or more NPs with biological activity from a source organism. There is much more to be learned from NPs than we can discover this narrow view. In this review, we discuss ways to harness the global properties of NPs.
Phase 1b study of crizotinib in combination with pembrolizumab in patients (pts) with untreated ALK-positive (+) advanced non-small cell lung cancer (NSCLC)
Authors: F.R. Vizcarrondo, S.P. Patel, N.A. Pennell, S. Pakkala, H. West, R. Kratzke, J. Tarazi, K. Wilner, A. Polli, W. Tan, Y. Liu, O. Valota, B. Piperdi, K.L. Reckamp
Journal: Annals of Oncology (2016)
MNGO-03. LONG TERM VOLUMETRIC ANALYSIS OF MENINGIOMAS TREATED WITH GAMMA KNIFE STEREOTACTIC RADIOSURGERY
Authors: John McGregor, Angel Long
Journal: Neuro-Oncology (2016)

Complete surgical resection of intracranial meningiomas including the dura of origin and infiltrated bone remains the treatment of choice for best long term control. Residual disease, tumor grade, location within the cranial vault, and patient co morbidities may limit the success of surgery alone. Stereotactic radiosurgery (SRS) expands the options for treatment. We review the outcomes in patients with meningiomas treated with SRS at our institution from 1999 – 2012 and assess the long term effects on lesion volumes. 78 patients with 89 presumed or confirmed meningiomas were treated with SRS over the 13 year period. Median age was 56 (range 17-84); 19 males and 59 females. Median marginal dose was 15.95 Gy (range 10 -31 Gy) to an averaged 51% isodose line (range 47 – 75%). 39 patients had surgery prior to treatment (50%). 10 patients had radiation therapy prior to SRS (13%). Patients were followed clinically and radiographically 1, 3, 5 and ≥10 years after SRS. Lesional volumes were measured at treatment and at long term follow up. 58 tumors (65%) were falcine/parasagital or cerebral convexities. 31 were skull base (34%). Histology included 27 WHO grade I, 17 WHO grade II and 1 WHO grade III meningiomas. 44 patients had no pathologic analysis. 7 lesions progressed requiring further treatment (8%); three at the skull base, and 4 in a convexity/parasagital location. Four of the progressive tumors were known WHO grade ll, 2 were WHO grade l, and 1 did not have confirmatory pathology. Three dimensional volume analyses of the lesions were performed at initial treatment and at long term follow-up. Radiosurgery is a reasonable adjunct to management of patients with primary, residual or recurrent meningiomas and presumed meningiomas. The control rates are > 90%. Volumetric comparisons allow improved analysis of the long term effects of SRS. Continued long term evaluations are needed.
Responses in specific metastases following treatment with lenvatinib (LN): Results from the phase 3 SELECT trial
Authors: B. Robinson, M. Schlumberger, L.J. Wirth, C.E. Dutcus, T.A. Binder, M. Guo, M. Taylor, S.B. Kim, M.K. Krzyzanowska, J. Capdevilla, S.I. Sherman, M. Tahara
Journal: Annals of Oncology (2016)
Outcome of Non-T-Cell-Depleted Hematopoietic Stem Cell Transplantation between HLA-Haploidentical Non-Inherited Maternal Antigen (NIMA)-Mismatched Family Members in Childhood.
Authors: Takao Yoshihara, Keiko Okada, Hiromasa Yabe, Michihiro Kobayashi, Atsushi Kikuta, Koji Kato, Naoto Adachi, Akira Kikuchi, Yasuzou Hirota, Hiroshi Kuroda, Yoshihisa Nagatoshi, Takeshi Inukai, Kazutoshi Koike, Hisato Kigasawa, Ryuhei Tanaka, Arata Watanabe
Journal: Blood (2005)
Switch from abiraterone + prednisone to abiraterone + dexamethasone after PSA progression under abiraterone + prednisone in asymptomatic metastatic castration-resistant prostate cancer (mCRPC) patients
Authors: C. Fenioux, C. Louvet, D. Prapotnich, S. Ropert, E. Barret, R. Sanchez-Salas, A. Mombet, N. Cathala, B. Poullennec, M.-L. Joulia, M. Ung, X. Cathelineau, M. Bennamoun
Journal: Annals of Oncology (2016)
Prognostic impact of Ki67 for resected early stage pure Invasive Lobular breast Cancer (ILC): cut-off analysis and clinical validation
Authors: L. Carbognin, I. Sperduti, A. Fabi, M.V. Dieci, I. Zampiva, G. Griguolo, S. Pilotto, V. Guarneri, M. Brunelli, R. Nortilli, E. Manfrin, E. Fiorio, V. Parolin, E. Filippi, F. Pellini, G.P. Pollini, C. Nisticò, P. Conte, G. Tortora, E. Bria
Journal: Annals of Oncology (2016)
GENT-44. LOWERED H3K27me3 AND DNA HYPOMETHYLATION DEFINE POORLY PROGNOSTIC PEDIATRIC POSTERIOR FOSSA EPENDYMOMAS
Authors: Sriram Venneti, Jill Bayliss, Piali Mukherjee, Chao Lu, Siddhant Jain, Daniel Martinez, Ashley Margol, Melike Pekmezci, Chan Chung, Richard Mc Eachin, Marcin Cieslik, Benjamin Garcia, Benita Tamrazi, Gaspare Larocca, Mariarita Santi, Peter Lewis, Ari Melnik, C Allis, Craig Thompson, Arul Chinnaiyan, Alexander Judkins
Journal: Neuro-Oncology (2016)

Childhood posterior fossa (PF) ependymomas cause significant morbidity and mortality. These tumors lack recurrent genetic alterations but exhibit CpG-island hypermethylation implicating epigenetic alterations in their pathogenesis. Further, histological grade does not reliably predict prognosis, highlighting the importance of developing more robust prognostic markers. We discovered global H3K27me3 reduction in a subset of these tumors analogous to H3K27M mutant high-grade gliomas. PF ependymomas with global reduction in H3K27me3 were transcriptionally similar to previously described PFA ependymomas. Further they displayed genome-wide DNA hypomethylation and altered H3K27me3 enrichment that rewired gene expression. Moreover, genome-wide DNA hypomethylation and H3K27me3 redistribution shared many similarities to H3K27M gliomas. Combined integrative analysis of both tumor types uncovered common epigenetic deregulation of select factors that control radial glial biology. Posterior fossa radial glia showed reduced H3K27me3, which suggests these cells as candidate cells-of-origin. Finally, H3K27me3 immunostaining served as a robust biomarker to stratify patients with poor prognosis and delineated radiologically invasive tumors. These data have clinical implications for biomarker development and to inform epigenetic approaches to treat PF ependymomas.
Evaluation of the derivation of human colon adenocarcinoma from Lgr5 colon stem cells.
Authors: V. K. Chiu, P. Paty, T. K. Chiu, A. Le Rolle, J. Shia, Z. Zeng, W. R. Jarnagin, M. R. Weiser, S. Rafii
Journal: Journal of Clinical Oncology (2011)

410 Background: Human colon stem cells share phenotypic hallmarks of self-renewal and proliferation that are associated with tumor cells. Lgr5 is a marker of colon stem cells and not colon differentiated cells. In mice, deletion of the adenomatous polyposis coli gene in colon stem cells but not in colon differentiated cells, rapidly gives rise to macroscopic adenomas. We investigated the role of Lgr5 colon stem cells in human colon tumors in relation to tumor cell of origin, tumor progression, tumor recurrence, and overall survival. Methods: Using in situ hybridization, we determined the histological distribution of Lgr5 mRNA in human colon specimens at different stages of tumor development and tumor recurrence after chemotherapy. Using gene expression analysis, we analysed Lgr5 mRNA expression levels in human normal colon (n = 33), normal liver (n = 13), colon adenomas (n = 45), primary colon adenocarcinomas (n = 170), liver metastates (n = 48) and lung metastates (n = 20). We examined the correlation between Lgr5 mRNA expression, K-ras mutation status and overall survival in stage IV colon adenocarcinomas. Results: Human normal colon Lgr5 mRNA was always expressed at basal level and restricted to human colon stem cells. In contrast, we observed an all (Lgr5 (+) ) or none (Lgr5 (-) ) expression in human colon adenomas, adenocarcinomas and liver metastases. When present Lgr5 mRNA expression was increased 3-10 fold compared to normal colon. The Lgr5 gene expression analysis provided similar results with increased expression in 66% of human colon adenomas, 62% of primary colon adenocarcinomas, 72% of colon liver metastases and 55% colon lung metastases when compared to normal colon. We have determined that 22.5% (18/80) of Lgr5 (+) and 46.4% (26/56) of Lgr5 (-) colon adenocarcinoma specimens have K-ras mutations. Kaplan-Meier estimates of median overall survival in Lgr5 (+) and Lgr5 (-) Stage IV colon adenocarcinomas were 20 months and 15 months, respectively. Conclusions: Human colon adenocarcinomas are derived predominantly from Lgr5 colon stem cells. Lgr5 (+) colon adenocarcinomas required less frequent K-ras mutation for tumor progression then Lgr5 (-) colon adenocarcinomas. No significant financial relationships to disclose.
STMC-22. A BIOSYNTHETIC METABOLIC PATHWAY IN GLIOBLASTOMA CONTROLS GROWTH VIA REACTIVE SPECIES BALANCE
Authors: Anh Tran, Kiera Walker, Lauren Hocevar, David Harrison, Wei Chen, Victor Darley-Usmar, Yancey Gillespie, Sara Cooper, Anita Hjelmeland
Journal: Neuro-Oncology (2016)

In glioblastoma (GBM; grade IV astrocytoma), subpopulations of highly tumorigenic cells called brain tumor initiating cells (BTICs) have been characterized by their unique capacity to promote tumor growth and therapeutic resistance. BTIC maintenance is increased via nitric oxide produced by nitric oxide synthases (NOS) in BTICs and the tumor vasculature. NOS require the co-factor tetrahydrobiopterin (BH4) for NO generation and will make superoxide if BH4 is deficient. As the first and rate-limiting enzyme of the de novo pathway synthesizing BH4 is GTP cyclohydrolase 1 (GCH1), GCH1 activity can control reactive nitrogen and oxygen species levels. We determined that GCH1 RNA and protein expression are increased in BTICs in comparison to non-BTICs. Overexpression of GCH1 in GBM cells increased cell growth in vitro and decreased survival in an intracranial GBM mouse model. In contrast, GCH1 knockdown with short hairpin RNA in GBM cells led to growth inhibition in vitro and also increased survival in animal models. When we inhibited GCH1 in BTICs with the small molecule inhibitor 2,4-diamino-6-hydroxypyrimidine (DAHP), neurosphere formation was decreased as was subcutaneous tumor growth. Effects of genetic or pharmacologic inhibition of GCH1 correlated with decreased NO and increased ROS production. In silico analyses demonstrate that higher GCH1 levels in glioma patients correlate with higher glioma grade, recurrence and worse survival. Together, our data suggest that upregulation of GCH1 in BTICs promotes tumor maintenance and is a good candidate target for therapeutic intervention in GBM.
The Prognostic Value of Whole-Body Suvmax of Nodal and Extranodal Lesions Detected By 18F-FDG PET-CT in Patients with Extranodal NK/T-Cell Lymphoma
Authors: Jin-Hua Liang, Chong-Yang Ding, Li Wang, Lei Fan, Tian-Nv Li, Jian-Yong Li, Wei Xu
Journal: Blood (2015)
Analysis of 148 cases of EGFR mutation-positive lung cancer patients
Authors: Yuko Abe, Yoshiro Tanio, Yuya Shirai, Yuichi Mitui, Koichi Ogawa, Yuki Akazawa, Kiyonobu Ueno, Kenichi Oomori, Shigetoshi Shimamoto, Hiroaki Fushimi
Journal: Annals of Oncology (2016)
GENT-40. DOT1L EPIGENETICALLY REGULATES AN EMT-LIKE PROCESS IN GBM BTICs
Authors: Danielle Bozek, H. Artee Luchman, Samuel Weiss
Journal: Neuro-Oncology (2016)

The median survival of patients diagnosed with Glioblastoma multiforme (GBM) remains poor. This may be in part due to cancer cell invasion outside the margin of tumor resection through an Epithelial-Mesenchymal Transition-like (EMT-like) phenomenon leading to disease recurrence. EMT is linked to invasion and metastasis of a number of cancers, and is characterized by loss of cell adhesion, increased cell motility and downregulation of E-cadherin. Epigenetic regulators affect chromatin structure by laying down epigenetic marks, which results in the regulation of DNA access to transcription factors. Epigenetics can be environmentally altered through cancer therapy and this may contribute to EMT in cancer cells. Disrupter of telomeric silencing-1-like (DOT1L) is a histone methyltransferase that catalyses the methylation of histone-3-lysine-79 (H3K79me) and is crucial for breast cancer tumorigenesis, invasion and metastasis. Recent studies have also shown that STAT3 is an important mediator of DOT1L regulation in colorectal cancer. Our group has previously demonstrated that the JAK2/STAT3 pathway is upregulated in GBM and essential to the growth and tumorigenic properties of brain tumor initiating cells (BTICs). We tested the hypothesis that DOT1L is directly regulated by STAT3 and promotes an EMT-like process in BTICs. Indeed, STAT3 inhibition using a JAK2/STAT3 inhibitor (R333) decreased protein expression of DOT1L and levels of H3K79me2. Activation of STAT3 in BTICs with Oncostatin M (OSM) treatment increased DOT1L expression and H3K79me2 levels. Furthermore, chromatin immunoprecipitation (ChIP) experiments showed that STAT3 directly transactivates DOT1L. Treatment with the DOT1L inhibitor EPZ-5676 decreased H3K79me2 levels and effectively decreased BTIC viability, proliferation and sphere initiating frequency in vitro. Moreover, EPZ-5676 treatment resulted in increased E-cadherin RNA levels and decreased both BTIC invasion and migration. Ongoing studies aim to further elucidate the role of DOT1L in BTICs through H3K79me2 ChIP-sequencing, RNA sequencing and in vivo analysis of GBM BTIC invasion with EPZ-5676 treatment.
Phase II study of cabazitaxel with or without abiraterone acetate and prednisone in patients with metastatic castrate resistant prostate cancer after prior docetaxel and abiraterone acetate
Authors: E.R. Kessler, D. Gao, T.W. Flaig, K. Breaker, M. Wold, M. Wacker, E.T. Lam
Journal: Annals of Oncology (2016)
A risk assessment model for predicting venous thromboembolic events in chemotherapy-treated germ-cell cancer
Authors: M.I. Luengo, D. Hervás, N. Sobrevilla, X. Garciadel Muro, J. Guma I. Padro, D. Castellano, J. Aparicio, A. Sánchez Muñoz, E. Buxo, A. Saenz, J.L. Aguilar, C. Valverde Morales, A. Fernández Aramburu, P. Maroto, M. Espinosa, P. Jimenez Fonseca, S. Ros, M. Margeli, J. Sastre, E. Gonzalez-Billalabeitia
Journal: Annals of Oncology (2016)