tbuckley/cabot-search huggingface dataset:
The androgen metabolite 5α-androstane-3β,17β-diol (3βAdiol) induces breast cancer growth via estrogen receptor: pharmacogenomic implications for aromatase therapy
Authors: Matthew Sikora, Kevin Cordero, Jose Larios, Michael Johnson, James Rae
Journal: Cancer Research (2008)

1586  Nearly 180,000 new cases of breast cancer will be diagnosed this year in the United States. It is known that estrogens play a central role in breast cancer biology. While the role of androgens is far less understood, they are believed to inhibit tumor growth. The steroid hormone precursor dehydroepiandrosterone (DHEA) is metabolized to testosterone (TS) by 3β- and 17β-hydroxysteroid dehydrogenases (HSD). TS can be converted to 17β-estradiol (E2) by CYP19 aromatase or to the potent androgen 5α-dihydrotestosterone (DHT) by 5α-reductase. DHT can be metabolized by 3β-HSD into 5α-androstane-3β,17β-diol (3βAdiol), which is further metabolized to an inactive compound by the genetically polymorphic cytochrome P450 7B1 (CYP7B1). It is believed that 3βAdiol is growth inhibitory to prostate cancer by activating estrogen receptor beta (ERβ), accordingly, CYP7B1 has been shown to be over-expressed during prostate cancer progression. However, the role of CYP7B1 in breast cancer development has not been explored. In breast cancer cell lines, 3βAdiol has been shown to induce gene transcription using ERβ-luciferase reporter systems, but studies with ERalpha (ERα) have produced mixed results. We hypothesized that 3βAdiol is a potent ERα agonist and that its production by breast cancer cells might present a mechanism for the acquisition of resistance to aromatase inhibitors (AIs). To test this hypothesis, the E2-dependant breast cancer cell lines MCF-7, BT-474, and T47D cell lines were grown in E2-free conditions, treated with increasing concentrations of TS, DHT, 3βAdiol or the synthetic androgen receptor (AR) agonist R1881, and monitored for proliferation. TS, DHT, and 3βAdiol induced proliferation in a dose-dependent fashion, whereas R1881 did not. The lack of R1881-induced growth and the observation that the AR antagonist bicalutamide was unable to block growth stimulation by TS, DHT and 3βAdiol suggest that the effects are being not mediated by AR. Furthermore, the aromatase inhibitors (AIs), while able to block TS-induced proliferation, had no effect on DHT- or 3βAdiol-induced growth. The growth effects of DHT and 3βAdiol were, however, both blocked by the ER antagonist ICI 182,780. As DHT is known to not bind ER, it is likely that DHT is metabolized to 3βAdiol, which then activates ER. These data demonstrate that androgen metabolites can induce ER-mediated proliferation in breast cancer cells, and suggest that while aromatase inhibition prevents TS metabolism into E2, TS can be metabolized by alternate pathways involving HSDs that produces a metabolite, 3βAdiol, with strong estrogenic properties. We propose that AI resistance may be caused by the production of 3βAdiol, which can induce breast cancer growth. Further, we postulate that polymorphisms that decrease functional CYP7B1 will cause increased 3βAdiol levels, and lead to AI resistance.
TK-Cells Safety and Efficacy in Allogeneic Hematopoietic Stem Cell Transplantation: Long-Term Clinical and Molecular Assessment in 128 Treated Patients.
Authors: Maria Teresa Lupo-Stanghellini, Giacomo Oliveira, Raffaella Greco, Luca Vago, Attilio Bondanza, Fabio Ciceri, Claudio Bordignon, Chiara Bonini
Journal: Blood (2012)
Gene Conversion of Sialic Acid Binding Domains in CD33-Related Siglecs by Adjacent Pseudogenes: A Novel Mechanism To Change Sialic Acid Binding Specificity.
Authors: Toshiyuki Hayakawa, Takashi Angata, Elliott H. Margulies, Tarjei Mikkelsen, Eric D. Green, Ajit Varki
Journal: Blood (2004)
High Expression of mRNA and Gene Amplification of Met In Myeloma Plasma Cells Characterize a More Aggressive Disease
Authors: Alberto Rocci, Manuela Gambella, Simona Aschero, Ileana Baldi, Livio Trusolino, Federica Cavallo, Alessandra Larocca, Paola Omedè, Andrea Bertotti, Vittorio Montefusco, Claudia Crippa, Francesca Patriarca, Anna Marina Liberati, Antonietta Falcone, Gianluca Isaia, Daniela Drandi, Marco Ladetto, Paolo M. Comoglio, Giovannino Ciccone, Mario Boccadoro, Antonio Palumbo
Journal: Blood (2010)
Development of a Measure of Health-Related Quality of Life for Non-Hodgkin’s Lymphoma Clinical Research: The Functional Assessment of Cancer Therapy - Lymphoma (FACT-Lym).
Authors: David Cella, Kimberly Webster, John Cashy, Lucie Kutikova, Michael F. Burgess, Boris K. Lin, Lee Bowman, Astra M. Liepa, Janine E. Gauthier, Stephanie A. Gregory, Stephen A. Johnson, Bruce D. Cheson
Journal: Blood (2005)
Evidence from the Oxford Classification cohort supports the clinical value of subclassification of focal segmental glomerulosclerosis in IgA nephropathy
Authors: Shubha S. Bellur, Fanny Lepeytre, Olga Vorobyeva, Stéphan Troyanov, H. Terence Cook, Ian S.D. Roberts, Charles E. Alpers, Alessandro Amore, Jonathan Barratt, Francois Berthoux, Stephen Bonsib, Jan A. Bruijn, Daniel C. Cattran, Rosanna Coppo, Vivette D'Agati, Giuseppe D'Amico, Steven Emancipator, Francesco Emma, John Feehally, Franco Ferrario, Fernando C. Fervenza, Sandrine Florquin, Agnes Fogo, Colin C. Geddes, Hermann-Josef Groene, Mark Haas, Andrew M. Herzenberg, Prue A. Hill, Ronald J. Hogg, Stephen I. Hsu, J. Charles Jennette, Kensuke Joh, Bruce A. Julian, Tetsuya Kawamura, Fernand M. Lai, Lei-Shi Li, Philip K.T. Li, Zhi-Hong Liu, Bruce Mackinnon, Sergio Mezzano, F. Paolo Schena, Yasuhiko Tomino, Patrick D. Walker, Haiyan Wang, Jan J. Weening, Nori Yoshikawa, Hong Zhang
Journal: Kidney International (2016)
Lysyl oxidase is a strong determinant of tumor cell colonization in bone. Short Title: LOX triggers tumor cell colonization in bone
Authors: Caroline Reynaud, Laura Ferreras, Paola Mauro, Casina Kan, Martine Croset, Edith Bonnelye, Floriane Pez, Clémence Thomas, Géraldine Aimond, Antoine Karnoub, Marie Brevet, Philippe Clézardin
Journal: Cancer Research (2016)

Lysyl oxidase (LOX) is a secreted copper-dependent amine oxidase whose primary function is to drive collagen crosslinking and extracellular matrix stiffness. LOX in colorectal cancer (CRC) synergizes with hypoxia-inducible factor-1 (HIF-1 to promote tumor progression. Here we investigated whether LOX/HIF1 endows CRC cells with full competence for aggressive colonization in bone. We show that a high LOX expression in primary tumors from CRC patients was associated with poor clinical outcome, irrespective of HIF-1. Additionally, LOX was expressed by tumor cells in the bone marrow from CRC patients with bone metastases. In vivo experimental studies show that LOX overexpression in CRC cells or systemic delivery of the conditioned medium from LOX-overexpressing CRC cells promoted tumor cell dissemination in the bone marrow and enhanced osteolytic lesion formation, irrespective of HIF-1. Conversely, silencing or pharmacological inhibition of LOX activity blocked dissemination of CRC cells in the bone marrow and tumor-driven osteolytic lesion formation. In vitro, tumor-secreted LOX supported the attachment and survival of CRC cells to and in the bone matrix, and inhibited osteoblast differentiation. LOX overexpression in CRC cells also induced a robust production of IL-6. In turn, both LOX and IL-6 were acting in concert to promote RANKL-dependent osteoclast differentiation, thereby creating an imbalance between bone resorption and bone formation. Collectively, our findings show that LOX supports CRC cell dissemination in the bone marrow and they reveal a novel mechanism through which LOX-driven IL-6 production by CRC cells impairs bone homeostasis.
High Resolution Array CGH Identifies TRAF3 as a Novel Tumor Suppressor in Multiple Myeloma.
Authors: Jonathan Keats, Rodger Tiedemann, Roelendt Schop, Michael Sebag, Marta Chesi, Scott Van Wier, Chang-Xin Shi, Yuan-Xiao Zhu, Angela Baker, Homer Fogle, Catherine Mancini, Tae-Hoon Chung, Philip Greipp, Angela Dispenzieri, Michael Barrett, Laurakay Bruhin, Keith Stewart, John Carpten, Rafael Fonseca, Peter Leif Bergsagel
Journal: Blood (2006)
Infrared Microspectroscopy Allows Direct Identification of Leukemic Cells Expressing T315I-Mutated BCR-ABL Via a Unique Spectral Signature
Authors: Christophe Sandt, Olivier Feraud, Marie Laure Bonnet, Rania Khedhir, Marie Claude Meunier, Paul Dumas, Annelise Bennaceur-Griscelli, Ali G Turhan
Journal: Blood (2014)
Incidence and Clinical Profile of JAK2 V617F Mutation in Myelofibrosis with Myeloid Metaplasia.
Authors: Giovanni Barosi, Monia Marchetti, Margherita Massa, Vittorio Rosti, Alessandro Vannucchi, Rosangela Invernizzi, Rita Campanelli, Gianluca Viarengo, Umberto Magrini, Gaetano Bergamaschi
Journal: Blood (2005)
Inhibition of p38α MAPK Reduces Tumor Burden, Prevents the Development of Myeloma Bone Disease, and Increases Survival in the 5T2 and 5T33 Murine Models of Myeloma.
Authors: Karin Vanderkerken, Satya Medicherla, Les Coulton, Benjamin Van Camp, Andy Protter, Linda Higgins, Eline Menu, Peter Croucher
Journal: Blood (2006)
The womb environment shapes respiratory health in offspring: a fascinating hypothesis
Authors: Franca Rusconi
Journal: European Respiratory Journal (2016)

Starting with the pioneering paper published in 1990 by D.J.P. Barker, "The fetal and infant origins of adult disease: the womb may be more important than the home" [1], and continuing with more recent papers on epigenetics and transgenerational developmental programming [2], the concept that in utero environment might play an important role on future health has reached the general public [3]. As far as respiratory health is concerned, we are all aware that asthma and allergic diseases often manifest themselves in early life, and that congenital factors play an important role in these [4]. Not only have prospective birth cohort studies been instrumental to investigate in utero determinants of chronic conditions such as asthma and IgE-associated diseases [5], but also studies based on several large population registries continue to contribute to better knowledge on this field [6]. Pre-eclampsia is detrimental to respiratory health in offspring and its effect is partly mediated by prematurity <http://ow.ly/kti0305B6lc>
Differential Role of the B-Cell Receptor Pathway in Diffuse Large Cell B Cell Lymphoma: Temsirolimus Has Additive Effects in Combination with the BTK Inhibitor PCI-32765 and PI3K Inhibitor Cal101 but Antagonizes Bortezomib in GCB Subtype
Authors: Anna-Katharina Zoellner, Stephan Bayerl, Marc Weinkauf, Georg Hess, Wolfgang Hiddemann, Martin H. Dreyling
Journal: Blood (2011)
Internalization of secreted antigen–targeted antibodies by the neonatal Fc receptor for precision imaging of the androgen receptor axis
Authors: Daniel L. J. Thorek, Philip A. Watson, Sang-Gyu Lee, Anson T. Ku, Stylianos Bournazos, Katharina Braun, Kwanghee Kim, Kjell Sjöström, Michael G. Doran, Urpo Lamminmäki, Elmer Santos, Darren Veach, Mesruh Turkekul, Emily Casey, Jason S. Lewis, Diane S. Abou, Marise R. H. van Voss, Peter T. Scardino, Sven-Erik Strand, Mary L. Alpaugh, Howard I. Scher, Hans Lilja, Steven M. Larson, David Ulmert
Journal: Science Translational Medicine (2016)

Targeting the androgen receptor (AR) pathway prolongs survival in patients with prostate cancer, but resistance rapidly develops. Understanding this resistance is confounded by a lack of noninvasive means to assess AR activity in vivo. We report intracellular accumulation of a secreted antigen-targeted antibody (SATA) that can be used to characterize disease, guide therapy, and monitor response. AR-regulated human kallikrein-related peptidase 2 (free hK2) is a prostate tissue-specific antigen produced in prostate cancer and androgen-stimulated breast cancer cells. Fluorescent and radio conjugates of 11B6, an antibody targeting free hK2, are internalized and noninvasively report AR pathway activity in metastatic and genetically engineered models of cancer development and treatment. Uptake is mediated by a mechanism involving the neonatal Fc receptor. Humanized 11B6, which has undergone toxicological tests in nonhuman primates, has the potential to improve patient management in these cancers. Furthermore, cell-specific SATA uptake may have a broader use for molecularly guided diagnosis and therapy in other cancers.
Cardiovascular Risk: Analysis of Known Factors in Patients After Treosulfan-Based Conditioning for Haploidentical and HLA-Identical Stem Cell Transplantation
Authors: Alessandra Forcina, Maria Teresa Lupo Stanghellini, Raffaella Greco, Alessandro Lorusso, Daniela Clerici, Jacopo Peccatori, Massimo Bernardi, Francesca Lunghi, Magda Marcatti, Lionello Camba, Elena Guggiari, Andrea Assanelli, Attilio Bondanza, Matteo Carrabba, Sarah Marktel, Consuelo Corti, Fabio Ciceri
Journal: Blood (2011)
Occult HIV-1 drug resistance to thymidine analogues following failure of first-line tenofovir combined with a cytosine analogue and nevirapine or efavirenz in sub Saharan Africa: a retrospective multi-centre cohort study
Authors: John Gregson, Pontiano Kaleebu, Vincent C Marconi, Cloete van Vuuren, Nicaise Ndembi, Raph L Hamers, Phyllis Kanki, Christopher J Hoffmann, Shahin Lockman, Deenan Pillay, Tulio de Oliveira, Nathan Clumeck, Gillian Hunt, Bernhard Kerschberger, Robert W Shafer, Chunfu Yang, Elliot Raizes, Rami Kantor, Ravindra K Gupta
Journal: The Lancet Infectious Diseases (2016)

BackgroundHIV-1 drug resistance to older thymidine analogue nucleoside reverse transcriptase inhibitor drugs has been identified in sub-Saharan Africa in patients with virological failure of first-line combination antiretroviral therapy (ART) containing the modern nucleoside reverse transcriptase inhibitor tenofovir. We aimed to investigate the prevalence and correlates of thymidine analogue mutations (TAM) in patients with virological failure of first-line tenofovir-containing ART.MethodsWe retrospectively analysed patients from 20 studies within the TenoRes collaboration who had locally defined viral failure on first-line therapy with tenofovir plus a cytosine analogue (lamivudine or emtricitabine) plus a non-nucleoside reverse transcriptase inhibitor (NNRTI; nevirapine or efavirenz) in sub-Saharan Africa. Baseline visits in these studies occurred between 2005 and 2013. To assess between-study and within-study associations, we used meta-regression and meta-analyses to compare patients with and without TAMs for the presence of resistance to tenofovir, cytosine analogue, or NNRTIs.FindingsOf 712 individuals with failure of first-line tenofovir-containing regimens, 115 (16%) had at least one TAM. In crude comparisons, patients with TAMs had lower CD4 counts at treatment initiation than did patients without TAMs (60·5 cells per μL [IQR 21·0–128·0] in patients with TAMS vs 95·0 cells per μL [37·0–177·0] in patients without TAMs; p=0·007) and were more likely to have tenofovir resistance (93 [81%] of 115 patients with TAMs vs 352 [59%] of 597 patients without TAMs; p<0·0001), NNRTI resistance (107 [93%] vs 462 [77%]; p<0·0001), and cytosine analogue resistance (100 [87%] vs 378 [63%]; p=0·0002). We detected associations between TAMs and drug resistance mutations both between and within studies; the correlation between the study-level proportion of patients with tenofovir resistance and TAMs was 0·64 (p<0·0001), and the odds ratio for tenofovir resistance comparing patients with and without TAMs was 1·29 (1·13–1·47; p<0·0001)InterpretationTAMs are common in patients who have failure of first-line tenofovir-containing regimens in sub-Saharan Africa, and are associated with multidrug resistant HIV-1. Effective viral load monitoring and point-of-care resistance tests could help to mitigate the emergence and spread of such strains.FundingThe Wellcome Trust.
Human Monocytes and Monocyte-Like Cells Are Highly Sensitive to Plitidepsin-Induced Cell Death In In Vitro Assays
Authors: Pablo E Morande, Samanta Zanetti, Mercedes Borge, Paula Nannini, Carolina Jancic, Raimundo Bezares, Carlos M. Galmarini, Romina Gamberale, Mirta Giordano
Journal: Blood (2010)
Effect of the Combination of Imatinib Mesylate (Glivec) and Curcumin in Chronicm Myeloid Leukemia Cell Line.
Authors: Young-Ju Kim, Yong-Hee Choi, Chang Up Kim, Eun Kyung Bae, Byung-Su Kim, Kwang-Sung Ahn, Jong-Seok Lee, Seonyang Park, Byoung Kook Kim, Sung-Soo Yoon
Journal: Blood (2004)
FLT3 Inhibitors Are Promising Salvage Therapy for Relapsed or Refractory Acute Myeloid Leukemia (AML) in Patients with FLT3-ITD Mutations,
Authors: Koichi Takahashi, Hagop M. Kantarjian, Naveen Pemmaraju, Gautam Borthakur, Stefan Faderl, Guillermo Garcia-Manero, Michael Andreeff, Sherry Pierce, Farhad Ravandi, Jorge E. Cortes
Journal: Blood (2011)
Monitoring of Hematopoietic Chimerism by Real-Time Quantitative PCR of Single Nucleotide Polymorphisms In Samples with Low DNA Quantities.
Authors: Christian Bach, Elmira Tomova, Katja Goldmann, Birgit Lauer, Wolf Roesler, Andreas Mackensen, Julia Winkler, Bernd M Spriewald
Journal: Blood (2010)
Relation of IL-18 Polymorphism to the Susceptibility and Clinical Feature of Multiple Myeloma in Japanese Patients
Authors: Takayuki Saitoh, Norihiko Moriyama, Tomonori Takani, Chiaki Ushie, Takumi Hoshino, Takeki Mitsui, Hiromi Koiso, Akihiko Yokohama, Hiroshi Handa, Norifumi Tsukamoto, Hatsue Ogawara, Morio Sawamura, Yoshihisa Nojima, Hirokazu Murakami
Journal: Blood (2011)
PDC-E2, a Common Auto Antigen in Primary Biliary Cirrhosis (PBC) Is Also a Target of an Antibody Response in Patients Who Achieve Complete Remission after Donor Lymphocyte Infusion.
Authors: Roberto Bellucci, Meagan Gallagher, Hong-Nam Nguyen, Edwin P. Alyea, Emmanuel Zorn, Kenneth C. Anderson, Nikhil C. Munshi, Jerome Ritz
Journal: Blood (2004)
Correlation of Secretory Activity of Neutrophils With Genotype in Patients With Familial Mediterranean Fever
Authors: Faekah Gohar, Banu Orak, Tilmann Kallinich, Marion Jeske, Mareike Lieber, Horst von Bernuth, Arnd Giese, Elisabeth Weissbarth‐Riedel, Johannes‐Peter Haas, Frank Dressler, Dirk Holzinger, Peter Lohse, Ulrich Neudorf, Elke Lainka, Claas Hinze, Katja Masjosthusmann, Christoph Kessel, Toni Weinhage, Dirk Foell, Helmut Wittkowski
Journal: Arthritis & Rheumatology (2016)

Familial Mediterranean fever (FMF) is an autoinflammatory disorder caused by pyrin-encoding MEFV mutations. Patients present with recurrent but self-limiting episodes of acute inflammation and often have persistent subclinical inflammation. The pathophysiology is only partially understood, but neutrophil overactivation is a hallmark of the disease. S100A12 is a neutrophil-derived proinflammatory danger signal that is strongly elevated in active FMF. This study was undertaken to characterize the secretory activity of neutrophils in vitro and investigate the association of S100A12 with disease activity and genotype in patients with FMF.Neutrophils from FMF patients carrying the p.M694V mutation (1 compound heterozygous and 5 homozygous) and neutrophils from 4 healthy control subjects were purified and stimulated in vitro. Neutrophil secretion of S100A12, interleukin-18 (IL-18), IL-1β, and caspase 1 was determined. Based on these in vitro analyses, serum concentrations of S100A12, IL-18, and IL-1β were also analyzed in 128 clinically and genetically characterized patients with FMF.In vitro, unstimulated neutrophils from p.M694V-positive patients spontaneously secreted more S100A12, IL-18, and caspase 1 compared to neutrophils from healthy controls. Serum concentrations of S100A12 correlated with disease activity and genotype, with the levels being highest in homozygous patients and with compound heterozygotes displaying higher levels than heterozygotes. Compared to individuals negative for the p.M694V mutation, heterozygous, compound heterozygous, or homozygous p.M694V-positive patients had higher serum levels of S100A12 and IL-18 during inactive and subclinical disease.The FMF phenotype is known to be more severe in patients carrying the p.M694V mutation. This report describes 2 molecules secreted by unconventional secretory pathways, S100A12 and IL-18, whose concentrations correlated with clinical disease activity and genotype in patients with FMF. In this clinically and genetically heterogeneous disease, management of these surrogate markers might help to improve patient care and outcomes.
Characterization of Rare, Dormant, and Therapy-Resistant Cells in Acute Lymphoblastic Leukemia
Authors: Sarah Ebinger, Erbey Ziya Özdemir, Christoph Ziegenhain, Sebastian Tiedt, Catarina Castro Alves, Michaela Grunert, Michael Dworzak, Christoph Lutz, Virginia A. Turati, Tariq Enver, Hans-Peter Horny, Karl Sotlar, Swati Parekh, Karsten Spiekermann, Wolfgang Hiddemann, Aloys Schepers, Bernhard Polzer, Stefan Kirsch, Martin Hoffmann, Bettina Knapp, Jan Hasenauer, Heike Pfeifer, Renate Panzer-Grümayer, Wolfgang Enard, Olivier Gires, Irmela Jeremias
Journal: Cancer Cell (2016)
Transfusion Burden and Outcomes in Patients with Low- or Unspecified-Grade Myelodysplastic Syndromes Treated with Erythropoiesis-Stimulating Agents: Analysis of a United States Commercial Claims Database
Authors: Maneesha Mehra, Ravi Potluri, Jianming He, Aleksandra Rizo, Suneel Mundle, Jacqueline Bussolari
Journal: Blood (2016)
Cytogenetic Clonal Evolution in MDS Is Associated with Shifts towards Unfavorable Karyotypes According to IPSS and Shorter Overall Survival: A Study on 988 MDS Patients Studied Sequentially by Chromosome Banding Analysis
Authors: Claudia Haferlach, Melanie Zenger, Tamara Alpermann, Susanne Schnittger, Wolfgang Kern, Torsten Haferlach
Journal: Blood (2011)
Oral Eltrombopag for the Long-Term Treatment of Patients with Chronic Idiopathic Thrombocytopenic Purpura: Results of a Phase III, Double- Blind, Placebo-Controlled Study (RAISE)
Authors: Gregory Cheng, Mansoor N Saleh, James B Bussel, Claus Marcher, Sandra Vasey, Bhabita Mayer, Manuel Aivado, Michael Arning, Nicole L. Stone
Journal: Blood (2008)
A Vaccination Regimen Incorporating the Synergistic Combination of CpG-Containing Oligodeoxynucleotides and IL-2 Can Elicit CD8+ T Cell Responses That Effect Anti-Tumor Immunity from T Cell Repertoires Undergoing Reconstitution by Homeostatic Peripheral Expansion after BMT.
Authors: James Kochenderfer, Christopher Chien, Jessica Simpson, Ronald Gress
Journal: Blood (2005)
Intensification of Post-Remissional Treatment in Adult Acute Lymphoblastic Leukemia (ALL) with t(4;11) or t(1;19): Results of the GIMEMA LAL 2000 Study.
Authors: Marco Vignetti, Giovanna Meloni, Monica Morselli, Alessandra Tedeschi, Felicetto Ferrara, Nicola Cantore, Giorgina Specchia, Francesco Di Raimondo, Anna Recchia, Simona Sica, Nicola Cascavilla, Andrea Camera, Francesco Fabbiano, Giuseppe Cimino, Marco Mancini, Paola Fazi, Roberto Foà, Franco Mandelli
Journal: Blood (2004)
Increased Levels of Myeloid-Derived Suppressor Cells (MDSCs) in Chronic Myeloid Leukemia and the Effect of Tyrosine Kinase Inhibitors on MDSCs in Vitro
Authors: Lisa H Christiansson, Stina Söderlund, Emma Svensson, Mats Bengtsson, Bengt Simonsson, Ulla Olsson-Strömberg, Angelica Loskog
Journal: Blood (2011)
Impaired Osteogenic Differentiation of Mesenchymal Stem Cells Derived From Multiple Myeloma Patients Is Associated with a Failure In the Deactivation of the NOTCH Pathway
Authors: Song Xu, Jinsong Hu, Dehui Xu, Isabelle Vande Broek, Xavier Leleu, Ben Van Camp, Karin Vanderkerken, Ivan Van Riet
Journal: Blood (2010)
Polyclonal Anti-Kel (KELGAM) Prevents Alloimmunization to Transfused Kel RBCs in a Murine Model
Authors: Sean R. Stowell, Connie M Arthur, Kathryn R. Girard-Pierce, Harold Clifford Sullivan, Manjula Santhanakrishnan, Prabitha Natarajan, Christopher A. Tormey, James C. Zimring, Jeanne E Hendrickson
Journal: Blood (2014)
TLR4 Asp299Gly Variant Confers Strong Protection against BK Virus-Associated Hemorrhagic Cystitis After Hematopoietic Stem Cell Transplantation in Children.
Authors: Bernd Gruhn, Norman Kloeppner, Nadine Pfaffendorf, Ilona Wolff, Daniel Steinbach, Felix Zintl, James F. Beck
Journal: Blood (2009)