tbuckley/cabot-search huggingface dataset:
MPTH-06. 1p/19q CO-DELETION STATUS PREDICTS SURVIVAL OUTCOMES IN NRG ONCOLOGY/RTOG 9802: A PHASE III TRIAL OF RT VS RT + PCV IN HIGH RISK LOW-GRADE GLIOMAS
Authors: Erica H. Bell, Peixin Zhang, Edward G. Shaw, Jan C. Buckner, Geoffrey R Barger, Stephen W. Coons, Dennis E. Bullard, Minesh P. Mehta, Mark R. Gilbert, Paul D. Brown, Keith J. Stelzer, Joseph P. McElroy, Jessica Fleming, Arup Chakraborty, Aline Paixao Becker, Kenneth D. Aldape, David G. Brachman, Albert D. Murtha, Christopher J Schultz, David Johnson, Stanley Z Gertler, Nadia N. Laack, Maria Werner-Wasik, Ian R. Crocker, Arnab Chakravarti
Journal: Neuro-Oncology (2016)

This study sought to determine the proportion of patients with 1p/19q co-deletion and its prognostic significance in the setting of NRG Oncology/RTOG 9802, a phase III trial of high-risk low-grade gliomas. Oncoscan and/or 450K methylation data were used to determine 1p/19q status. Univariable (UVAs) and multivariable analyses (MVAs) were performed using the Cox proportional hazard model. Hazard ratios for the effect of 1p/19q co-deletion on survival outcomes were calculated. Patient pretreatment characteristics and treatment assignment were included as covariates in MVAs. Of all the randomized and eligible patients in NRG Oncology/RTOG 9802, 77 (30.7%) had tissues available and sufficient DNA for profiling. Of these patients, 28 (36.4%) were 1p/19q co-deleted, 47 (61.0%) were non-co-deleted, and 2 (2.6%) were undeterminable. Majority (85.7%) of the co-deleted patients had oligodendroglioma as opposed to astrocytoma/oligoastrocytoma, whereas 17.0% of non-co-deleted patients had oligodendroglioma. Upon UVAs, 1p/19q co-deletion was significantly correlated with better OS (HR= 0.25; 95% CI: 0.11-0.55; p<0.001) and PFS (HR= 0.38; 95% CI 0.21-0.69; p <0.001). Upon MVAs, the statistical significance was maintained, with a HR=0.21 (95% CI: 0.09-0.46; p<0.001) for OS and a HR=0.35 (95% CI: 0.19-0.64; p<0.001) for PFS. 1p/19q co-deletion was a significant independent prognostic biomarker of high-risk low-grade gliomas in NRG Oncology/RTOG 9802. Our analyses underscore the prognostic value of 1p/19q co-deletion. Importantly, this is one of the first studies to validate its prognostic significance in a grade II cohort using rigorous MVAs with prospectively-collected, well-annotated clinical data. Analysis of 1p/19 co-deletion in combination with IDH mutations is ongoing and will be presented. Additional efforts are underway to increase our sample size for the predictive analyses. FUNDING: U10CA21661, U10CA180868, U10CA180822, and U10CA37422 (NCI). Also, R01CA108633, R01CA169368, RC2CA148190, U10CA180850-01 (NCI), Brain Tumor Funders Collaborative Grant, and The Ohio State University CCC (all to AC).
Pathology-targeted cell delivery via injectable micro-scaffold capsule mediated by endogenous TGase
Authors: Chunxiao Qi, Yaqian Li, Patrick Badger, Hongsheng Yu, Zhifeng You, Xiaojun Yan, Wei Liu, Yan Shi, Tie Xia, Jiahong Dong, Chenyu Huang, Yanan Du
Journal: Biomaterials (2017)
Prospective analysis in GIST patients on the role of alpha-1 acid glycoprotein (AGP) in imatinib exposure
Authors: S. Bins, K. Eechoute, J.S.L. Kloth, F.M. de Man, A. Oosten, P. de Bruijn, S. Sleijfer, R. Mathijssen
Journal: Annals of Oncology (2016)
Brief Chemoimmunotherapy R-FND with Rituximab Consolidation Followed by Randomization Between Rituximab Maintenance Vs. Observation As First Line Treatment in Elderly Patients with Advanced Follicular Lymphoma (FL): Final Results of a Prospective Randomized Trial by Italian Lymphoma Foundation (FIL)
Authors: Umberto Vitolo, Marco Ladetto, Carola Boccomini, Andrea Evangelista, Enrica Gamba, Eleonora Russo, Alessandra Tucci, Annalisa Chiarenza, Antonello Pinto, Amalia De Renzo, Francesco Zaja, Andrea Gallamini, Alessia Bari, Isabel Alvarez, Elisa Bernocco, Mario Petrini, Guido Parvis, Benedetta Puccini, Paolo Corradini, Tommasina Perrone, Sharon Supekar, Annalisa Chiappella, Barbara Botto, Barbara Mantoan, Federico De Angelis, Luca Baldini, Giuseppe Rossi
Journal: Blood (2011)
Screening for Lynch syndrome among endometrial cancer patients less than 60 years
Authors: E. Aguirre, M. Mele, N. Tuset, A. Velasco, J. Tarragona, M. Sampayo, S. Serrano, F. Riu, M. Rodriguez-Balada, X. Matias-Guiu, E. Garcia, E. Ortega, J. BalmaÑa
Journal: Annals of Oncology (2016)
Effectiveness and safety of Everolimus-Exemestane (EVE-EXE) in unselected patients (pts) with HR + /HER2- Metastatic Breast Cancer (MBC): Our experience in clinical practice
Authors: A. Mafodda, R. Giannicola, D. Azzarello, P. Del Medico, M. Raffaele, C. Giuffrè, R. Maisano
Journal: Annals of Oncology (2016)
ATIM-22. PLACEBO CONTROLLED DOUBLE BLIND PHASE IIB/III TRIAL OF AUTOLOGOUS FORMALIN-FIXED TUMOR VACCINE (AFTV-GBM) FOR NEWLY DIAGNOSED GLIOBLASTOMA
Authors: Takashi Maruyama
Journal: Neuro-Oncology (2016)

There has been a growing interest in therapeutic modalities based on tumor-specific immune reactions for glioblastoma(GBM). Autologous formalin-fixed tumor vaccine(AFTV) for GBM is an emerging innovative treatment approach, which aims at stimulating patient’s own immune system. Based on retrospectively analyzed clinical results of AFTV phase I/II trials, we are conducting double-blind phase IIb/III clinical trial. We have finished two phase I/II trials of AFTV in ACNU era and TMZ era. Newly diagnosed GBM with KPS>60, 16-75yo, more than 80% removal were enrolled for the analysis. Three courses of AFTV were administered after initial treatment radiation without chemotherapy in ACNU era (UMIN0002) and radiation with TMZ in TMZ era as first line therapy(UMIN1426). Median overall survival (mOS) and progression free survival (mPFS) were 19.8 and 7.6 months respectively in UMIN0002. Second AFTV trial resulted in 22,2 and 8,2 months in UMIN1426. There were no significant adverse events of more than grade2. The results of these trials demonstrate the feasibility of AFTV as concomitant treatment of 1stline therapy. We are ongoing multicenter double-blind prospective randomized phase II/III trial. The study is designed as prospective placebo-control double blind trial. 60 pts were enrolled for phase IIb part. Three course of AFTV were administered before, end and one month after initial treatment of chemo and radiation therapy. OS as primary endpoint and PFS, response rate and QOL are observing. We introduce the rationale and study design of this clinical trial.
Retargeting of Citokine-Induced Killer (CIK) Cells with Molecularly Engrafted T-Cell Receptors (TCR): A Preclinical in Vitro and In Vivo Study
Authors: Angela Rita Elia, Giorgio Inghirami, Paola Circosta, Flavio Cristofani, Nathalie Santoro, Dario Sangiolo, Corrado Tarella, Alessandro Cignetti
Journal: Blood (2011)
Effect of Methyl Aminolevulinate Photodynamic Therapy With and Without Ablative Fractional Laser Treatment in Patients With Microinvasive Squamous Cell Carcinoma
Authors: Seung-Hwan Choi, Ki-Ho Kim, Ki-Hoon Song
Journal: JAMA Dermatology (2017)

<h3>Importance</h3> Surgical excision is the standard treatment for cutaneous squamous cell carcinoma (SCC). However, microinvasive SCC (Clark level II) is limited to the papillary dermis, and it should be differentiated from invasive SCC. Ablative fractional laser-primed photodynamic therapy (AFL-PDT) may have enhanced efficacy. <h3>Objective</h3> To compare 1 session of AFL-PDT with 2 sessions of conventional methyl aminolevulinate-PDT (MAL-PDT) for the treatment of microinvasive SCC. <h3>Design, Setting, and Participants</h3> A 2-armed, randomized, single-blind, comparative trial of 45 patients with histologically proven microinvasive SCC. Twenty-one patients were randomized to treatment with a single AFL-PDT session, and 24 patients were randomized to 2 MAL-PDT sessions with a 1-week interval between sessions using a computer-generated program. Standard pretreatment such as curettage was not performed prior to PDT owing to a tendency to bleed. The efficacy, recurrence rate, cosmetic outcomes, and safety were assessed 1 week, 3, 12, and 24 months after the last treatment. <h3>Interventions</h3> AFL was performed with an ablation depth of 550 µm to 600 µm, coagulation level of 1, treatment density of 22%, and a single pulse. Then, MAL cream was applied under occlusion for 3 hours and illuminated by using a red light-emitting diode light at 37 J/cm<sup>2</sup>. A second session of MAL-PDT was administered after 7 days. <h3>Main Outcomes and Measures</h3> The primary outcome measures were the lesion response at 3 and 12 months, and the recurrence rate 12 months after the last treatment. <h3>Results</h3> Twenty-one patients (6 men, 15 women) with a mean (SD) age of 76 (6) years were randomized to treatment with a single AFL-PDT session, and 24 patients (11 men, 13 women) with a mean (SD) age of 75 (6) years were randomized to 2 MAL-PDT sessions. The overall complete response rates 3 months after treatment were 84.2% with AFL-PDT and 52.4% with MAL-PDT (<i>P</i> = .03). These differences in efficacy remained significant at the 24-month follow-up. The recurrence rate was significantly lower with AFL-PDT (12.5%) than with MAL-PDT (63.6%) at 24 months (<i>P</i> = .006). AFL-PDT and MAL-PDT did not differ significantly with respect to the cosmetic outcomes, adverse events, or pain intensity. <h3>Conclusions and Relevance</h3> AFL-PDT can be used as an alternative treatment option for patients with microinvasive SCC who are not suitable for surgical treatment. <h3>Trial Registration</h3> clinicaltrials.gov Identifier:NCT02666534
A Phase I/II Dose Escalation Trial of ONCOHIST® (Recombinant Human Histone H1.3) in Patients with Relapsed or Refractory Acute Myeloid Leukemia.
Authors: Michael Zeppezauer, Grazina Formicka-Zeppezauer, Peter Gross, Hans Joernvall, Joerg Schubert, Michael Pfreundschuh
Journal: Blood (2007)
Implementation of An Aggressive Risk Stratified Treatment Protocol for Children and Adolescents with Acute Lymphoblastic Leukemia in a Developing Country
Authors: Samar A. Muwakkit, Carol Al-Aridi, Ahmad Samra, Raya Saab, Rami Mahfouz, Chantal Farra, Sima Jeha, Miguel R. Abboud
Journal: Blood (2011)
Association between polymorphisms in the leptin promoter and leptin receptor genes and cancer in a mediterranean population of the PREDIMED study
Authors: J.B. Ramirez Sabio, J.V. Sorlí, C. Ortega-Azorín, P. Carrasco, O. Portolés, E.M. Asensio, D. Corella
Journal: Annals of Oncology (2016)
Frequency of driver mutations in EGFR wt NSCLC using mass spectrometry: Experience of Area Vasta Romagna
Authors: E. Chiadini, L. Capelli, A. Delmonte, N. De Luigi, C. Dazzi, C. Casanova, A. Gamboni, M. Papi, M.M. Tumedei, S. Bravaccini, A. Dubini, M. Puccetti, L. Crinò, P. Ulivi
Journal: Annals of Oncology (2016)
Efficacy of osimertinib in combination with Hedgehog pathway inhibitors in reverting T790M-mediated resistence
Authors: G. Esposito, C.M. Della Corte, F. Papaccio, G. Viscardi, M. Fasano, T. Troiani, E. Martinelli, F. Ciardiello, F. Morgillo
Journal: Annals of Oncology (2016)
Incidence and Prognostic Impact of SNPs Regulating PU.1 Gene Expression in AML
Authors: Nicolas Boissel, Olivier Nibourel, Jean-Baptiste Micol, Nathalie Philippe, M. Crepin, Aline Renneville, Christine Terre, Sylvie Castaigne, Xavier Thomas, Herve Dombret, Claude Preudhomme
Journal: Blood (2008)
Appendiceal neuroendocrine tumors: a large multicentre Italian series. Preliminary result
Authors: G. Lamberti, G. Rossi, F. Grillo, F. Spada, S. Pusceddu, M. Rinzivillo, S. Massironi, S. Tafuto, A. Faggiano, L. Antonuzzo, G. Luppi, M. Albertelli, N. Fazio, C. Vernieri, G. Delle Fave, N. Brighi, D. Ferone, D. Campana
Journal: Annals of Oncology (2016)
French real-life efficacy of 1st line gefitinib in EGFR mutation-positive NSCLC in the prospective EPIDAURE study: Results by EGFR exon 19 Del and L858R mutation subtypes
Authors: M. Perol, J.-F. Morère, E. Fabre, B. Lemaire, I. Monnet, E. Brambilla, V. Rondeau, M. Licour, J. Cadranel
Journal: Annals of Oncology (2016)
ACE and CXCL10 as predictive biomarkers in the LEA study
Authors: Jdela Haba, E. Aranda Aguilar, S. Morales, J.A. García-Sáenz, A. Guerrero, N. Martínez, A. Antón, M. Muñoz, M. Ramos, M. Gil-Gil, M. Margelí, S. Servitja, B. Bermejo, J. Cruz, A. Rodríguez Lescure, M. Casas, M. Sánchez-Aragó, R. Caballero, E. Carrasco, M. Martin
Journal: Annals of Oncology (2016)
PDTB-25. YAP FUNCTION IN PEDIATRIC GLIOBLASTOMAS
Authors: Renee Read, Anna Kenney, Matthew Schniederjan, Jeffrey J. Olson
Journal: Neuro-Oncology (2016)

Malignant high-grade gliomas (HGGs), neoplasms of glial cells and their precursors, such as glioblastomas (GBMs) and diffuse intrinsic pontine gliomas (DIPGs), are the most deadly primary brain tumors in children, and are incurable with current therapies. The most frequent genetic lesions in pediatric HGGs (pHGGs) include amplification/mutation/overexpression of receptor tyrosine kinases (RTKs), such as PDGFRA, and neomorphic K27M mutations in histone H3 proteins that dominantly block H3-K27 methylation and prevent normal epigenetic gene silencing. Current data indicates that RTK signaling and H3-K27M mutations cooperate to drive tumor pathology and confer therapeutic resistance. To understand how these mutations drive tumorigenesis, my research program uses a multidisciplinary approach that includes functional screening in Drosophila glioma models and drug testing in patient-derived HGG tumor stem cell cultures. Our studies yielded strong preliminary evidence that the YAP transcriptional activator is overexpressed and activated in RTK-mutant pHGG cells, and that YAP transcriptional activity is required for proliferation and survival of pHGG cells, particularly in pHGGs harboring H3-K27M mutations. YAP family transcription factors can normally stimulate expansion of stem/progenitor cell populations in response to physiological RTK signaling. Established YAP transcriptional target genes, which are normally controlled by methylation and epigenetic silencing, include genes that can drive HGG tumor cell self-renewal, proliferation, and therapeutic resistance when overexpressed. Therefore, we hypothesize that, as a consequence of oncogenic RTK alterations, YAP becomes constitutively activated to drive a gene expression program that promotes uncontrolled expansion of neural stem/progenitor cells to create malignant tumors, and that this is exacerbated by H3-K27M epigenetic dysregulation. In testing this hypothesis, we generated compelling preliminary data showing that inhibition of YAP specifically provokes growth arrest and cell death of RTK-overexpressing H3-K27M-mutant pHGG cells. Our research indicates that YAP inhibition may be a promising therapeutic strategy for pHGGs.
Subcutaneous Bortezomib in Combination Regimens in Newly Diagnosed Patients with Myeloma or Systemic AL Amyloidosis: High Response Rates and Minimal Toxicity.
Authors: Gunjan L Shah, Esha Kaul, Shelly Fallo, Furha I. Cossor, Hedy Smith, Andreas K. Klein, Kenneth B. Miller, Raymond L. Comenzo
Journal: Blood (2012)
IMST-54. GLIOBLASTOMA EXTRACELLULAR VESICLES INDUCE IMMUNOSUPPRESSION VIA PD-L1
Authors: Timothy Peterson, Jasmine Tyson
Journal: Neuro-Oncology (2016)

Glioblastoma multiforme (GBM) induces potent immunosuppression both within the tumor and systemically. The mechanisms underlying this have not been fully elucidated. GBM shed large numbers of extracellular vesicles (EV’s). Here, we test the hypothesis that GBM-EV’s contribute to immunosuppression. EV’s were isolated from cultured human GBM cell lines, GBM patient serum, and healthy donor serum by serial centrifugation. Nanosight nanoparticle tracking was used to determine EV frequency and size distribution. Western blot and ELISA were used to determine tumor-associated antigen and PD-L1 expression. GBM EV’s from wild type and PD-L1-overexpressing cells were cultured with healthy donor CD14+ monocytes or CD3+ T cells. Binding was determined by confocal microscopy. Induction of CD14+/HLA-DR- monocytic myeloid-derived suppressor cells (MDSC’s) and CD4+ and CD8+ regulatory T cells (Treg) were determined by flow cytometry. T cell proliferation was assessed by flow cytometry and CFSE staining. GBM’s shed large amounts of EV’s including both exosomes (<100nm) and microvesicles (100-500nm) in vitro. EV’s with similar size distribution are found in GBM patients’ serum at increased frequency compared with healthy donors. Tumor-associated antigens (ErbB2, MAGEA3) can be detected in GBM patients’ serum EV’s. Some GBM-derived EV’s express the immunosuppressive protein PD-L1 and bind both T cells and monocytes through PD-1. GBM EV’s induce MDSC differentiation in normal monocytes in vitro(27.5%+/-5.62%) compared to media (5.24%+/-0.77; P=0.0078) and this was further increased by PD-L1 overexpressing EV’s (54.28%+/-5.48%; P=0.0143). GBM EV-induced MDSC’s inhibited T cell proliferation in response to anti-CD3 (65.98%+/-5.64% vs. 40.40%+/-7.99%; P=0.0399). GBM EV’s also showed trends towards inducing both CD4 and CD8 Treg’s in a PD-L1-dependent fashion. GBM EV’s contain both immunosuppressive molecules and tumor-associated antigens. Their presence in GBM patients’ serum suggests potential to mediate systemic immunosuppression. In keeping with this, GBM EV’s induce immunosuppressive changes in leukocytes in a PD-L1-dependent fashion.
Donor-Recipient HLA-Matching of Unrelated Cord Blood Units At High-Resolution Reveals High Degrees of HLA-Mismatch and Alters Graft Selection
Authors: Parastoo B Dahi, Doris M Ponce, Katherine L Evans, Marissa N Lubin, Anne Marie R Gonzales, Courtney Byam, Rosanna Ferrante, Melissa Sideroff, Deborah Wells, Sergio A. Giralt, Nancy A. Kernan, Andromachi Scaradavou, Juliet N Barker
Journal: Blood (2012)
Modelling relapse in patients with high-risk localised prostate cancer treated randomly in the GETUG 12 phase III trial reveals two populations of relapsing patients
Authors: C. Vicier, L. Faivre, F. Lesaunier, R. Delva, G. Gravis, F. Rolland, F. Priou, J.-M. Ferrero, N. Houede, L. Mourey, C. Theodore, I. Krakowski, J.-F. Berdah, M. Baciuchka, B. Laguerre, A. Flechon, S. Oudard, M. Habibian, S. Culine, K. Fizazi
Journal: Annals of Oncology (2016)
Complex chromosomal rearrangements by single catastrophic pathogenesis in NUT midline carcinoma
Authors: J.-K. Lee, S. Louzada, Y. An, S.Y. Kim, S. Kim, J. Youk, S. Park, S.H. Koo, B. Keam, Y.K. Jeon, J.-L. Ku, F. Yang, T.M. Kim, Y.S. Ju
Journal: Annals of Oncology (2016)

Nuclear protein in testis (NUT) midline carcinoma (NMC) is a rare aggressive malignancy often occurring in the tissues of midline anatomical structures. Except for the pathognomonic BRD3/4-NUT rearrangement, the comprehensive landscape of genomic alterations in NMCs has been unexplored.We investigated three NMC cases, including two newly diagnosed NMC patients in Seoul National University Hospital, and a previously reported cell line (Ty-82). Whole-genome and transcriptome sequencing were carried out for these cases, and findings were validated by multiplex fluorescence in situ hybridization and using individual fluorescence probes.Here, we present the first integrative analysis of whole-genome sequencing, transcriptome sequencing and cytogenetic characterization of NUT midline carcinomas. By whole-genome sequencing, we identified a remarkably similar pattern of highly complex genomic rearrangements (previously denominated as chromoplexy) involving the BRD3/4-NUT oncogenic rearrangements in two newly diagnosed NMC cases. Transcriptome sequencing revealed that these complex rearrangements were transcribed as very simple BRD3/4-NUT fusion transcripts. In Ty-82 cells, we also identified a complex genomic rearrangement involving the BRD4-NUT rearrangement underlying the simple t(15;19) karyotype. Careful inspections of rearrangement breakpoints indicated that these rearrangements were likely attributable to single catastrophic events. Although the NMC genomes had >3000 somatic point mutations, canonical oncogenes or tumor suppressor genes were rarely affected, indicating that they were largely passenger events. Mutational signature analysis showed predominant molecular clock-like signatures in all three cases (accounting for 54%-75% of all base substitutions), suggesting that NMCs may arise from actively proliferating normal cells.Taken together, our findings suggest that a single catastrophic event in proliferating normal cells could be sufficient for neoplastic transformation into NMCs.
Targeting Hedgehog in pancreatic cancer: An innovative approach but not for all tumors.
Authors: Kalliopi Andrikou, Luca Faloppi, Cristian Loretelli, Alessandra Mandolesi, Maristella Bianconi, Mario Scartozzi, Rossana Berardi, Italo Bearzi, Stefano Cascinu
Journal: Journal of Clinical Oncology (2013)

205 Background: Exocrine pancreatic cancer is the fifth cause of cancer-related death in Europe and has a very poor prognosis for all disease stages. To date no medical treatment has significantly increased patients' survival. One of the reasons for pancreatic cancer's chemoresistance is the complex tumor architecture: cancer cells are surrounded by a dense desmoplastic stroma that blocks drugs delivery. Moreover, pancreatic cancer is characterized by a marked heterogeneity of cells, including cancer stem cells (CSCs) that act as tumor-initiating cells and hierarchically control the differentiated cancer cells. Recent studies in multiple pancreatic cancer model systems have implicated the Hedgehog signaling pathway in these tumor-stromal interactions. The Hedgehog signaling pathway, a crucial regulator of proliferation and differentiation during embryonic development, has been reported to be aberrant and SMO overexpression seems to be a mechanism of activation of this pathway in human pancreatic cancer fibroblasts. Several studies are ongoing to evaluate the potential role of Hedgehog inhibitors, we investigated the contribution of Hedgehog to pancreatic progression and aggressiveness, evaluating the associated of stemness and desmoplastic reaction. Methods: In 110 histological samples of pancreatic ductal adenocarcinoma were performed molecular biology assessment of SPARC, CD133, CD44, CD24, OCT3/4, SHH, IHH, DHH, SMO, PTCH1, PTCH2. Results: Our analysis showed a strictly correlation between overexpression of SMO and high levels of SPARC (p=0.0005) and stemness markers CD133 (p=0.04) and OCT3/4 (p=0.0023) Conclusions: Our data demonstrate a critical and conserved role of Hedgehog signaling in the regulation of stem cell lineages and in the determination of a pronounced desmoplastic reaction determining chemoresistance and disease progression. We can speculate that patients with an aggressive profile defined by SMO overexpression would be the best candidates for treatment with Hedgehog inhibitors. This evidence suggests that this pathway may hold promise for new therapeutic approaches.
Inmune Reconstitution After Autologous Stem Cell Trasplantation: Is There Any Difference Between HIV+ and HIV- Patients?
Authors: Mariana Bastos Oreiro, Alicia Roldan, Javier Anguita, Cristina Pascual, Ana Perez, Pascual Balsalobre, Mi Kwon, Gabriela Rodriguez Macias, Jorge Gayoso, Ismael Buno, Jose Luis Diez-Martin
Journal: Blood (2012)
Autologous Hematopoetic Stem Cell Transplantation as An Intensive Consolidation Therapy for Adult Patients in Remission from Acute Myeloid Leukemia.
Authors: Sonja G Genadieva-Stavrik, Alexandra Pivkova, Zlate Stojanoski, Svetlana Krstevska-Balkanov, Borce Georgievski
Journal: Blood (2010)