tbuckley/cabot-search huggingface dataset:
Long-term follow up of patients with follicular lymphoma (FL) receiving high dose therapy (HDT) with autologous haematopoietic progenitor cell support at St. Bartholomew’s Hospital (SBH)
Authors: A. J. Davies, J. Apostolidis, I. N. Micallef, S. Montoto, J. Matthews, T. A. Lister, A. Z. S. Rohatiner
Journal: Journal of Clinical Oncology (2005)

6568 Background: HDT supported by autologous haematopoietic progenitor cells has been investigated as consolidation of 2nd or subsequent remission of FL at SBH. Long-term follow up data are reported. Methods: Between June 1985 and Dec. 2001, 125 patients (pts) median age 45 years (range 25–62) received cyclophosphamide + total body irradiation (CY+TBI), supported by either antibody purged marrow (100 pts), or peripheral blood progenitor cells (PBPC) (5 pts) until Feb 1997, and thereafter, BCNU, etoposide, cytarabine and melphalan with PBPC (20 pts). At the time of HDT, 85 pts were in 2nd remission, 28 in 3rd, and 12 in ≥4th; 45 pts were in CR and 80 in PR following a median of 3 (2–9) prior therapies. Median follow-up is 11.7 yrs (0–19.1) and 10.8 yrs (1.3–19.1) for surviving pts. Results: At 5, 10 and 15 yrs, Kaplan-Meier estimates for freedom from recurrence (FFR) are: 56%, 46%, and 43% respectively, for progression free survival: 45%, 32%, 28% and for overall survival (OS): 69%, 48% and 39%. To date, there is no difference in OS according to regimen. OS was superior in pts receiving HDT in 2nd compared to subsequent remissions (p<0.005). Sixty-one patients have recurred (median time to recurrence 1.6 yrs (0.2 to 12.0), 90% within 6 yrs; 17 asymptomatic recurrences were detected following annual surveillance CT and bone marrow examination. Histology at recurrence was FL in 48 pts, transformation to DLBCL in 13 pts. Comparison of pts receiving HDT in 2nd remission with conventionally treated historical controls treated at SBH demonstrates a continuing significant superiority in FFR (p<0.01) and a trend towards significant improvement in OS (p=0.05). Duration of 2nd remission exceeded that of 1st remission in 73% of pts. tMDS/tAML has developed in 21 pts (17%), all post CY+TBI, at a median 4.7 yrs (0.7–13.9). Death in remission occurred in 24 pts (5 early treatment-related, 11 tMDS/tAML, 4 other 2nd malignancy, 3 unrelated causes,1 unknown). Conclusions: For a subset of patients with FL, HDT has resulted in prolonged FFR however this benefit has been tempered by late toxicity. Performed in 2nd remission, HDT significantly modifies the clinical course of FL. No significant financial relationships to disclose.
Nilotinib Treatment in Pediatric Patients (pts) with Philadelphia Chromosome- Positive (Ph+) Leukemia Refractory to Prior Tyrosine Kinase Inhibitor (TKI) Therapy: Results from Nilotinib Compassionate Use Program
Authors: Alan S. Wayne, Carla Renata Macedo, Tomasz Szczudlo, Richard C. Woodman
Journal: Blood (2008)
Corticosteroids and infliximab impair the performance of interferon-γ release assays used for diagnosis of latent tuberculosis
Authors: Alexander Edwards, Yifang Gao, Raymond N Allan, Darran Ball, Hans de Graaf, Tracy Coelho, Vanessa Clifford, Nigel Curtis, Anthony Williams, Saul N Faust, Salah Mansour, Ben Marshall, Paul Elkington, Marc Tebruegge
Journal: Thorax (2017)

The impact of immunosuppression on interferon-γ release assays and novel cytokine biomarkers of TB infection, mycobacteria-specific IL-2, IP-10 and TNF-α responses was investigated in an ex vivo model. Cytokine responses in standard QuantiFERON-TB Gold in-Tube (QFT-GIT) assays were compared with duplicate assays containing dexamethasone or infliximab. Dexamethasone converted QFT-GIT results from positive to negative in 30% of participants. Antigen-stimulated interferon-γ, IL-2 and TNF-α responses were markedly reduced, but IP-10 responses were preserved. Infliximab caused QFT-GIT result conversion in up to 30% of participants and substantial reductions in all cytokine responses. Therefore, corticosteroids and anti-TNF-α agents significantly impair interferon-γ release assay performance. IP-10 may be a more robust TB biomarker than interferon-γ in patients receiving corticosteroids.
Non Malignant Late Complications After Allogeneic Hematopoietic Stem Cell Transplantation (allo-HSCT); Korean Experience
Authors: Silvia Park, Su Jin Lee, Won jin Chang, Chi Hoon Maeng, Jung Yong Hong, Moon Ki Choi, Sung Hee Lim, Ji Yun Lee, Chul Won Jung, Jun Ho Jang, Kihyun Kim, Young Saing Kim, Je-Hwan Lee, Sung-Soo Yoon
Journal: Blood (2012)
Shape-controlled fabrication of magnetite silver hybrid nanoparticles with high performance magnetic hyperthermia
Authors: Qi Ding, Dongfang Liu, Dawei Guo, Fang Yang, Xingyun Pang, Renchao Che, Naizhen Zhou, Jun Xie, Jianfei Sun, Zhihai Huang, Ning Gu
Journal: Biomaterials (2017)
LY2784544, a Novel JAK2 Inhibitor, Decreases In Vitro Growth of Hematopoietic Human Progenitors From JAK2 V617F Positive Polycythemia Vera Patients
Authors: Lourdes Florensa, Beatriz Bellosillo, Leonor Arenillas, Liandong Ma, Richard Walgren, Alberto Alvarez, Judit Gonzalez, Rosa M Vila, Raquel Longarón, Carles Besses
Journal: Blood (2010)
Abstract B15: Anti-metastatic activity of RGD-specific cadherin-17-targeting monoclonal antibodies in colorectal cancer
Authors: Rubén Bartolomé, Sofia Torres, Beatriz Escudero-Paniagua, Carmen Aizpurua, Eva Calviño, Juan I. Imbaud, Ignacio Casal
Journal: Cancer Research (2017)

Abstract Most colorectal cancer deaths occur as a consequence of late diagnosis and the appearance of metastasis. We demonstrated that a RGD motif present in liver-intestine cadherin, also known as cadherin 17 (CDH17), plays a critical role in the liver metastasis of colorectal cancer by interacting with α2β1 integrin. CDH17 is able to induce a conformational change in β1 integrin to promote a high affinity conformation. This change is dependent of the RGD motif present in domain 6 of CDH17. The same activation was observed after cell exposition to 9 amino acid peptides containing the RGD motif and the flanking sequences from CDH17. Commercial antibodies anti-CDH17 did not cause any effect on β1 integrin activation. Here, we have used peptides containing the RGD motif and their flanking sequences in CDH17 to retrieve four highly selective monoclonal antibodies with anti-metastatic activity. Only CDH17 RGD-specific monoclonal antibodies inhibited β1 integrin activation in colorectal cancer cells. This inhibition provoked a significant reduction in cell adhesion and proliferation of metastatic cells. In addition, the treatment with these four anti-cadherin RGD antibodies impaired the activation of FAK, JNK and ERK kinases, which are critical for cell adhesion and proliferation. Moreover, RGD-specific monoclonal antibodies were able to cause a significant increase in mouse survival after intra-splenic injection together with highly metastatic cells, as determined by Kaplan-Meier survival analysis and log-rank curves. However, this effect on survival was different for each monoclonal antibody, suggesting a relevant impact of the RGD binding orientation in antibody recognition. As a conclusion, we propose that blocking the interaction between RGD cadherins and α2β1 integrin with highly selective monoclonal antibodies constitutes a promising therapy against colon cancer progression and liver metastasis. Citation Format: Rubén Bartolomé, Sofia Torres, Beatriz Escudero-Paniagua, Carmen Aizpurua, Eva Calviño, Juan I. Imbaud, Ignacio Casal. Anti-metastatic activity of RGD-specific cadherin-17-targeting monoclonal antibodies in colorectal cancer. [abstract]. In: Proceedings of the AACR Special Conference on Colorectal Cancer: From Initiation to Outcomes; 2016 Sep 17-20; Tampa, FL. Philadelphia (PA): AACR; Cancer Res 2017;77(3 Suppl):Abstract nr B15.
IPI and R-IPI in Korean DLBCL Patients Treated with R-CHOP.
Authors: Sung-Hwa Bae, Hun-Mo Ryoo, Min Kyoung Kim, Kyung Hee Lee, Myung Soo Hyun, Hawk Kim, Jea-Hoo Park, Won-Sik Lee, Young-Don Joo
Journal: Blood (2007)
Sex-Based Differences in Cardiometabolic Biomarkers
Authors: Jeanney Lew, Monika Sanghavi, Colby R. Ayers, Darren K. McGuire, Torbjørn Omland, Dorothee Atzler, Maria O. Gore, Ian Neeland, Jarett D. Berry, Amit Khera, Anand Rohatgi, James A. de Lemos
Journal: Circulation (2017)

Background: Few data are available comparing cardiovascular disease (CVD) biomarker profiles between women and men in the general population. We analyzed sex-based differences in multiple biomarkers reflecting distinct pathophysiological pathways, accounting for differences between women and men in CVD risk factors, body composition, and cardiac morphology. Methods: A cross-sectional analysis was performed using data from the Dallas Heart Study, a multiethnic population-based study. Associations between sex and 30 distinct biomarkers representative of 6 pathophysiological categories were evaluated using multivariable linear regression adjusting for age, race, traditional CVD risk factors, kidney function, insulin resistance, MRI and dual-energy x-ray absorptiometry measures of body composition and fat distribution, and left ventricular mass. Results: After excluding participants with CVD, the study population included 3439 individuals, mean age 43 years, 56% women, and 52% black. Significant sex-based differences were seen in multiple categories of biomarkers, including lipids, adipokines, and biomarkers of inflammation, endothelial dysfunction, myocyte injury and stress, and kidney function. In fully adjusted models, women had higher levels of high-density lipoprotein cholesterol and high-density lipoprotein particle concentration, leptin, d -dimer, homoarginine, and N-terminal pro B-type natriuretic peptide, and lower levels of low-density lipoprotein cholesterol, adiponectin, lipoprotein-associated phospholipase A2 mass and activity, monocyte chemoattractant protein-1, soluble endothelial cell adhesion molecule, symmetrical dimethylarginine, asymmetrical dimethylarginine, high-sensitivity troponin T, and cystatin C. Conclusions: Biomarker profiles differ significantly between women and men in the general population. Sex differences were most apparent for biomarkers of adiposity, endothelial dysfunction, inflammatory cell recruitment, and cardiac stress and injury. Future studies are needed to characterize whether pathophysiological processes delineated by these biomarkers contribute to sex-based differences in the development and complications of CVD.
Specific Regulation of NFAT (Nuclear Factors of Activated T Cells) Expression in CD34+ Cells Differentiating into Diverse Hematopoietic Lineages.
Authors: Alexander Kiani, Hanna Kuithan, Friederike Kuithan, Satu Kyttaelae, Ivonne Habermann, Martin Bornhaeuser, Gerhard Ehninger
Journal: Blood (2006)
TMIC-13MUTANT<i>IDH1/2</i>SUPPRESSES LOCAL AND SYSTEMIC THROMBOSIS IN GLIOMA PATIENTS
Authors: Steven Schwarze, Laith Khoury, Cheddhi Thomas, Carolina Benjamin, Rui Chen, Li Chen, Yinxing Liu, Kristine Song, Caleb Dawson, Donato Pacione, David Zagzag, Thomas McIntyre, Matija Snuderl, Craig Horbinski
Journal: Neuro-Oncology (2015)

Mutations in isocitrate dehydrogenase 1 and 2 (mutIDH1/2) are common in gliomas, resulting in enzymes that produce D-2-hydroxyglutarate (D-2-HG). The effects of mutIDH1/2 on the microenvironment, including thrombosis, are not known. In discovery and validation cohorts of World Health Organization (WHO) grade II-IV gliomas from two institutions (total N = 317), microthrombi were present in 85-90% of wild-type gliomas but in only 2-6% of mutant gliomas (P < 0.0001), and their absence was an independent predictor of mutIDH1/2. Systemic hypercoagulation occurred in 25-30% of patients with wild-type IDH1/2 gliomas, but in 0% of patients with mutIDH1/2 gliomas (P < 0.0001). The prognostic strength of microthrombi was comparable to necrosis and microvascular proliferation, the current WHO criteria for a diagnosis of glioblastoma. In silico analysis of 428 gliomas from The Cancer Genome Atlas (TCGA) revealed that, in the coagulome, the mRNA with the strongest inverse relationship to mutIDH1/2 was F3, encoding tissue factor procoagulant (P = 1.06E-52). MutIDH1/2 gliomas in the TCGA also had significantly elevated F3 promoter methylation (P < 0.0001). In a separate tissue microarray containing 95 gliomas, mutIDH1/2 tumors showed dramatically reduced tissue factor protein expression (P < 0.0001). Additionally, D-2-HG inhibited human platelet aggregation by blocking intracellular calcium accumulation. In human in vitro and mouse in vivo models, mutIDH1 and D-2-HG lowered free serum calcium by up to 40% and markedly impaired coagulation (P < 0.0001). In sum, mutIDH1/2 enzymes have potent antithrombotic activity within gliomas and systemically. These findings have profound implications for the pathologic evaluation of gliomas, the effect of altered isocitrate metabolism on tumor microenvironment and calcium homeostasis, and the pre-and postoperative management of these patients.
MODELING and Targeting ERG-INDUCED Acute MYELOID LEUKEMIA (AML).
Authors: Gil Smooha, Yehudit Birger, Liat Goldberg, Jasmine Jacob-Hirsch, Ninette Amariglio, Gideon Rechavi, Ditsa Levanon, Yoram Groner, Anat Taragan, Yoel Kloog, Jeremy Q Wen, John Crispino, Michael D. Radmacher, Guido Marcucci, Clara D. Bloomfield, Shai Izraeli
Journal: Blood (2009)
STEM-13EXPRESSION OF STEM CELL, PROLIFERATION AND CHEMORESISTANCE MARKERS IN GLIOMA CELLS IN THE TUMOR PERIPHERY
Authors: Sune Munthe, Stine Asferg Petterson, Rikke Hedegaard Dahlrot, Frantz Rom Poulsen, Bjarne Winther Kristensen
Journal: Neuro-Oncology (2015)

Gliomas are highly infiltrative tumors incurable with surgery. Although surgery removes the bulk tumor, tumor cells in the periphery are left behind resulting in tumor relapses. The aim of the present study was to characterize the phenotype of tumor cells in the periphery focusing on tumor stemness, proliferation and chemoresistance. This was investigated in situ in patient glioma tissue as well as in orthotopic glioblastoma xenografts. We identified 26 gliomas having the R132 mutation in Isocitrate DeHydrogenase 1 (mIDH1). A double immunofluorescence approach identifying mIDH1 positive tumor cells and a panel of markers was used. The panel comprised of five different stem cell markers (CD133, Musashi-1, Bmi-1, Sox-2 and Nestin), the proliferation marker Ki-67 as well as MGMT. Computer-based automated classifiers were designed to measure the mIDH1 positive nucleus area-fraction of the chosen markers. Moreover orthotopic glioblastoma xenografts from five different patient-derived spheroid cultures were obtained. A double immunofluorescence approach identifying vimentin positive tumor cells and the same panel of markers were used, except MGMT since most tumors were MGMT methylated. The results showed that tumor cells in the periphery of patient gliomas expressed stem cell markers, however at a significantly lower level than in the tumor core. The Ki-67 level was significantly reduced, whereas the reduction in the MGMT level did not reach significance. In orthotopic glioblastoma xenografts same results were obtained for Sox-2, Nestin and Ki-67, where as the other markers were expressed at the same level in core and periphery. In conclusion tumor cells in the periphery of patient gliomas displayed reduced but to a large degree preserved stemness and proliferation. Novel therapies aiming at preventing recurrence should therefore take tumor stemness into account. Orthotopic glioblastoma xenografts to a large degree mimic patient tumors and therefore have a promising translational potential.
Iron Chelation Therapy in Transfusion Dependent Patients with Thalassemia and Minimal Liver Iron Load
Authors: Antonios Kattamis, Konstantinos Stokidis, Theoni Petropoulou, Dimitra Kyriacopoulou, Polyxeni Delaporta, Ioannis Papassotiriou, Vassilis Ladis
Journal: Blood (2010)
High Resolution Genomic Profiling Using Single Nucleotide Polymorphism Microarrays Reveals Novel Genomic Lesions in Hairy Cell Leukaemia and Hairy-Cell Leukaemia Variant
Authors: Sarah L Hockley, Monica Else, Paola E Leone, Brian A Walker, Alison Morilla, Daniel Catovsky, Gareth J Morgan, Estella Matutes, David Gonzalez
Journal: Blood (2008)
Pharmacological inhibition of porcupine induces regression of experimental skin fibrosis by targeting Wnt signalling
Authors: Chih-Wei Chen, Christian Beyer, Jun Liu, Christiane Maier, Chun Li, Thuong Trinh-Minh, Xiaohan Xu, Stuart H Cole, Mindy H Hsieh, Nicholas Ng, Alana Althage, Shelly Meeusen, Shifeng Pan, Eric C Svensson, H Martin Seidel, Georg Schett, Peter Gergely, Jennifer L Harris, Jörg H W Distler
Journal: Annals of the Rheumatic Diseases (2017)

Wnt signalling has been implicated in activating a fibrogenic programme in fibroblasts in systemic sclerosis (SSc). Porcupine is an O-acyltransferase required for secretion of Wnt proteins in mammals. Here, we aimed to evaluate the antifibrotic effects of pharmacological inhibition of porcupine in preclinical models of SSc.The porcupine inhibitor GNF6231 was evaluated in the mouse models of bleomycin-induced skin fibrosis, in tight-skin-1 mice, in murine sclerodermatous chronic-graft-versus-host disease (cGvHD) and in fibrosis induced by a constitutively active transforming growth factor-β-receptor I.Treatment with pharmacologically relevant and well-tolerated doses of GNF6231 inhibited the activation of Wnt signalling in fibrotic murine skin. GNF6231 ameliorated skin fibrosis in all four models. Treatment with GNF6231 also reduced pulmonary fibrosis associated with murine cGvHD. Most importantly, GNF6231 prevented progression of fibrosis and showed evidence of reversal of established fibrosis.These data suggest that targeting the Wnt pathway through inhibition of porcupine provides a potential therapeutic approach to fibrosis in SSc. This is of particular interest, as a close analogue of GNF6231 has already demonstrated robust pathway inhibition in humans and could be available for clinical trials.
Google Trends terms reporting rhinitis and related topics differ in European countries
Authors: J. Bousquet, I. Agache, J. M. Anto, K. C. Bergmann, C. Bachert, I. Annesi‐Maesano, P. J. Bousquet, G. D'Amato, P. Demoly, G. De Vries, E. Eller, W.J. Fokkens, J. Fonseca, T. Haahtela, P. W. Hellings, J. Just, T. Keil, L. Klimek, P. Kuna, K. C. Lodrup Carlsen, R. Mösges, R. Murray, K. Nekam, G. Onorato, N. G. Papadopoulos, B. Samolinski, P. Schmid‐Grendelmeier, M. Thibaudon, P. Tomazic, M. Triggiani, A. Valiulis, E. Valovirta, M. Van Eerd, M. Wickman, T. Zuberbier, A. Sheikh
Journal: Allergy (2017)

Google Trends (GT) searches trends of specific queries in Google and reflects the real-life epidemiology of allergic rhinitis. We compared Google Trends terms related to allergy and rhinitis in all European Union countries, Norway and Switzerland from 1 January 2011 to 20 December 2016. The aim was to assess whether the same terms could be used to report the seasonal variations of allergic diseases. Using the Google Trend 5-year graph, an annual and clear seasonality of queries was found in all countries apart from Cyprus, Estonia, Latvia, Lithuania and Malta. Different terms were found to demonstrate seasonality depending on the country - namely 'hay fever', 'allergy' and 'pollen' - showing cultural differences. A single set of terms cannot be used across all European countries, but allergy seasonality can be compared across Europe providing the above three terms are used. Using longitudinal data in different countries and multiple terms, we identified an awareness-related spike of searches (December 2016).
Platelet-localized FXI promotes a vascular coagulation-inflammatory circuit in arterial hypertension
Authors: Sabine Kossmann, Jeremy Lagrange, Sven Jäckel, Kerstin Jurk, Moritz Ehlken, Tanja Schönfelder, Yvonne Weihert, Maike Knorr, Moritz Brandt, Ning Xia, Huige Li, Andreas Daiber, Matthias Oelze, Christoph Reinhardt, Karl Lackner, Andras Gruber, Brett Monia, Susanne H. Karbach, Ulrich Walter, Zaverio M. Ruggeri, Thomas Renné, Wolfram Ruf, Thomas Münzel, Philip Wenzel
Journal: Science Translational Medicine (2017)

Multicellular interactions of platelets, leukocytes, and the blood vessel wall support coagulation and precipitate arterial and venous thrombosis. High levels of angiotensin II cause arterial hypertension by a complex vascular inflammatory pathway that requires leukocyte recruitment and reactive oxygen species production and is followed by vascular dysfunction. We delineate a previously undescribed, proinflammatory coagulation-vascular circuit that is a major regulator of vascular tone, blood pressure, and endothelial function. In mice with angiotensin II-induced hypertension, tissue factor was up-regulated, as was thrombin-dependent endothelial cell vascular cellular adhesion molecule 1 expression and integrin αMβ2- and platelet-dependent leukocyte adhesion to arterial vessels. The resulting vascular inflammation and dysfunction was mediated by activation of thrombin-driven factor XI (FXI) feedback, independent of factor XII. The FXI receptor glycoprotein Ibα on platelets was required for this thrombin feedback activation in angiotensin II-infused mice. Inhibition of FXI synthesis with an antisense oligonucleotide was sufficient to prevent thrombin propagation on platelets, vascular leukocyte infiltration, angiotensin II-induced endothelial dysfunction, and arterial hypertension in mice and rats. Antisense oligonucleotide against FXI also reduced the increased blood pressure and attenuated vascular and kidney dysfunction in rats with established arterial hypertension. Further, platelet-localized thrombin generation was amplified in an FXI-dependent manner in patients with uncontrolled arterial hypertension, suggesting that platelet-localized thrombin generation may serve as an inflammatory marker of high blood pressure. Our results outline a coagulation-inflammation circuit that promotes vascular dysfunction, and highlight the possible utility of FXI-targeted anticoagulants in treating hypertension, beyond their application as antithrombotic agents in cardiovascular disease.
Mutations in Ribosomal Protein Genes of Diamond-Blackfan Anemia Patients in Japan.
Authors: Yuki Konno, Tsutomu Toki, Satoru Tandai, Gang Xu, Kiminori Terui, Shouichi Ohga, Seiji Kojima, Ryu Yanagisawa, Kenichi Koike, Daiichiro Hasegawa, Yoshiyuki Kosaka, Rie Kanei, Tsuyoshi Imai, Teruaki Hongo, Myoung-Ja Park, Arata Watanabe, Etsuro Ito
Journal: Blood (2009)
The Useful Individualized Assessment of Immunosuppressive Therapy with Cyclosporine A (CsA) after Allogeneic Stem Cell Transplantation by Simultaneous Analyses of Cytokine Production among CD4+ T Cells and Blood CsA Levels.
Authors: Nobuhiro Tsukada, Tatsuo Furukawa, Hiromi Ito, Noriko Izumi, Akihito Momoi, Kiyoshi Okazuka, Keiichiro Honma, Masayoshi Masuko, Shigeo Hashimoto, Sadao Aoki, Yoshifusa Aizawa
Journal: Blood (2004)
Weekly Combination Chemotherapy with Cyclophosphamide, Bortezomib and Dexamethasone (CyBorD) for Newly Diagnosed Patients with Advanced Cardiac Disease Due to Systemic AL Amyloidosis
Authors: Furha I. Cossor, Adam Boruchov, Michael Danso, Michael Edward Lee, Ayan Patel, Eric Winer, Rodney Falk, Raymond L. Comenzo
Journal: Blood (2011)
Genome-Wide Profiling Reveals Recurring Molecular Defects in Relapsed Childhood Acute Lymphoblastic Leukemia (ALL): A Children’s Oncology Group Study.
Authors: Jun Yang, Deepa Bhojwani, Wenjian Yang, Yiping Fan, Meenakshi Devidas, Stephen Hunger, Cheryl Willman, Elizabeth Raetz, Mary V. Relling, William L. Carroll
Journal: Blood (2007)