tbuckley/cabot-search huggingface dataset:
A novel humanized mouse model with significant improvement of class-switched, antigen-specific antibody production
Authors: Hua Yu, Chiara Borsotti, Jean-Nicolas Schickel, Shu Zhu, Till Strowig, Elizabeth E. Eynon, Davor Frleta, Cagan Gurer, Andrew J. Murphy, George D. Yancopoulos, Eric Meffre, Markus G. Manz, Richard A. Flavell
Journal: Blood (2017)
Molecular and Structural Characterization of the SH3 Domain of AHI-1 in Regulation of Cellular Resistance of BCR-ABL+ Chronic Myeloid Leukemia Cells to Tyrosine Kinase Inhibitors
Authors: Xiaohu Liu, Min Chen, Paolo Lobo, Jianghong An, SW. Grace Cheng, Annie Moradian, Gregg B. Morin, Filip Van Petegem, Xiaoyan Jiang
Journal: Blood (2011)
Lipidic nanoparticle CPT-11 in a bioluminescent orthotopic pancreas cancer model
Authors: Byron Hann, Karissa Peth, Donghui Wang, Stephan Gysin, Shang Li, Erika Kullberg, Yun Hom, Matthew Goldman, Margaret Tempero, John Park
Journal: Cancer Research (2007)

5648  Efforts to treat pancreas cancer have been hampered by a lack of effective therapeutic options as well as predictive preclinical models. We hypothesized that nanoparticle agents encapsulating potent cytotoxic compounds may be useful against pancreatic cancer; and that antibody-targeted versions directed against EGFR may further increase efficacy against EGFR-overexpressing pancreatic cancers. We applied a liposome-based drug loading and stabilization technique to generate nanoliposomal CPT-11, a novel lipidic nanoparticle agent containing the prodrug CPT-11 (irinotecan) that has entered clinical trials. In addition, Fab9 fragments of C225 were conjugated to nanoliposomal CPT-11 to generate EGFR-targeted immunoliposomal CPT-11.  Another objective of this study was to develop a bioluminescent-based orthotopic xenograft model of pancreas cancer with EGFR-overexpression to test this therapeutic approach. COLO357, a human pancreatic cell line, was passaged multiple times in vivo to generate the sub-line L3.6pl. This cell line was subsequently modified by lentiviral transduction to generate a firefly luciferase-expressing cell line, L3.6pl-T. L3.6pl-T cells were injected, during surgery, directly into the pancreas of a nude mouse to generate a tumor xenograft. Following ip administration of luciferin, animals were immediately imaged using a Xenogen IVIS 100 bioluminescent imager, and subsequently imaged at weekly intervals. Tumor burden was quantified by measuring luminescence. The signal was quantified by defining regions of interest (ROIs) and measuring photons/sec/str.  Agents evaluated in this model included EGFR-targeted immunoliposomal CPT-11, nanoliposomal CPT-11, free drug or vehicle control. All treatments were administered i.v. by tail vein beginning at 7 days post- tumor implantation and continued weekly for a total of three treatments. Both nanoliposomal CPT-11 and immunoliposomal CPT-11 showed potent antitumor activity, including durable tumor regressions, and were markedly superior to the equivalent dose of free drug. While both nanoparticle constructs were highly potent, the immunoliposome agent appeared to provide more prolonged duration of responses than the non-targeted version. Systemic toxicity was not observed with any treatment.  We conclude that nanoparticle-mediated delivery of CPT-11 via nanoliposomal CPT-11 or anti-EGFR immunoliposomal CPT-11 greatly enhances antitumor efficacy in the orthotopic COLO357 pancreatic xenograft model. This therapeutic approach offers potential advantages for pancreatic cancer treatment, and this type of model system may be useful in preclinical evaluation.
Haploidentical Natural Killer (NK) Cells Expanding In Vivo After Adoptive Transfer Exhibit Hyperfunction That Partially Overcomes Self Tolerance and Leads to Clearance of Refractory Leukemia
Authors: Sarah Cooley, Bree Foley, Michael R Verneris, David McKenna, Xianghua Luo, Kathryn E. Dusenbery, Bruce R. Blazar, Daniel J. Weisdorf, Jeffrey S. Miller
Journal: Blood (2011)
A Functional Genetic Screen Identifies the Phosphoinositide 3-kinase Pathway as a Determinant of Resistance to Fibroblast Growth Factor Receptor Inhibitors in FGFR Mutant Urothelial Cell Carcinoma
Authors: Liqin Wang, Tonći Šuštić, Rodrigo Leite de Oliveira, Cor Lieftink, Pasi Halonen, Marieke van de Ven, Roderick L. Beijersbergen, Michel M. van den Heuvel, René Bernards, Michiel S. van der Heijden
Journal: European Urology (2017)
The Role of Efflux Pumps in Tuberculosis Treatment and Their Promise as a Target in Drug Development: Unraveling the Black Box
Authors: Lindsey H.M. te Brake, Gerjo J. de Knegt, Jurriaan E. de Steenwinkel, Teunis J.P. van Dam, David M. Burger, Frans G.M. Russel, Reinout van Crevel, Jan B. Koenderink, Rob E. Aarnoutse
Journal: The Annual Review of Pharmacology and Toxicology (2017)

Insight into drug transport mechanisms is highly relevant to the efficacious treatment of tuberculosis (TB). Major problems in TB treatment are related to the transport of antituberculosis (anti-TB) drugs across human and mycobacterial membranes, affecting the concentrations of these drugs systemically and locally. Firstly, transporters located in the intestines, liver, and kidneys all determine the pharmacokinetics and pharmacodynamics of anti-TB drugs, with a high risk of drug-drug interactions in the setting of concurrent use of antimycobacterial, antiretroviral, and antidiabetic agents. Secondly, human efflux transporters limit the penetration of anti-TB drugs into the brain and cerebrospinal fluid, which is especially important in the treatment of TB meningitis. Finally, efflux transporters located in the macrophage and Mycobacterium tuberculosis cell membranes play a pivotal role in the emergence of phenotypic tolerance and drug resistance, respectively. We review the role of efflux transporters in TB drug disposition and evaluate the promise of efflux pump inhibition from a novel holistic perspective.
Prospective Study of Peri-Transplant Use of Sorafenib As Remission Maintenance for FLT3-ITD Patients Undergoing Allogeneic Transplantation
Authors: Keith W. Pratz, Ivana Gojo, Judith E. Karp, Leo Luznik, B. Douglas Smith, Richard J Jones, Jackie Greer, Christopher Gocke, Maria R. Baer, Vu H. Duong, John J Wright, Michelle A. Rudek, Ashkan Emadi, Mark J. Levis
Journal: Blood (2015)
SDX-101 Is Cytotoxic and Overcomes Drug Resistance in Multiple Myeloma.
Authors: Makoto Hamasaki, Teru Hideshima, Kenji Ishitsuka, Hiroshi Yasui, Norihiko Shiraishi, Shaji Kumar, Noopur Raje, Aldo M. Roccaro, Yu-Tzu Tai, Reshma Shiringarpure, Lorenzo Leoni, Sarath Kanekal, Gary Elliott, Nikhil C. Munshi, Kenneth C. Anderson
Journal: Blood (2004)
CODOX-M/IVAC (NCI 89-C-41) for Children and Adolescents with Small Non-Cleaved and Large B-Cell Lymphomas. A 14 Years Monocentric Experience.
Authors: Maria Luisa Moleti, Anna Maria Testi, Luigi Malandruccolo, Elisabetta Todisco, Edoardo Pescarmona, Pietro Martino, Francesca Paoloni, Walter Barberi, Cecilia Alfieri, Giovanna Palumbo, Fiorina Giona, Robert Foà
Journal: Blood (2004)
Evaluation of Prognostic Variables and Scoring Systems in Normal Karyotyped Myelodisplastic Patients
Authors: Carolina B Belli, Mabel Lardo, Guillermo Arrossagaray, Juan Francisco Sakamoto, María Gabriela Flores, Pedro Negri Aranguren, Raquel Maria Bengio, Irene Larripa, Pedro Raul Perez Bianco
Journal: Blood (2008)
Correlation of antimuscarinic acetylcholine receptor antibody titers and antidesmoglein antibody titers with the severity of disease in patients with pemphigus
Authors: Manimegalai Jeyasekaran Dhanabhakya Lakshmi, Telanseri Jaykar Jaisankar, Medha Rajappa, Devinder Mohan Thappa, Laxmisha Chandrashekar, Dakshinamurthy Divyapriya, Malathi Munisamy, Gunaseelan Revathy
Journal: Journal of the American Academy of Dermatology (2017)
Ninety Percent Sustained Complete Response (CR) Rate Projected 4 Years after Onset of CR in Gene Expression Profiling (GEP)-Defined Low-Risk Multiple Myeloma (MM) Treated with Total Therapy 3 (TT3): Basis for GEP-Risk-Adapted TT4 and TT5
Authors: Bart Barlogie, Elias J. Anaissie, John D. Shaughnessy, Frits van Rhee, Mauricio Pineda-Roman, Jeff Haessler, Klaus A. Hollmig, Yazan Alsayed, Sarah Waheed, Monica Graziutti, Elias Kiwan, John Crowley
Journal: Blood (2008)
Epigenomic reprogramming during pancreatic cancer progression links anabolic glucose metabolism to distant metastasis
Authors: Oliver G McDonald, Xin Li, Tyler Saunders, Rakel Tryggvadottir, Samantha J Mentch, Marc O Warmoes, Anna E Word, Alessandro Carrer, Tal H Salz, Sonoko Natsume, Kimberly M Stauffer, Alvin Makohon-Moore, Yi Zhong, Hao Wu, Kathryn E Wellen, Jason W Locasale, Christine A Iacobuzio-Donahue, Andrew P Feinberg
Journal: Nature Genetics (2017)
Sixteen novel mutations in <i>PNPLA1</i> in patients with autosomal recessive congenital ichthyosis reveal the importance of an extended patatin domain in <i>PNPLA1</i> that is essential for proper human skin barrier function
Authors: A.D. Zimmer, G.J. Kim, A. Hotz, E. Bourrat, I. Hausser, C. Has, V. Oji, K. Stieler, A. Vahlquist, V. Kunde, B. Weber, F.P.W. Radner, S. Leclerc-Mercier, N. Schlipf, P. Demmer, J. Küsel, J. Fischer
Journal: British Journal of Dermatology (2017)

Autosomal recessive congenital ichthyosis (ARCI) is a genetically heterogeneous group of rare Mendelian skin disorders characterized by cornification and differentiation defects of keratinocytes. Mutations in nine genes including PNPLA1 are known to cause nonsyndromic forms of ARCI. To date, only 10 distinct pathogenic mutations in PNPLA1 have been reported. To identify new causative PNPLA1 mutations. We screened genetically unresolved cases, including our ARCI collection, comprising more than 700 families. Screening for mutations was performed either by direct Sanger sequencing or in combination with a multigene panel, followed by sequence and mutation analysis. Here we report on 16 novel mutations present in patients from 17 families. While all previously reported mutations and most of our novel mutations are located within the core patatin domain, we report five novel PNPLA1 mutations that are downstream of this domain. Thus, as recently described for PNPLA2, we hypothesize that a region larger than the core domain is required for full enzymatic activity of PNPLA1 in human skin barrier formation. We estimate the frequency of PNPLA1 mutations among patients with ARCI to be around 3%. Most of our patients were born as collodion babies and showed a relatively mild ichthyosis phenotype. In four unrelated patients we observed a cyclic scaling course, which seems to be a potential phenotypic variation in a small percentage of patients with PNPLA1 mutations. The variability of the clinical manifestations and the lack of typical clinical features are specific for patients with PNPLA1 mutations, and emphasize the importance of DNA sequencing for differential diagnosis of ARCIs.
Final Clinical Results of a Phase 2 NCI Multicenter Study of Romidepsin in Recurrent Cutaneous T-Cell Lymphoma (Molecular Analyses Included).
Authors: Susan Bates, Richard Piekarz, John Wright, Robin Frye, William Douglas Figg, Steven L. Allen, Michael Craig, Larisa Geskin, Laura Hutchins, David Joske, Mark Kirschbaum, John P. Leonard, Miles Prince, Craig B. Reeder, Maryalice Stetler- Stevenson, Alex Ling, Jean Nichols
Journal: Blood (2008)
Protein Kinase Cδ Differentially Regulates Platelet Functional Responses.
Authors: Ramya Chari, Todd Getz, Bela Nagy, Kamala Bhavaraju, Yingying Mao, Yamini Saraswathy Bynagari, Swaminathan Murugappan, Keiko Nakayama, James Daniel, Satya P. Kunapuli
Journal: Blood (2008)
Combination of the Hedgehog Pathway Inhibitor LDE225 and Nilotinib Eliminates Chronic Myeloid Leukemia Stem and Progenitor Cells.
Authors: David A Irvine, Bin Zhang, Elaine K Allan, Tessa L Holyoake, Marion Dorsch, Paul W Manley, Ravi Bhatia, Mhairi Copland
Journal: Blood (2009)
ChIP-Chip in Primary AML Blasts Identifies Peroxiredoxin-II as An Epigenetically Silenced Tumor Suppressor.
Authors: Shuchi Agrawal-Singh, Markus Wiechmann, Sandra Doths, Christina Nolte, Nils Heinrich Thoennissen, Hans-Ulrich Klein, Martin Dugas, Wolfgang E. Berdel, Steffen Koschmieder, Hubert Serve, Carsten Mueller-Tidow
Journal: Blood (2008)
Maintenance sunitinib postchemotherapy (CT) in patients (pts) with advanced urothelial carcinoma (UC): A randomized placebo controlled phase II trial
Authors: D. Bradley, S. Daignault, D. C. Smith, D. Nanus, S. Tagawa, W. M. Stadler, J. Garcia, R. Dreicer, M. Al-Hawary, M. Hussain
Journal: Journal of Clinical Oncology (2009)

5073 Background: Although response to CT is common in pts with advanced UC it is rarely durable. Sunitinib is an oral small molecule inhibitor of receptor tyrosine kinases regulating angiogenesis including VEGFR-1, -2, -3, and PDGFR-α, -β with demonstrated antitumor activity in a variety of solid tumors. Inhibition of angiogenesis following CT may delay disease progression. Therefore, we are evaluating maintenance sunitinib in a phase II study. Methods: Pts with advanced UC, &gt; stable disease (SD) after 4–6 cycles of CT, a performance status (PS) 0–2, adequate organ function and &lt; 42 days from last CT dose were randomized to sunitinib 50 mg or placebo; 4 weeks (wks) on 2 off in 6 wk cycles. Pts were stratified by response to CT. Disease was assessed every 12 wks. Pts were unblinded for progression or unacceptable adverse events (AEs), with placebo pts offered open label sunitinib. The primary end point is 6 month progression rate using a modified version of the randomized selection design (Simon 1985). 42 pts/arm are to be accrued to allow selection of the superior arm with 90% probability. Other endpoints include safety, response rate (RR), time to progression, median survival, RR to open label sunitinib and correlation of changes in serum VEGF and sVEGFR-2 levels with outcome. Results: To date, 28 pts have been registered and 26 have completed &gt; 12 wks of therapy. Median age is 69 years (48–81) and PS is 1 (37% PS 0, 52% PS 1). 12% had a complete response (CR) to prior CT, 46% a partial response (PR) and 42% SD. 14 pts have progressed after a median of 2 cycles (range 1–12). 7 pts received open label sunitinib at progression, 1/7 remains on treatment. Median duration on open label therapy is 2.2 months (11 days-15 months). Best response to open label therapy to date is progressive disease (2 pts), SD (2 pts) for 24 wks, PR in 1 pt through 60 weeks and 2 pts have not reached first assessment. Grade 3 AEs on open label sunitinib included: bladder hemorrhage, increased creatinine, fatigue, thrombocytopenia and hand-and-foot syndrome. No grade 4 or 5 AEs were observed. Conclusions: Preliminary results indicate that maintenance sunitinib post CT is feasible in advanced UC pts and is associated with clinical activity. Supported by Pfizer. [Table: see text]
Guarana (Paullinia cupana) controls the progression of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone induced lung carcinogenesis in mice: a role for inhibition of CREB/ATF-1 activation
Authors: Heidge Fukumasu, Maria Zaidan-Dagli
Journal: Cancer Research (2008)

AACR Annual Meeting-- Apr 12-16, 2008; San Diego, CA

5475 

The needs of new agents or substances are urgent regarding cancer treatment and prevention. Guarana ( Paullinia cupana Mart. var. sorbilis ) was shown to present chemopreventive effect in a hepatocarcinogenesis model and growth control in Melanoma and Ehrlich tumor cells in vivo . It is known that tobacco consumption is the main cause of lung cancer, which is the most frequent cause of cancer deaths worldwide. The aim of this work was to study the chemopreventive effect of guarana on NNK-induced lung carcinogenesis. Sixty 42-day-old A/J female mice were injected with NNK (200mg/kg, I.P.), separated into three groups [CT, GA (100mg/kg) and GB (2000mg/kg)] and were treated up to 54 weeks with guarana mixed in powder ration. After euthanasia, lung lesions were counted, excised and fixed in formalin or snap frozen. Histopathology and morphometrical analyses were performed and immunohistochemistry for PCNA and phosphorylated CREB (Ser133) were conducted with DAB-LSAB method. At last, for statistical analysis non-parametric tests as Kruskal-Wallis or Mann-Whitney were used depending on the number of groups compared. Guarana (2000mg/kg) treatment after 52 weeks reduced body weight (CT=23.5±3.3, n=20; GA=24.2±2.5, n=19; GB=21.6±1.9g, n=21; p=0.009). All animals treated with NNK presented lung macroscopic lesions (CT=9.3±5.1; GA=12.3±3.5; GB=11.3±4.0; p=0.0604), and interestingly, a decreased percentage of lesions greater than 2.5mm were noted in guarana (GB) treated animals (CT=45.5±19.6%; GA=38.1±18.4%; GB=14.5±9.5%; p<0.0001). Histopathology and morphometrical analysis indicated that guarana reduced the malignancy of lung lesions (CT=1.7±0.4; GA=1.6±0.3; GB=1.5±0.3; p=0.0424) and led to a tendency of decreased tumor burden (CT=8.2±5.8%; GA=7.2±3.7%; GB=4.4±3.3%; p=0.0653). At a molecular level, guarana-treated animals presented lung tumors with less PCNA positive cells, indicating slower cell proliferation (CT=29.9±11.2%, n=6; GB=17.3±6.5%, n=7; p=0.0221). Accordingly, after phospho-CREB immunohistochemical analysis, which indicates that the transcription factor CREB/ATF-1 is in its active form, it was possible to note that guarana induced a growth control effect in lung tumor cells by reducing CREB activation (CT=63.9±5.6%, n=4; GB=47.0±5.2%, n=4; p=0.0286) and consequently control the progression of NNK-induced lung carcinogenesis. Our efforts are now directed to study which protein(s) phosphorylated CREB in these lung tumors as p38/MAPK, ERK1/2 and SAPK/JNK1, 2, 3 and identify the guarana targets responsible for such effects.
5-Azacytidine, Valproic Acid and ALL-Trans Retinoic Acid in INT-2/High Risk Myelodysplastic Syndromes: Results of the GIMEMA MDS0205 Multicenter Trial
Authors: Maria Teresa Voso, Valeria Santini, Carlo Finelli, Lorenza Borin, Emanuele Angelucci, Giuseppe Fioritoni, Benedetta Neri, Agostino Cortellezi, Oreste Villani, Francesco Buccisano, Giovanni Martinelli, Maria Concetta Petti, Gina Zini, Alfonso Piciocchi, Paola Fazi, Giuliana Alimena, Marco Gobbi, Vincenzo Liso, Giuseppe Leone
Journal: Blood (2008)
Tyrosine kinase blocking collagen IV–derived peptide suppresses ocular neovascularization and vascular leakage
Authors: Raquel Lima e Silva, Yogita Kanan, Adam C. Mirando, Jayoung Kim, Ron B. Shmueli, Valeria E. Lorenc, Seth D. Fortmann, Jason Sciamanna, Niranjan B. Pandey, Jordan J. Green, Aleksander S. Popel, Peter A. Campochiaro
Journal: Science Translational Medicine (2017)

An integrin-binding peptide derived from collagen IV prevents ligand-induced activation of multiple tyrosine kinase receptors and strongly suppresses ocular neovascularization and vascular leakage.
Mesenchymal Stem Cells Promote the Engraftment of Cord Blood CD34+ Cells but Do Not Accelarate Platelet Recovery NOD/SCID Mice.
Authors: Yvette van Hensbergen, Helen de Boer, Manon C. Slot, Laurus F. Schipper, Anneke Brand, Willem E. Fibbe
Journal: Blood (2005)
Metformin Inhibits Hepatic mTORC1 Signaling via Dose-Dependent Mechanisms Involving AMPK and the TSC Complex
Authors: Jessica J. Howell, Kristina Hellberg, Marc Turner, George Talbott, Matthew J. Kolar, Debbie S. Ross, Gerta Hoxhaj, Alan Saghatelian, Reuben J. Shaw, Brendan D. Manning
Journal: Cell Metabolism (2017)
Mature Erythroblasts Die of Autophagy and Induce Autophagy of Immature Erythroblasts, Limiting the Final Cellular Output In Human Erythroid Massive Amplification (HEMA) Culture
Authors: Giovanni Migliaccio, Francesca Masiello, Valentina Tirelli, Massimo Sanchez, Lilian Varricchio, Carolyn Whitsett, Anna Rita F Migliaccio
Journal: Blood (2010)
Positive Predictive Value of Progressively Elevated D-Dimer Levels in Patients with a Suspected First Deep Vein Thrombosis.
Authors: Sarah Louise Dunbar Takach Lapner, Lori Ann Linkins, Shannon M. Bates, Jim Julian, James D. Douketis, Sameer Parpia, Sam Schulman, Clive Kearon
Journal: Blood (2012)
Change in Liver Iron Concentration (LIC), Serum Ferritin (SF) and Labile Plasma Iron (LPI) Over 1 Year of Deferasirox (DFX/Exjade®) Therapy in a Cohort of Myelodysplastic Patients
Authors: Peter L Greenberg, Charles Schiffer, Charles A Koller, Tara Glynos, Carole Paley
Journal: Blood (2008)
Gene Transfer of Canine FVIIa Results in Partial Correction of Canine Hemophilia: A Model for FVIII/FIX Gene-Based Bypassing Agents.
Authors: Paris Margaritis, Elise Roy, Harre D. Downey, Shangzen Zhou, Elizabeth Merricks, Aaron Dillow, Timothy C. Nichols, Katherine A. High
Journal: Blood (2007)
Survival in Children with Perinatally Acquired Human Immunodeficiency Virus Type 1 Infection
Authors: G B Scott, C Hutto, R W Makuch, M T Mastrucci, T O'Connor, C D Mitchell, E J Trapido, W P Parks
Journal: New England Journal of Medicine (1989)

We describe our experience at Jackson Memorial Hospital in Miami, Florida, with 172 children who were given diagnoses of perinatally acquired infection with human immunodeficiency virus type 1 (HIV-1). The 146 mothers of the children acquired HIV-1 through heterosexual contact (69 percent), intravenous drug use (30 percent), or blood transfusion (1 percent). The children presented with symptomatic disease at a median age of eight months; only 21 percent presented after the age of two years. The most common first manifestations of disease were lymphoid interstitial pneumonia (in 17 percent), encephalopathy (in 12 percent), recurrent bacterial infections (in 10 percent), and candida esophagitis (in 8 percent), for which the median survival times from diagnosis were 72, 11, 50, and 12 months, respectively. Nine percent of the children had Pneumocystis carinii pneumonia at a median age of five months and had a median survival of only one month. The median survival for all 172 children was 38 months from the time of diagnosis. Mortality was highest in the first year of life (17 percent), and by proportional-hazard analysis the probability of long-term survival is low. In multivariate analyses, early age at diagnosis and the first identifiable pattern of clinical disease were found to be independently related to survival. We conclude that children with perinatally acquired HIV-1 infection have a very poor prognosis and that most become symptomatic before one year of age. Early diagnosis is important, since there is only a short interval in which to initiate prophylactic or antiviral treatment before progressive disease begins.
Early CP CML, Nilotinib 400 mg Twice Daily Frontline: Beyond 3 Years, Results Remain Excellent and Stable (A GIMEMA CML Working Party Trial)
Authors: Gabriele Gugliotta, Fausto Castagnetti, Massimo Breccia, Luciano Levato, Adele Capucci, Mario Tiribelli, Alfonso Zaccaria, Monica Bocchia, Antonio Cuneo, Fabio Stagno, Giorgina Specchia, Maurizio Musso, Bruno Martino, Michele Cedrone, Tamara Intermesoli, Francesca Palandri, Simona Soverini, Carmen Baldazzi, Sandra Durante, Nicoletta Testoni, Giuliana Alimena, Fabrizio Pane, Giuseppe Saglio, Michele Baccarani, Giovanni Martinelli, Gianantonio Rosti
Journal: Blood (2011)
Antibody 10-1074 suppresses viremia in HIV-1-infected individuals
Authors: Marina Caskey, Till Schoofs, Henning Gruell, Allison Settler, Theodora Karagounis, Edward F Kreider, Ben Murrell, Nico Pfeifer, Lilian Nogueira, Thiago Y Oliveira, Gerald H Learn, Yehuda Z Cohen, Clara Lehmann, Daniel Gillor, Irina Shimeliovich, Cecilia Unson-O'Brien, Daniela Weiland, Alexander Robles, Tim Kümmerle, Christoph Wyen, Rebeka Levin, Maggi Witmer-Pack, Kemal Eren, Caroline Ignacio, Szilard Kiss, Anthony P West, Hugo Mouquet, Barry S Zingman, Roy M Gulick, Tibor Keler, Pamela J Bjorkman, Michael S Seaman, Beatrice H Hahn, Gerd Fätkenheuer, Sarah J Schlesinger, Michel C Nussenzweig, Florian Klein
Journal: Nature Medicine (2017)