tbuckley/cabot-search huggingface dataset:
Genetic Predisposition to an Impaired Metabolism of the Branched-Chain Amino Acids and Risk of Type 2 Diabetes: A Mendelian Randomisation Analysis
Authors: Luca A. Lotta, Robert A. Scott, Stephen J. Sharp, Stephen Burgess, Jian’an Luan, Therese Tillin, Amand F. Schmidt, Fumiaki Imamura, Isobel D. Stewart, John R. B. Perry, Luke Marney, Albert Koulman, Edward D. Karoly, Nita G. Forouhi, Rasmus J. O. Sjögren, Erik Näslund, Juleen R. Zierath, Anna Krook, David B. Savage, Julian L. Griffin, Nishi Chaturvedi, Aroon D. Hingorani, Kay-Tee Khaw, Inês Barroso, Mark I. McCarthy, Stephen O’Rahilly, Nicholas J. Wareham, Claudia Langenberg
Journal: PLoS Medicine (2016)

Background Higher circulating levels of the branched-chain amino acids (BCAAs; i.e., isoleucine, leucine, and valine) are strongly associated with higher type 2 diabetes risk, but it is not known whether this association is causal. We undertook large-scale human genetic analyses to address this question. Methods and Findings Genome-wide studies of BCAA levels in 16,596 individuals revealed five genomic regions associated at genome-wide levels of significance (p < 5 × 10−8). The strongest signal was 21 kb upstream of the PPM1K gene (beta in standard deviations [SDs] of leucine per allele = 0.08, p = 3.9 × 10−25), encoding an activator of the mitochondrial branched-chain alpha-ketoacid dehydrogenase (BCKD) responsible for the rate-limiting step in BCAA catabolism. In another analysis, in up to 47,877 cases of type 2 diabetes and 267,694 controls, a genetically predicted difference of 1 SD in amino acid level was associated with an odds ratio for type 2 diabetes of 1.44 (95% CI 1.26–1.65, p = 9.5 × 10−8) for isoleucine, 1.85 (95% CI 1.41–2.42, p = 7.3 × 10−6) for leucine, and 1.54 (95% CI 1.28–1.84, p = 4.2 × 10−6) for valine. Estimates were highly consistent with those from prospective observational studies of the association between BCAA levels and incident type 2 diabetes in a meta-analysis of 1,992 cases and 4,319 non-cases. Metabolome-wide association analyses of BCAA-raising alleles revealed high specificity to the BCAA pathway and an accumulation of metabolites upstream of branched-chain alpha-ketoacid oxidation, consistent with reduced BCKD activity. Limitations of this study are that, while the association of genetic variants appeared highly specific, the possibility of pleiotropic associations cannot be entirely excluded. Similar to other complex phenotypes, genetic scores used in the study captured a limited proportion of the heritability in BCAA levels. Therefore, it is possible that only some of the mechanisms that increase BCAA levels or affect BCAA metabolism are implicated in type 2 diabetes. Conclusions Evidence from this large-scale human genetic and metabolomic study is consistent with a causal role of BCAA metabolism in the aetiology of type 2 diabetes.
Combining Anti-Mir-155 with Chemotherapy for the Treatment of Lung Cancers
Authors: Katrien Van Roosbroeck, Francesca Fanini, Tetsuro Setoyama, Cristina Ivan, Cristian Rodriguez-Aguayo, Enrique Fuentes-Mattei, Lianchun Xiao, Ivan Vannini, Roxana S. Redis, Lucilla D'Abundo, Xinna Zhang, Milena S. Nicoloso, Simona Rossi, Vianey Gonzalez-Villasana, Rajesha Rupaimoole, Manuela Ferracin, Fortunato Morabito, Antonino Neri, Peter P. Ruvolo, Vivian R. Ruvolo, Chad V. Pecot, Dino Amadori, Lynne Abruzzo, Steliana Calin, Xuemei Wang, M. James You, Alessandra Ferrajoli, Robert Orlowski, William Plunkett, Tara M. Lichtenberg, Ramana V. Davuluri, Ioana Berindan-Neagoe, Massimo Negrini, Ignacio I. Wistuba, Hagop M. Kantarjian, Anil K. Sood, Gabriel Lopez-Berestein, Michael J. Keating, Muller Fabbri, George A. Calin
Journal: Clinical Cancer Research (2016)

Purpose: The oncogenic miR-155 is upregulated in many human cancers, and its expression is increased in more aggressive and therapy-resistant tumors, but the molecular mechanisms underlying miR-155-induced therapy resistance are not fully understood. The main objectives of this study were to determine the role of miR-155 in resistance to chemotherapy and to evaluate anti-miR-155 treatment to chemosensitize tumors.Experimental Design: We performed in vitro studies on cell lines to investigate the role of miR-155 in therapy resistance. To assess the effects of miR-155 inhibition on chemoresistance, we used an in vivo orthotopic lung cancer model of athymic nude mice, which we treated with anti-miR-155 alone or in combination with chemotherapy. To analyze the association of miR-155 expression and the combination of miR-155 and TP53 expression with cancer survival, we studied 956 patients with lung cancer, chronic lymphocytic leukemia, and acute lymphoblastic leukemia.Results: We demonstrate that miR-155 induces resistance to multiple chemotherapeutic agents in vitro, and that downregulation of miR-155 successfully resensitizes tumors to chemotherapy in vivo We show that anti-miR-155-DOPC can be considered non-toxic in vivo We further demonstrate that miR-155 and TP53 are linked in a negative feedback mechanism and that a combination of high expression of miR-155 and low expression of TP53 is significantly associated with shorter survival in lung cancer.Conclusions: Our findings support the existence of an miR-155/TP53 feedback loop, which is involved in resistance to chemotherapy and which can be specifically targeted to overcome drug resistance, an important cause of cancer-related death. Clin Cancer Res; 23(11); 2891-904. ©2016 AACR.
MRI Prospective Survey on Cardiac and Hepatic Iron in Thalassemia Intermedia Patients Treated with Desferrioxamine, Deferiprone and Deferasirox
Authors: Antonella Meloni, Aurelio Maggio, Anna Pietrapertosa, Pier Paolo Bitti, Sabrina Armari, Antonio Cardinale, Maria Paola Carta, Paolo Preziosi, Elisabetta Chiodi, Vincenzo Positano, Maria Giovanna Neri, Alessia Pepe
Journal: Blood (2014)
In Vitro Decitabine Treatment Demonstrates Heterogeneous Changes in Methylation and Gene Expression in Primary AML Samples.
Authors: David H Spencer, Jeffery M. Klco, Tamara Lamprecht, Todd Wylie, Vincent Magrini, Jasreet Hundal, Jason Walker, Nobish Varghese, Matthew R Meyer, Petra Gilmore, Reid Townsend, Elaine R. Mardis, Timothy J. Ley
Journal: Blood (2012)
Quitting smoking reduces mortality at any age, study of over 70s finds
Authors: Susan Mayor
Journal: BMJ (2016)

Quitting smoking at any age is associated with reduced mortality, as a study in people aged over 70 found that current smokers had higher mortality than former smokers, including those who quit in their 60s.1

Most studies on smoking and mortality have focused on middle aged populations, and little evidence existed of the benefit of quitting in elderly people.

The new study …
FTY720-Induced Sequestration of Donor T Cells in Lymph Nodes Leads to Activation-Induced Apoptosis of Alloreactive T Cells and Reduced Graft-Versus-Host Disease.
Authors: Daigo Hashimoto, Shoji Asakura, Ken-ichi Matsuoka, Yukimi Sakoda, Mitsune Tanimoto, Takanori Teshima
Journal: Blood (2004)
Bortezomib with Dexamethasone in Newly Diagnosed Patients with Primary Systemic Light Chain Amyloidosis or Multiple Myeloma-Associated AL Amyloidosis
Authors: Beihui Huang, Juan Li, Junru Liu, Dong Zheng, Mei Chen, Zhenhai Zhou, Duorong Xu, Waiyi Zou
Journal: Blood (2012)
Clinical Efficacy of Lenalidomide in Fludarabine-Refractory Chronic Lymphocytic Leukemia Patients.
Authors: Asher A. Chanan-Khan, Myron S. Czuczman, Swaminathan Padmanabhan, Michael J. Keating, Susan M. O’Brien, William G. Wierda, Alessandra Ferrajoli
Journal: Blood (2007)
Hepcidin detects iron deficiency in <scp>S</scp>ri <scp>L</scp>ankan adolescents with a high burden of hemoglobinopathy: A diagnostic test accuracy study
Authors: Katherine Wray, Angela Allen, Emma Evans, Chris Fisher, Anuja Premawardhena, Lakshman Perera, Rexan Rodrigo, Gayan Goonathilaka, Lebbe Ramees, Craig Webster, Andrew E Armitage, Andrew M Prentice, David J Weatherall, Hal Drakesmith, Sant‐Rayn Pasricha
Journal: American Journal of Hematology (2016)

Abstract Anemia affects over 800 million women and children globally. Measurement of hepcidin as an index of iron status shows promise, but its diagnostic performance where hemoglobinopathies are prevalent is unclear. We evaluated the performance of hepcidin as a diagnostic test of iron deficiency in adolescents across Sri Lanka. We selected 2273 samples from a nationally representative cross‐sectional study of 7526 secondary schoolchildren across Sri Lanka and analyzed associations between hepcidin and participant characteristics, iron indices, inflammatory markers, and hemoglobinopathy states. We evaluated the diagnostic accuracy of hepcidin as a test for iron deficiency with estimation of the AUC ROC , sensitivity/specificity at each hepcidin cutoff, and calculation of the Youden Index to find the optimal threshold. Hepcidin was associated with ferritin, sTfR, and hemoglobin. The AUC ROC for hepcidin as a test of iron deficiency was 0.78; hepcidin outperformed Hb and sTfR. The Youden index‐predicted cutoff to detect iron deficiency (3.2 ng/mL) was similar to thresholds previously identified to predict iron utilization and identify deficiency in African populations. Neither age, sex, nor α‐ or β‐thalassemia trait affected diagnostic properties of hepcidin. Hepcidin pre‐screening would prevent most iron‐replete thalassemia carriers from receiving iron whilst still ensuring most iron deficient children were supplemented. Our data indicate that the physiological relationship between hepcidin and iron status transcends specific populations. Measurement of hepcidin in individuals or populations could establish the need for iron interventions.
Impact of Rituximab-Based Therapy After Histological Transformation on High-Dose Therapy and Autologous Stem Cell Transplantation in Follicular Transformed Lymphomas
Authors: Jose Manuel Calvo-Villas, Alejandro Martín, Carlos Panizo, Juan Manuel Sancho, Alba Redondo, José David González-Sanmiguel, Blanca Sanchez Gonzalez, Maria José Requena, Eva González-Barca, María José Rodríguez-Salazar, Nerea Castro, Viviana Paredes, Jorge Gayoso, Dolores Caballero
Journal: Blood (2011)
Higher Doses of Transplanted CD34+, CD3+ and CD8+ Cells Are Associated with Better Donor T-Cell Chimerism and Less Graft Rejection, but Not with GVHD after Nonmyeloablative Conditioning for Unrelated Hematopoietic Cell Transplantation.
Authors: Frederic Baron, Michael Maris, Barry Storer, Brenda Sandmaier, Jens Panse, Thomas Chauncey, Mohamed Sorror, Marie Terese Little, David Maloney, Rainer Storb, Shelly Heimfeld
Journal: Blood (2004)
Recombinant DEK Regulates Hematopoietic Stem and Progenitor Cells in a CXCR2- GαI Protein-Dependent Manner
Authors: Maegan L. Capitano, Nirit Mor-Vaknin, Maureen Legendre, Scott Cooper, David Markovitz, Hal E. Broxmeyer
Journal: Blood (2014)
New insights into the generation and role of de novo mutations in health and disease
Authors: Rocio Acuna-Hidalgo, Joris A. Veltman, Alexander Hoischen
Journal: Genome biology (2016)

Aside from inheriting half of the genome of each of our parents, we are born with a small number of novel mutations that occurred during gametogenesis and postzygotically. Recent genome and exome sequencing studies of parent–offspring trios have provided the first insights into the number and distribution of these de novo mutations in health and disease, pointing to risk factors that increase their number in the offspring. De novo mutations have been shown to be a major cause of severe early-onset genetic disorders such as intellectual disability, autism spectrum disorder, and other developmental diseases. In fact, the occurrence of novel mutations in each generation explains why these reproductively lethal disorders continue to occur in our population. Recent studies have also shown that de novo mutations are predominantly of paternal origin and that their number increases with advanced paternal age. Here, we review the recent literature on de novo mutations, covering their detection, biological characterization, and medical impact.
Interferon regulatory factor 2 protects mice from lethal viral neuroinvasion
Authors: Melody M.H. Li, Leonia Bozzacco, Hans-Heinrich Hoffmann, Gaëlle Breton, Jakob Loschko, Jing W. Xiao, Sébastien Monette, Charles M. Rice, Margaret R. MacDonald
Journal: The Journal of Experimental Medicine (2016)

The host responds to virus infection by activating type I interferon (IFN) signaling leading to expression of IFN-stimulated genes (ISGs). Dysregulation of the IFN response results in inflammatory diseases and chronic infections. In this study, we demonstrate that IFN regulatory factor 2 (IRF2), an ISG and a negative regulator of IFN signaling, influences alphavirus neuroinvasion and pathogenesis. A Sindbis virus strain that in wild-type (WT) mice only causes disease when injected into the brain leads to lethal encephalitis in Irf2−/− mice after peripheral inoculation. Irf2−/− mice fail to control virus replication and recruit immune infiltrates into the brain. Reduced B cells and virus-specific IgG are observed in the Irf2−/− mouse brains despite the presence of peripheral neutralizing antibodies, suggesting a defect in B cell trafficking to the central nervous system (CNS). B cell–deficient μMT mice are significantly more susceptible to viral infection, yet WT B cells and serum are unable to rescue the Irf2−/− mice. Collectively, our data demonstrate that proper localization of B cells and local production of antibodies in the CNS are required for protection. The work advances our understanding of host mechanisms that affect viral neuroinvasion and their contribution to immunity against CNS infections.
Brief Report: Vitamin D Deficiency Is Associated With Endothelial Dysfunction and Increases Type I Interferon Gene Expression in a Murine Model of Systemic Lupus Erythematosus
Authors: John A. Reynolds, Avi Z. Rosenberg, Carolyne K. Smith, Jamie C. Sergeant, Gillian I. Rice, Tracy A. Briggs, Ian N. Bruce, Mariana J. Kaplan
Journal: Arthritis & Rheumatology (2016)

Patients with systemic lupus erythematosus (SLE) have an increased risk of cardiovascular disease (CVD) and impaired endothelial repair. Although vitamin D deficiency is associated with increased CVD risk in the general population, a causal relationship has not been demonstrated. We aimed to determine whether vitamin D deficiency directly modulates endothelial dysfunction and immune responses in a murine model of SLE.Vitamin D deficiency was induced in lupus-prone MRL/lpr mice by dietary restriction for 6 weeks. Endothelium-dependent vasorelaxation was quantified using aortic ring myography, and endothelial repair mechanisms were assessed by evaluating the phenotype and function of bone marrow endothelial progenitor cells (EPCs) and with the use of an in vivo Matrigel plug model. Lupus disease activity was determined by evaluating expression of interferon-stimulated genes (ISGs) in splenic tissue, positivity for serum autoantibodies, and renal histology. To validate the findings, expression of ISGs was also measured in whole blood from vitamin D-deficient and vitamin D-sufficient patients with SLE.Vitamin D deficiency resulted in impaired endothelium-dependent vasorelaxation and decreases in neoangiogenesis without a change in the total number of EPCs. There were no differences in anti-double-stranded DNA titers, proteinuria, or glomerulonephritis (activity or chronicity) between vitamin D-deficient or sufficient mice. Vitamin D deficiency was associated with a trend toward increased ISG expression both in mice and in patients with SLE.These findings indicate that vitamin D deficiency is associated with hampered vascular repair and reduced endothelial function, and may modulate type I interferon responses.
Factors Affecting Quality of Life During and After Stem Cell Transplantation in Long Term Survivors – Comparison of Autologous and Allogeneic Stem Cell Transplantation
Authors: Katerina Benesova, Marie Trnkova, Miriam Lanska, Veronika Valkova, Katerina Steinerova, Zdenek Koristek, Jan Novak, Ludek Raida, Petra Keslova, Blanka Vackova, Klara Kruntoradova, Tomas Dolezal, Marek Trneny
Journal: Blood (2012)
GWAS of clinically defined gout and subtypes identifies multiple susceptibility loci that include urate transporter genes
Authors: Akiyoshi Nakayama, Hirofumi Nakaoka, Ken Yamamoto, Masayuki Sakiyama, Amara Shaukat, Yu Toyoda, Yukinori Okada, Yoichiro Kamatani, Takahiro Nakamura, Tappei Takada, Katsuhisa Inoue, Tomoya Yasujima, Hiroaki Yuasa, Yuko Shirahama, Hiroshi Nakashima, Seiko Shimizu, Toshihide Higashino, Yusuke Kawamura, Hiraku Ogata, Makoto Kawaguchi, Yasuyuki Ohkawa, Inaho Danjoh, Atsumi Tokumasu, Keiko Ooyama, Toshimitsu Ito, Takaaki Kondo, Kenji Wakai, Blanka Stiburkova, Karel Pavelka, Lisa K Stamp, Nicola Dalbeth, Yutaka Sakurai, Hiroshi Suzuki, Makoto Hosoyamada, Shin Fujimori, Takashi Yokoo, Tatsuo Hosoya, Ituro Inoue, Atsushi Takahashi, Michiaki Kubo, Hiroshi Ooyama, Toru Shimizu, Kimiyoshi Ichida, Nariyoshi Shinomiya, Tony R Merriman, Hirotaka Matsuo
Journal: Annals of the Rheumatic Diseases (2016)

Objective A genome-wide association study (GWAS) of gout and its subtypes was performed to identify novel gout loci, including those that are subtype-specific. Methods Putative causal association signals from a GWAS of 945 clinically defined gout cases and 1213 controls from Japanese males were replicated with 1396 cases and 1268 controls using a custom chip of 1961 single nucleotide polymorphisms (SNPs). We also first conducted GWASs of gout subtypes. Replication with Caucasian and New Zealand Polynesian samples was done to further validate the loci identified in this study. Results In addition to the five loci we reported previously, further susceptibility loci were identified at a genome-wide significance level (p&lt;5.0×10 −8 ): urate transporter genes ( SLC22A12 and SLC17A1 ) and HIST1H2BF-HIST1H4E for all gout cases, and NIPAL1 and FAM35A for the renal underexcretion gout subtype. While NIPAL1 encodes a magnesium transporter, functional analysis did not detect urate transport via NIPAL1, suggesting an indirect association with urate handling. Localisation analysis in the human kidney revealed expression of NIPAL1 and FAM35A mainly in the distal tubules, which suggests the involvement of the distal nephron in urate handling in humans. Clinically ascertained male patients with gout and controls of Caucasian and Polynesian ancestries were also genotyped, and FAM35A was associated with gout in all cases. A meta-analysis of the three populations revealed FAM35A to be associated with gout at a genome-wide level of significance (p meta =3.58×10 −8 ). Conclusions Our findings including novel gout risk loci provide further understanding of the molecular pathogenesis of gout and lead to a novel concept for the therapeutic target of gout/hyperuricaemia.
The Effects of Co-Stimulatory Endodomains on the Fate of T Cells Expressing a Tumor Directed Chimeric Antigen Receptor (CAR) In Human Subjects with B Cell Malignancies
Authors: Barbara Savoldo, Carlos A. Ramos, Catherine M. Bollard, Enli Liu, Martha Mims, Michael Keating, Adrian P. Gee, Zhuyong Mei, Cliona M Rooney, Helen E Heslop, Malcolm K. Brenner, Gianpietro Dotti
Journal: Blood (2010)
The Hybrid Regimen of ABVD/BEACOPP May Overcome the High-Risk Features of the Advanced Stage Hodgkin Lymphoma
Authors: Ahmed Alaskar, Ahmad Al Ameer, Gasmelseed Ahmed, Ayman Alhejazi, Khadega Abuelgasim, Giamal Gmati, Mushtaq Rather, Mohsen Al Zahrani
Journal: Blood (2014)
Randomized Prospective Biomarker Trial of ERCC1 for Comparing Platinum and Nonplatinum Therapy in Advanced Non–Small-Cell Lung Cancer: ERCC1 Trial (ET)
Authors: Siow Ming Lee, Mary Falzon, Fiona Blackhall, James Spicer, Marianne Nicolson, Abhro Chaudhuri, Gary Middleton, Samreen Ahmed, Jonathan Hicks, Barbara Crosse, Mark Napier, Julian M. Singer, David Ferry, Conrad Lewanski, Martin Forster, Sally-Ann Rolls, Arrigo Capitanio, Robin Rudd, Natasha Iles, Yenting Ngai, Michael Gandy, Rachel Lillywhite, Allan Hackshaw
Journal: Journal of Clinical Oncology (2017)

Purpose Retrospective studies indicate that expression of excision repair cross complementing group 1 (ERCC1) protein is associated with platinum resistance and survival in non–small-cell lung cancer (NSCLC). We conducted the first randomized trial, to our knowledge, to evaluate ERCC1 prospectively and to assess the superiority of nonplatinum therapy over platinum doublet therapy for ERCC1-positive NSCLC as well as noninferiority for ERCC1-negative NSCLC. Patients and Methods This trial had a marker-by-treatment interaction phase III design, with ERCC1 (8F1 antibody) status as a randomization stratification factor. Chemonaïve patients with NSCLC (stage IIIB and IV) were eligible. Patients with squamous histology were randomly assigned to cisplatin and gemcitabine or paclitaxel and gemcitabine; nonsquamous patients received cisplatin and pemetrexed or paclitaxel and pemetrexed. Primary end point was overall survival (OS). We also evaluated an antibody specific for XPF (clone 3F2). The target hazard ratio (HR) for patients with ERCC1-positive NSCLC was ≤ 0.78. Results Of patients, 648 were recruited (177 squamous, 471 nonsquamous). ERCC1-positive rates were 54.5% and 76.7% in nonsquamous and squamous patients, respectively, and the corresponding XPF-positive rates were 70.5% and 68.5%. Accrual stopped early in 2012 for squamous patients because OS for nonplatinum therapy was inferior to platinum therapy (median OS, 7.6 months [paclitaxel and gemcitabine] v 10.7 months [cisplatin and gemcitabine]; HR, 1.46; P = .02). Accrual for nonsquamous patients halted in 2013. Median OS was 8.0 (paclitaxel and pemetrexed) versus 9.6 (cisplatin and pemetrexed) months for ERCC1-positive patients (HR, 1.11; 95% CI, 0.85 to 1.44), and 10.3 (paclitaxel and pemetrexed) versus 11.6 (cisplatin and pemetrexed) months for ERCC1-negative patients (HR, 0.99; 95% CI, 0.73 to 1.33; interaction P = .64). OS HR was 1.09 (95% CI, 0.83 to 1.44) for XPF-positive patients, and 1.39 (95% CI, 0.90 to 2.15) for XPF-negative patients (interaction P = .35). Neither ERCC1 nor XPF were prognostic: among nonsquamous patients, OS HRs for positive versus negative were ERCC1, 1.11 ( P = .32), and XPF, 1.08 ( P = .55). Conclusion Superior outcomes were observed for patients with squamous histology who received platinum therapy compared with nonplatinum chemotherapy; however, selecting chemotherapy by using commercially available ERCC1 or XPF antibodies did not confer any extra survival benefit.
A Phase II Study of MESA Chemotherapy for Newly Diagnosed, Relapsed or Refractory Extranodal Natural Killer (NK)/T-Cell Lymphoma, Nasal Type: A Multicenter Trial of Northern-West of China
Authors: Rong Liang, Gao Guangxun, Chen Jie Ping, Jishi Wang, Xiao min Wang, Yun Zeng, Xie qun Chen, Liang Zhang
Journal: Blood (2015)
Randomized Phase II Trial of Pentostatin, Cyclophosphamide, and Rituximab with or without Concurrent Avastin for Previously Untreated B-Chronic Lymphocytic Leukemia (CLL)
Authors: Tait D. Shanafelt, Betsy R. LaPlant, Timothy G Call, Daniel Nikcevich, Jose F. Leis, Wei Ding, Adam Pettinger, Daniel L. Van Dyke, Diane F. Jelinek, Curtis A. Hanson, Neil E. Kay
Journal: Blood (2014)
Use of the Novel Monoclonal Assay for the Measurement of Circulating Free Light Chain in the Diagnosis, Prognostication of Survival and Assessment of Response to Therapy in AL Amyloidosis
Authors: Giovanni Palladini, Tiziana Bosoni, Paolo Milani, Laura Pirolini, Andrea Foli, Filomena Li Bergolis, Francesca Lavatelli, Leda Roggeri, Elena Cigalini, Ilaria Repetti, Veronica Valentini, Simona Casarini, Riccardo Albertini, Giampaolo Merlini
Journal: Blood (2012)
High Level Expression of a Membrane-Anchored Inhibitor of HIV Infection in Murine Hematopoietic Stem and Progenitor Cells Does Not Pertubate Serial Multilineage Repopulation.
Authors: Axel Schambach, Bernhard Schiedlmeier, Jens Bohne, Dorothee von Laer, Geoff Margison, Christopher Baum
Journal: Blood (2004)
Role of CD137/4-1BB and Its Ligand in the NK Cell Mediated Immune Surveillance of Acute Myeloid Leukemia.
Authors: Tina Baessler, Matthias Krusch, Katrin M. Baltz, Benjamin J. Schmiedel, Helga M. Schmetzer, Lothar Kanz, Helmut R. Salih
Journal: Blood (2007)