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1. Elucidating mechanisms of genetic cross-disease associations at the PROCR vascular disease locus (vol 13, 1222, 2022)

Author

Stacey, D, Chen, LY, Stanczyk, PJ, Howson, JMM, Mason, AM, Burgess, S, MacDonald, S, Langdown, J, McKinney, H, Downes, K, Farahi, N, Peters, JE, Basu, S, Pankow, JS, Tang, WH, Pankratz, N, Sabater-Lleal, M, de Vries, PS, Smith, NL, Dehghan, A, Heath, AS, Morrison, AC, Reiner, AP, Johnson, A, Richmond, A, Peters, A, Vlieg, AV, McKnight, B, Psaty, BM, Hayward, C, Ward-Caviness, C, O'Donnell, C, Chasman, D, Strachan, DP, Tregouet, DA, Mook-Kanamori, D, Gill, D, Thibord, F, Asselbergs, FW, Leebeek, FWG, Rosendaal, FR, Davies, G, Homuth, G, Temprano, G, Campbell, H, Taylor, HA, Bressler, J, Huffman, JE, Rotter, JI, Yao, J, Wilson, JF, Bis, JC, Hahn, JM, Desch, KC, Wiggins, KL, Raffield, LM, Bielak, LF, Yanek, LR, Kleber, ME, Mueller, M, Kavousi, M, Mangino, M, Conomos, MP, Liu, ML, Brown, MR, Jhun, MA, Chen, MH, de Maat, MPM, Peyser, PA, Elliot, P, Wei, P, Wild, PS, Morange, PE, van der Harst, P, Yang, Q, Le, NQ, Marioni, R, Li, RF, Damrauer, SM, Cox, SR, Trompet, S, Felix, SB, Volker, U, Koenig, W, Jukema, JW, Guo, XQ, Gelinas, AD, Schneider, DJ, Janjic, N, Samani, NJ, Ye, S, Summers, C, Chilvers, ER, Danesh, J, and Paul, DS

Published
2022

2. Genomic and transcriptomic association studies identify 16 novel susceptibility loci for venous thromboembolism

Author

Lindstrom, S, Wang, L, Smith, EN, Gordon, W, Vlieg, AV, de Andrade, M, Brody, JA, Pattee, JW, Haessler, J, Brumpton, B, Chasman, DI, Suchon, P, Chen, MH, Turman, C, Germain, M, Wiggins, KL, MacDonald, J, Braekkan, SK, Armasu, SM, Pankratz, N, Jackson, RD, Nielsen, JB, Giulianini, F, Puurunen, MK, Ibrahim, M, Heckbert, SR, Damrauer, SM, Natarajan, P, Klarin, D, de Vries, PS, Sabater-Lleal, M, Huffman, JE, Bammler, TK, Frazer, KA, McCauley, BM, Taylor, K, Pankow, JS, Reiner, AP, Gabrielsen, ME, Deleuze, JF, O'Donnell, CJ, Kim, J, McKnight, B, Kraft, P, Hansen, JB, Rosendaal, FR, Heit, JA, Psaty, BM, Tang, WH, Kooperberg, C, Hveem, K, Ridker, PM, Morange, PE, Johnson, AD, Kabrhel, C, Tregouet, DA, Smith, NL, Busenkell, E, Judy, R, Lynch, J, Levin, M, Aragam, JHK, Chaffin, M, Haas, M, Assimes, TL, Huang, J, Lee, KM, Shao, Q, Huang, YF, Sun, YV, Vujkovic, M, Saleheen, D, Miller, DR, Reaven, P, DuVall, S, Boden, W, Pyarajan, S, Henke, P, Gaziano, JM, Concato, J, Rader, DJ, Cho, K, Chang, KM, Wilson, PWF, Tsao, PS, Kathiresan, S, Obi, A, Million Veteran Program, CHARGE Hemostasis Working Grp, and INVENT Consortium

Subjects
cardiovascular diseases, equipment and supplies
Abstract

Venous thromboembolism (VTE) is a significant contributor to morbidity and mortality. To advance our understanding of the biology contributing to VTE, we conducted a genome-wide association study (GWAS) of VTE and a transcriptome-wide association study (TWAS) based on imputed gene expression from whole blood and liver. Wemeta-analyzedGWAS data from18 studies for 30 234 VTE cases and 172 122 controls and assessed the association between 12 923 718 genetic variants and VTE. We generated variant prediction scores of gene expression from whole blood and liver tissue and assessed them for association with VTE. Mendelian randomization analyses were conducted for traits genetically associated with novel VTE loci. We identified 34 independent genetic signals for VTE risk from GWAS meta-analysis, of which 14 are newly reported associations. This included 11 newly associated genetic loci (C1orf198, PLEK, OSMR-AS1, NUGGC/SCARA5, GRK5, MPHOSPH9, ARID4A, PLCG2, SMG6, EIF5A, and STX10) of which 6 replicated, and 3 new independent signals in 3 known genes. Further, TWAS identified 5 additional genetic loci with imputed gene expression levels differing between cases and controls in whole blood (SH2B3, SPSB1, RP11-747H7.3, RP4-737E23.2) and in liver (ERAP1). At some GWAS loci, we found suggestive evidence that the VTE association signal for novel and previously known regions colocalized with expression quantitative trait locus signals. Mendelian randomization analyses suggested that blood traits may contribute to the underlying risk of VTE. To conclude, we identified 16 novel susceptibility loci for VTE; for some loci, the association signals are likely mediated through gene expression of nearby genes.

Published
2019

3. Causal effect of plasminogen activator inhibitor type 1 on coronary heart disease

Author

Song, C, Burgess, S, Eicher, JD, O'Donnell, CJ, Johnson, AD, Huang, J, Sabater-Lleal, M, Asselbergs, FW, Tregouet, D, Shin, SY, Ding, J, Baumert, J, Oudot-Mellakh, T, Folkersen, L, Smith, NL, Williams, SM, Ikram, MA, Kleber, ME, Becker, DM, Truong, V, Mychaleckyj, JC, Tang, W, Yang, Q, Sennblad, B, Moore, JH, Williams, FMK, Dehghan, A, Silbernagel, G, Schrijvers, EMC, Smith, S, Karakas, M, Tofler, GH, Silveira, A, Navis, GJ, Lohman, K, Chen, MH, Peters, A, Goel, A, Hopewell, JC, Chambers, JC, Saleheen, D, Lundmark, P, Psaty, BM, Strawbridge, RJ, Boehm, BO, Carter, AM, Meisinger, C, Peden, JF, Bis, JC, McKnight, B, Öhrvik, J, Taylor, K, Franzosi, MG, Seedorf, U, Collins, R, Franco-Cereceda, A, Syvänen, AC, Goodall, AH, Yanek, LR, Cushman, M, Müller-Nurasyid, M, Folsom, AR, Basu, S, Matijevic, N, Van Gilst, WH, Kooner, JS, Danesh, J, Clarke, R, Meigs, JB, Kathiresan, S, Reilly, MP, Klopp, N, Harris, TB, Winkelmann, BR, Grant, PJ, Hillege, HL, Watkins, H, Spector, TD, Becker, LC, Tracy, RP, März, W, Uitterlinden, AG, Eriksson, P, Cambien, F, Morange, PE, Koenig, W, Soranzo, N, Van der Harst, P, Liu, Y, Hamsten, A, Ehret, GB, Munroe, PB, Rice, KM, Bochud, M, Chasman, DI, Smith, AV, Epidemiology, Internal Medicine, Radiology & Nuclear Medicine, Virology, Clinical Genetics, Obstetrics & Gynecology, and Gastroenterology & Hepatology

Subjects
0301 basic medicine, Blood Glucose, Aging, Cardiac & Cardiovascular Systems, Epidemiology, medicine.medical_treatment, Genome-wide association study, Coronary Disease, Review, Coronary Artery Disease, 030204 cardiovascular system & hematology, Cardiorespiratory Medicine and Haematology, Cardiovascular, chemistry.chemical_compound, 0302 clinical medicine, Risk Factors, single nucleotide polymorphism, GENETIC-VARIANTS, Odds Ratio, ARTERY-DISEASE, METABOLIC SYNDROME, genome‐wide association study, INSULIN-RESISTANCE, education.field_of_study, Systematic Review and Meta‐Analysis, Fibrinolysis, Incidence, Mendelian Randomization Analysis, Single Nucleotide, C-REACTIVE PROTEIN, 3. Good health, Observational Studies as Topic, plasminogen activator inhibitor type 1, Heart Disease, CARDIOVASCULAR-DISEASE, Plasminogen activator inhibitor-1, Cardiology, Cardiology and Cardiovascular Medicine, Risk assessment, Lipoproteins, HDL, Life Sciences & Biomedicine, medicine.medical_specialty, HDL, Lipoproteins, Population, Polymorphism, Single Nucleotide, Risk Assessment, 03 medical and health sciences, Genetic, Association Studies, Clinical Research, Internal medicine, Mendelian randomization, Plasminogen Activator Inhibitor 1, Journal Article, medicine, Humans, Genetic Predisposition to Disease, GENOME-WIDE ASSOCIATION, Polymorphism, coronary heart disease, education, Heart Disease - Coronary Heart Disease, Science & Technology, genome-wide association study, business.industry, coronary heart disease ■ genome‐wide association study ■ Mendelian randomization ■ plasminogen activator inhibitor type 1 ■ single nucleotide polymorphism, Odds ratio, SUMMARIZED DATA, 030104 developmental biology, Endocrinology, MYOCARDIAL-INFARCTION, chemistry, Multivariate Analysis, Cardiovascular System & Cardiology, business, Biomarkers, Genome-Wide Association Study
Abstract

Background Plasminogen activator inhibitor type 1 ( PAI ‐1) plays an essential role in the fibrinolysis system and thrombosis. Population studies have reported that blood PAI ‐1 levels are associated with increased risk of coronary heart disease ( CHD ). However, it is unclear whether the association reflects a causal influence of PAI ‐1 on CHD risk. Methods and Results To evaluate the association between PAI ‐1 and CHD , we applied a 3‐step strategy. First, we investigated the observational association between PAI ‐1 and CHD incidence using a systematic review based on a literature search for PAI ‐1 and CHD studies. Second, we explored the causal association between PAI ‐1 and CHD using a Mendelian randomization approach using summary statistics from large genome‐wide association studies. Finally, we explored the causal effect of PAI ‐1 on cardiovascular risk factors including metabolic and subclinical atherosclerosis measures. In the systematic meta‐analysis, the highest quantile of blood PAI ‐1 level was associated with higher CHD risk comparing with the lowest quantile (odds ratio=2.17; 95% CI: 1.53, 3.07) in an age‐ and sex‐adjusted model. The effect size was reduced in studies using a multivariable‐adjusted model (odds ratio=1.46; 95% CI : 1.13, 1.88). The Mendelian randomization analyses suggested a causal effect of increased PAI ‐1 level on CHD risk (odds ratio=1.22 per unit increase of log‐transformed PAI ‐1; 95% CI : 1.01, 1.47). In addition, we also detected a causal effect of PAI ‐1 on elevating blood glucose and high‐density lipoprotein cholesterol. Conclusions Our study indicates a causal effect of elevated PAI ‐1 level on CHD risk, which may be mediated by glucose dysfunction.

Published
2017

4. The plasminogen activator inhibitor-1 -675 4G/5G genotype influences the risk of myocardial infarction associated with elevated plasma proinsulin and insulin concentrations in men from Europe: the HIFMECH study

Author

Juhan Vague I, Morange PE, Frere C, Aillaud MF, Alessi MC, Hawe E, Boquist S, Tornvall P, Yudkin JS, Tremoli E, Margaglione M, Hamsten A, Humphries SE, HIFMECH Study Group, DI MINNO, GIOVANNI, Juhan Vague, I, Morange, Pe, Frere, C, Aillaud, Mf, Alessi, Mc, Hawe, E, Boquist, S, Tornvall, P, Yudkin, J, Tremoli, E, Margaglione, M, DI MINNO, Giovanni, Hamsten, A, Humphries, Se, and HIFMECH Study, Group

Subjects
Male, medicine.medical_specialty, Genotype, medicine.medical_treatment, Myocardial Infarction, chemistry.chemical_compound, Insulin resistance, Risk Factors, Internal medicine, Plasminogen Activator Inhibitor 1, Humans, Insulin, Medicine, Myocardial infarction, Proinsulin, Hemostasis, Polymorphism, Genetic, business.industry, Hematology, Odds ratio, Middle Aged, medicine.disease, Europe, Endocrinology, chemistry, Case-Control Studies, Plasminogen activator inhibitor-1, Insulin Resistance, business, Plasminogen activator, Body mass index
Abstract

Summary. Although the potential role of plasminogen activator inhibitor-1 (PAI-1) in the development of coronary artery disease is strongly supported by its biological characteristics, results of clinical studies remain controversial. Objectives: To investigate whether plasma PAI-1 concentrations and the −675 4G/5G polymorphism located in the PAI-1 gene could constitute risk markers for myocardial infarction (MI). Patients and methods: We used a European case–control study, the HIFMECH study, comparing 598 men with MI and 653 age-matched controls. Results: Insulin resistance explained a major part of the variation in PAI-1 (24%) whereas inflammation had only a minor contribution (0.01%). For both cases and controls plasma PAI-1 concentrations were significantly higher in the North than the South, and in both regions were higher in individuals with MI compared with control subjects [overall odds ratio (OR) for a 1 SD increase = 1.54, 95% confidence interval (CI) 1.34, 1.77]. This difference was observed in all the centers studied. Overall, the difference between cases and control subjects remained significant after controlling for inflammation variables (OR = 1.30, 95% CI 1.08, 1.57), but lost significance after controlling for insulin resistance variables (OR = 1.17, 95% CI 0.98, 1.40). The 4G allele was associated with significantly higher PAI-1 levels in cases but not controls and, taken independently, did not modify the risk of MI (P = 0.9). However, a significant interaction was observed with both insulin or proinsulin and the risk of MI (P = 0.05 and 0.02, respectively), but not with triglycerides or body mass index (BMI). The insulin or proinsulin effect on risk was observed only in the carriers of the 4G/4G genotype. This interaction appeared not to be mediated by plasma PAI-1 antigen concentrations (P = 0.01 and 0.02 after adjustment for PAI-1 plasma levels). The interaction with proinsulin but not insulin remained statistically significant after further adjustment for other factors associated with insulin resistance (triglycerides and BMI) and C-reactive protein (P = 0.01). Conclusion: This study suggests that PAI-1 has a role in risk of MI in the presence of underlying insulin resistance. A significant interaction between insulin or proinsulin and the −675 4G/5G polymorphism was observed in risk for MI. The mechanisms for these interactions remain to be determined.

Published
2003

5. Plasma thrombin-activatable fibrinolysis inhibitor antigen concentration and genotype in relation to myocardial infarction in the north and south of Europe

Author

Juhan Vague I, Morange PE, Aubert H, Henry M, Aillaud MF, Alessi MC, Samnegård A, Hawe E, Yudkin J, Margaglione M, Hamsten A, Humphries SE, HIFMECH Study Group, DI MINNO, GIOVANNI, Juhan Vague, I, Morange, Pe, Aubert, H, Henry, M, Aillaud, Mf, Alessi, Mc, Samnegård, A, Hawe, E, Yudkin, J, Margaglione, M, DI MINNO, Giovanni, Hamsten, A, Humphries, Se, and HIFMECH Study, Group

Subjects
Male, Carboxypeptidase B2, medicine.medical_specialty, Genotype, medicine.medical_treatment, Population, Myocardial Infarction, Lower risk, Linkage Disequilibrium, Fibrin, Antigen, Risk Factors, Internal medicine, Fibrinolysis, medicine, Humans, Thrombophilia, Myocardial infarction, Antigens, education, Alleles, education.field_of_study, Polymorphism, Genetic, biology, business.industry, Thrombin, Case-control study, Odds ratio, Middle Aged, medicine.disease, Surgery, Europe, Genetics, Population, Endocrinology, Case-Control Studies, biology.protein, Cardiology and Cardiovascular Medicine, business
Abstract

The thrombin-activatable fibrinolysis inhibitor (TAFI) is a recently described inhibitor of fibrinolysis that decreases plasminogen binding to the fibrin surface. The plasma TAFI concentration is almost entirely genetically determined. We investigated whether plasma TAFI levels and polymorphisms located in the TAFI gene could constitute risk markers of myocardial infarction (MI). Plasma TAFI antigen (Ag) levels were assayed by ELISA and 2 TAFI gene polymorphisms (Ala147Thr and C+1542G in the 3′ untranslated region) were determined in a large European case-control study. This study compared 598 men recruited 3 to 6 months after MI with 653 age-matched controls from North Europe (Stockholm, Sweden, and London, England) and South Europe (Marseilles, France, and San Giovanni Rotondo, Italy). A TAFI Ag value above the 90th percentile was associated with a significantly lower risk of MI (odds ratio 0.55, P P P =0.03) and San Giovanni Rotondo ( P =0.03); the odds ratio for the entire cohort was 0.78 ( P

Published
2002

7. Hypofibrinolysis and increased PAI-1 are linked to atherothrombosis via insulin resistance and obesity

Author

Juhan-Vague, I., Marie-christine ALESSI, and Morange, Pe

Subjects
Polymorphism, Genetic, Adipose Tissue, Cardiovascular Diseases, Fibrinolysis, Plasminogen Activator Inhibitor 1, Animals, Humans, Thrombosis, Obesity, Insulin Resistance
Abstract

Plasminogen activator inhibitor 1 (PAI-1) is the primary physiological inhibitor of plasminogen activation in vivo. Circulating PAI-1 levels are elevated in patients with coronary heart disease and may play an important role in the development of atherothrombosis by decreasing fibrin degradation. Increased PAI-1 expression can also directly influence vessel wall remodelling. Prospective cohort studies have underlined the association between increased plasma PAI-1 levels and the risk of coronary events, but the predictive capacity of PAI-1 disappeared after adjustments for insulin resistance markers. The insulin resistance syndrome, which is characterized partly by obesity with visceral fat accumulation, is considered as a major regulator of PAI-1 expression. Recently, production of PAI-1 by adipose tissue, in particular by fat from omentum, has been evidenced, and it has been proposed that it could be responsible for the elevated plasma PAI-1 level observed in insulin resistance. The role of stroma cells, tumour necrosis factor (TNF)-alpha and transforming growth factor (TGF)-beta as possible enhancers of PAI-1 synthesis are presently emphasized. Glucocorticoids and insulin may also be implicated. Moreover, a weak genetic control of plasma PAI-1 concentration has been described in patients with high plasma levels of PAI-1. The role of PAI-1 in the development of adipose tissue metabolism is important to consider as PAI-1 -/- mice submitted to a high-fat diet showed changes in cell composition of adipose tissue and in plasma insulin and triglyceride levels.

8. The European Hematology Association Roadmap for European Hematology Research: a consensus document

Author

Engert, Andreas, Balduini, Carlo, Brand, Anneke, Coiffier, Bertrand, Cordonnier, Catherine, Doehner, Hartmut, de Wit, Thom Duyvene, Eichinger, Sabine, Fibbe, Willem, Green, Tony, de Haas, Fleur, Iolascon, Achille, Jaffredo, Thierry, Rodeghiero, Francesco, Salles, Gilles, Schuringa, Jan Jacob, Andre, Marc, Andre-Schmutz, Isabelle, Bacigalupo, Andrea, Bochud, Pierre-Yves, den Boer, Monique, Bonini, Chiara, Camaschella, Clara, Cant, Andrew, Cappellini, Maria Domenica, Cazzola, Mario, Lo Celso, Cristina, Dimopoulos, Meletios, Douay, Luc, Dzierzak, Elaine, Einsele, Hermann, Ferreri, Andres, De Franceschi, Lucia, Gaulard, Philippe, Gottgens, Berthold, Greinacher, Andreas, Gresele, Paolo, Gribben, John, de Haan, Gerald, Hansen, John-Bjarne, Hochhaus, Andreas, Kadir, Rezan, Kaveri, Srini, Kouskoff, Valerie, Kuehne, Thomas, Kyrle, Paul, Ljungman, Per, Maschmeyer, Georg, Mendez-Ferrer, Simon, Milsom, Michael, Mummery, Christine, Ossenkoppele, Gert, Pecci, Alessandro, Peyvandi, Flora, Philipsen, Sjaak, Reitsma, Pieter, Maria Ribera, Jose, Risitano, Antonio, Rivella, Stefano, Ruf, Wolfram, Schroeder, Timm, Scully, Marie, Socie, Gerard, Staal, Frank, Stanworth, Simon, Stauder, Reinhard, Stilgenbauer, Stephan, Tamary, Hannah, Theilgaard-Monch, Kim, Thein, Swee Lay, Tilly, Herve, Trneny, Marek, Vainchenker, William, Vannucchi, Alessandro Maria, Viscoli, Claudio, Vrielink, Hans, Zaaijer, Hans, Zanella, Alberto, Zolla, Lello, Zwaginga, Jaap Jan, Martinez, Patricia Aguilar, van den Akker, Emile, Allard, Shubha, Anagnou, Nicholas, Andolfo, Immacolata, Andrau, Jean-Christophe, Angelucci, Emanuele, Anstee, David, Aurer, Igor, Avet-Loiseau, Herve, Aydinok, Yesim, Bakchoul, Tamam, Balduini, Alessandra, Barcellini, Wilma, Baruch, Dominique, Baruchel, Andre, Bayry, Jagadeesh, Bento, Celeste, van den Berg, Anke, Bernardi, Rosa, Bianchi, Paola, Bigas, Anna, Biondi, Andrea, Bohonek, Milos, Bonnet, Dominique, Borchmann, Peter, Borregaard, Niels, Braekkan, Sigrid, van den Brink, Marcel, Brodin, Ellen, Bullinger, Lars, Buske, Christian, Butzeck, Barbara, Cammenga, Jorg, Campo, Elias, Carbone, Antonino, Cervantes, Francisco, Cesaro, Simone, Charbord, Pierre, Claas, Frans, Cohen, Hannah, Conard, Jacqueline, Coppo, Paul, Vives Corrons, Joan-Lluis, da Costa, Lydie, Davi, Frederic, Delwel, Ruud, Dianzani, Irma, Domanovic, Dragoslav, Donnelly, Peter, Drnovsek, Tadeja Dovc, Dreyling, Martin, Du, Ming-Qing, Dufour, Carlo, Durand, Charles, Efremov, Dimitar, Eleftheriou, Androulla, Elion, Jacques, Emonts, Marieke, Engelhardt, Monika, Ezine, Sophie, Falkenburg, Fred, Favier, Remi, Federico, Massimo, Fenaux, Pierre, Fitzgibbon, Jude, Flygare, Johan, Foa, Robin, Forrester, Lesley, Galacteros, Frederic, Garagiola, Isabella, Gardiner, Chris, Garraud, Olivier, van Geet, Christel, Geiger, Hartmut, Geissler, Jan, Germing, Ulrich, Ghevaert, Cedric, Girelli, Domenico, Godeau, Bertrand, Goekbuget, Nicola, Goldschmidt, Hartmut, Goodeve, Anne, Graf, Thomas, Graziadei, Giovanna, Griesshammer, Martin, Gruel, Yves, Guilhot, Francois, von Gunten, Stephan, Gyssens, Inge, Halter, Jorg, Harrison, Claire, Harteveld, Cornelis, Hellstrom-Lindberg, Eva, Hermine, Olivier, Higgs, Douglas, Hillmen, Peter, Hirsch, Hans, Hoskin, Peter, Huls, Gerwin, Inati, Adlette, Johnson, Peter, Kattamis, Antonis, Kiefel, Volker, Kleanthous, Marina, Klump, Hannes, Krause, Daniela, Hovinga, Johanna Kremer, Lacaud, Georges, Lacroix-Desmazes, Sebastien, Landman-Parker, Judith, LeGouill, Steven, Lenz, Georg, von Lilienfeld-Toal, Marie, von Lindern, Marieke, Lopez-Guillermo, Armando, Lopriore, Enrico, Lozano, Miguel, MacIntyre, Elizabeth, Makris, Michael, Mannhalter, Christine, Martens, Joost, Mathas, Stephan, Matzdorff, Axel, Medvinsky, Alexander, Menendez, Pablo, Migliaccio, Anna Rita, Miharada, Kenichi, Mikulska, Malgorzata, Minard, Veronique, Montalban, Carlos, de Montalembert, Mariane, Montserrat, Emili, Morange, Pierre-Emmanuel, Mountford, Joanne, Muckenthaler, Martina, Mueller-Tidow, Carsten, Mumford, Andrew, Nadel, Bertrand, Navarro, Jose-Tomas, el Nemer, Wassim, Noizat-Pirenne, France, O'Mahony, Brian, Oldenburg, Johannes, Olsson, Martin, Oostendorp, Robert, Palumbo, Antonio, Passamonti, Francesco, Patient, Roger, de Latour, Regis Peffault, Pflumio, Francoise, Pierelli, Luca, Piga, Antonio, Pollard, Debra, Raaijmakers, Marc, Radford, John, Rambach, Ralf, Rao, A. Koneti, Raslova, Hana, Rebulla, Paolo, Rees, David, Ribrag, Vincent, Rijneveld, Anita, Rinalducci, Sara, Robak, Tadeusz, Roberts, Irene, Rodrigues, Charlene, Rosendaal, Frits, Rosenwald, Andreas, Rule, Simon, Russo, Roberta, Saglio, Guiseppe, Sanchez, Mayka, Scharf, Ruediger E., Schlenke, Peter, Semple, John, Sierra, Jorge, So-Osman, Cynthia, Manuel Soria, Jose, Stamatopoulos, Kostas, Stegmayr, Bernd, Stunnenberg, Henk, Swinkels, Dorine, Taborda Barata, Joao Pedro, Taghon, Tom, Taher, Ali, Terpos, Evangelos, Thachil, Jecko, Tissot, Jean Daniel, Touw, Ivo, Toye, Ash, Trappe, Ralf, Traverse-Glehen, Alexandra, Unal, Sule, Vaulont, Sophie, Viprakasit, Vip, Vitolo, Umberto, van Wijk, Richard, Wojtowicz, Agnieszka, Zeerleder, Sacha, Zieger, Barbara, Centre de Recherche des Cordeliers (CRC), Université Pierre et Marie Curie - Paris 6 (UPMC)-École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Pierre et Marie Curie - Paris 6 - UFR de Médecine Pierre et Marie Curie (UPMC), Université Pierre et Marie Curie - Paris 6 (UPMC), Université Sorbonne Paris Cité (USPC), Institut National de la Santé et de la Recherche Médicale (INSERM), University Hospital of Cologne [Cologne], Laboratoire de Biologie du Développement (LBD), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Biologie Paris Seine (IBPS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS), Service d’Hématologie [Centre Hospitalier Lyon Sud - HCL], Centre Hospitalier Lyon Sud [CHU - HCL] (CHLS), Hospices Civils de Lyon (HCL)-Hospices Civils de Lyon (HCL), Hospices Civils de Lyon (HCL), Department of Internal Medicine I, Medizinische Universität Wien = Medical University of Vienna, Service d'Hématologie [CHRU Nancy], Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy), Ege Üniversitesi, Engert, Andrea, Balduini, Carlo, Brand, Anneke, Coiffier, Bertrand, Cordonnier, Catherine, Döhner, Hartmut, De Wit, Thom Duyvené, Eichinger, Sabine, Fibbe, Willem, Green, Tony, De Haas, Fleur, Iolascon, Achille, Jaffredo, Thierry, Rodeghiero, Francesco, Sall Es, Gille, Schuringa, Jan Jacob, André, Marc, Andre Schmutz, Isabelle, Bacigalupo, Andrea, Bochud, Pierre Yve, Den Boer, Monique, Bonini, Chiara, Camaschella, Clara, Cant, Andrew, Cappellini, Maria Domenica, Cazzola, Mario, Celso, Cristina Lo, Dimopoulos, Meletio, Douay, Luc, Dzierzak, Elaine, Einsele, Hermann, Ferreri, André, De Franceschi, Lucia, Gaulard, Philippe, Gottgens, Berthold, Greinacher, Andrea, Gresele, Paolo, Gribben, John, De Haan, Gerald, Hansen, John Bjarne, Hochhaus, Andrea, Kadir, Rezan, Kaveri, Srini, Kouskoff, Valerie, Kühne, Thoma, Kyrle, Paul, Ljungman, Per, Maschmeyer, Georg, Méndez Ferrer, Simón, Milsom, Michael, Mummery, Christine, Ossenkoppele, Gert, Pecci, Alessandro, Peyvandi, Flora, Philipsen, Sjaak, Reitsma, Pieter, Ribera, José Maria, Risitano, ANTONIO MARIA, Rivella, Stefano, Ruf, Wolfram, Schroeder, Timm, Scully, Marie, Socie, Gerard, Staal, Frank, Stanworth, Simon, Stauder, Reinhard, Stilgenbauer, Stephan, Tamary, Hannah, Theilgaard Mönch, Kim, Thein, Swee Lay, Tilly, Hervé, Trneny, Marek, Vainchenker, William, Vannucchi, Alessandro Maria, Viscoli, Claudio, Vrielink, Han, Zaaijer, Han, Zanella, Alberto, Zolla, Lello, Zwaginga, Jaap Jan, Martinez, Patricia Aguilar, Van Den Akker, Emile, Allard, Shubha, Anagnou, Nichola, Andolfo, Immacolata, Andrau, Jean Christophe, Angelucci, Emanuele, Anstee, David, Aurer, Igor, Avet Loiseau, Hervé, Aydinok, Yesim, Bakchoul, Tamam, Balduini, Alessandra, Barcellini, Wilma, Baruch, Dominique, Baruchel, André, Bayry, Jagadeesh, Bento, Celeste, Van Den Berg, Anke, Bernardi, Rosa, Bianchi, Paola, Bigas, Anna, Biondi, Andrea, Bohonek, Milo, Bonnet, Dominique, Borchmann, Peter, Borregaard, Niel, Brækkan, Sigrid, Van Den Brink, Marcel, Brodin, Ellen, Bullinger, Lar, Buske, Christian, Butzeck, Barbara, Cammenga, Jörg, Campo, Elia, Carbone, Antonino, Cervantes, Francisco, Cesaro, Simone, Charbord, Pierre, Claas, Fran, Cohen, Hannah, Conard, Jacqueline, Coppo, Paul, Vives Corron, Joan Llui, Da Costa, Lydie, Davi, Frederic, Delwel, Ruud, Dianzani, Irma, Domanović, Dragoslav, Donnelly, Peter, Drnovšek, Tadeja Dovč, Dreyling, Martin, Du, Ming Qing, Dufour, Carlo, Durand, Charle, Efremov, Dimitar, Eleftheriou, Androulla, Elion, Jacque, Emonts, Marieke, Engelhardt, Monika, Ezine, Sophie, Falkenburg, Fred, Favier, Remi, Federico, Massimo, Fenaux, Pierre, Fitzgibbon, Jude, Flygare, Johan, Foà, Robin, Forrester, Lesley, Galacteros, Frederic, Garagiola, Isabella, Gardiner, Chri, Garraud, Olivier, Van Geet, Christel, Geiger, Hartmut, Geissler, Jan, Germing, Ulrich, Ghevaert, Cedric, Girelli, Domenico, Godeau, Bertrand, Gökbuget, Nicola, Goldschmidt, Hartmut, Goodeve, Anne, Graf, Thoma, Graziadei, Giovanna, Griesshammer, Martin, Gruel, Yve, Guilhot, Francoi, Von Gunten, Stephan, Gyssens, Inge, Halter, Jörg, Harrison, Claire, Harteveld, Corneli, Hellström Lindberg, Eva, Hermine, Olivier, Higgs, Dougla, Hillmen, Peter, Hirsch, Han, Hoskin, Peter, Huls, Gerwin, Inati, Adlette, Johnson, Peter, Kattamis, Antoni, Kiefel, Volker, Kleanthous, Marina, Klump, Hanne, Krause, Daniela, Hovinga, Johanna Kremer, Lacaud, George, Lacroix Desmazes, Sébastien, Landman Parker, Judith, Legouill, Steven, Lenz, Georg, Von Lilienfeld Toal, Marie, Von Lindern, Marieke, Lopez Guillermo, Armando, Lopriore, Enrico, Lozano, Miguel, Macintyre, Elizabeth, Makris, Michael, Mannhalter, Christine, Martens, Joost, Mathas, Stephan, Matzdorff, Axel, Medvinsky, Alexander, Menendez, Pablo, Migliaccio, Anna Rita, Miharada, Kenichi, Mikulska, Malgorzata, Minard, Véronique, Montalbán, Carlo, De Montalembert, Mariane, Montserrat, Emili, Morange, Pierre Emmanuel, Mountford, Joanne, Muckenthaler, Martina, Müller Tidow, Carsten, Mumford, Andrew, Nadel, Bertrand, Navarro, Jose Toma, El Nemer, Wassim, Noizat Pirenne, France, O’Mahony, Brian, Oldenburg, Johanne, Olsson, Martin, Oostendorp, Robert, Palumbo, Antonio, Passamonti, Francesco, Patient, Roger, De Latour, Regis Peffault, Pflumio, Francoise, Pierelli, Luca, Piga, Antonio, Pollard, Debra, Raaijmakers, Marc, Radford, John, Rambach, Ralf, Koneti Rao, A., Raslova, Hana, Rebulla, Paolo, Rees, David, Ribrag, Vincent, Rijneveld, Anita, Rinalducci, Sara, Robak, Tadeusz, Roberts, Irene, Rodrigues, Charlene, Rosendaal, Frit, Rosenwald, Andrea, Rule, Simon, Russo, Roberta, Saglio, Guiseppe, Sanchez, Mayka, Scharf, Rüdiger E., Schlenke, Peter, Semple, John, Sierra, Jorge, So Osman, Cynthia, Soria, José Manuel, Stamatopoulos, Kosta, Stegmayr, Bernd, Stunnenberg, Henk, Swinkels, Dorine, Barata, João Pedro Taborda, Taghon, Tom, Taher, Ali, Terpos, Evangelo, Thachil, Jecko, Tissot, Jean Daniel, Touw, Ivo, Toye, Ash, Trappe, Ralf, Traverse Glehen, Alexandra, Unal, Sule, Vaulont, Sophie, Viprakasit, Vip, Vitolo, Umberto, Van Wijk, Richard, Wójtowicz, Agnieszka, Zeerleder, Sacha, Zieger, Barbara, Hematology, Service d'hématologie clinique, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Henri Mondor-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), University of York [York, UK], Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS), Centre National de la Recherche Scientifique (CNRS), Centre de Recherche en Cancérologie de Lyon (UNICANCER/CRCL), Centre Léon Bérard [Lyon]-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Pediatrics, Cell biology, Erasmus MC other, Pulmonary Medicine, Medical Oncology, Other departments, AII - Amsterdam institute for Infection and Immunity, Medical Microbiology and Infection Prevention, ACS - Amsterdam Cardiovascular Sciences, Clinical Haematology, Engert, A, Balduini, C, Brand, A, Coiffier, B, Cordonnier, C, Döhner, H, De, Wit, Td, Eichinger, S, Fibbe, W, Green, T, de Haas, F, Iolascon, A, Jaffredo, T, Rodeghiero, F, Salles, G, Schuringa, Jj, and the other authors of the EHA Roadmap for European Hematology, Research, Cancer Research UK, Biotechnology and Biological Sciences Research Council (BBSRC), Université Pierre et Marie Curie - Paris 6 (UPMC)-École Pratique des Hautes Études (EPHE), De Wit, T, De Haas, F, Sall Es, G, Schuringa, J, André, M, Andre Schmutz, I, Bacigalupo, A, Bochud, P, Den Boer, M, Bonini, C, Camaschella, C, Cant, A, Cappellini, M, Cazzola, M, Celso, C, Dimopoulos, M, Douay, L, Dzierzak, E, Einsele, H, Ferreri, A, De Franceschi, L, Gaulard, P, Gottgens, B, Greinacher, A, Gresele, P, Gribben, J, De Haan, G, Hansen, J, Hochhaus, A, Kadir, R, Kaveri, S, Kouskoff, V, Kühne, T, Kyrle, P, Ljungman, P, Maschmeyer, G, Méndez Ferrer, S, Milsom, M, Mummery, C, Ossenkoppele, G, Pecci, A, Peyvandi, F, Philipsen, S, Reitsma, P, Ribera, J, Risitano, A, Rivella, S, Ruf, W, Schroeder, T, Scully, M, Socie, G, Staal, F, Stanworth, S, Stauder, R, Stilgenbauer, S, Tamary, H, Theilgaard Mönch, K, Thein, S, Tilly, H, Trneny, M, Vainchenker, W, Vannucchi, A, Viscoli, C, Vrielink, H, Zaaijer, H, Zanella, A, Zolla, L, Zwaginga, J, Martinez, P, Van Den Akker, E, Allard, S, Anagnou, N, Andolfo, I, Andrau, J, Angelucci, E, Anstee, D, Aurer, I, Avet Loiseau, H, Aydinok, Y, Bakchoul, T, Balduini, A, Barcellini, W, Baruch, D, Baruchel, A, Bayry, J, Bento, C, Van Den Berg, A, Bernardi, R, Bianchi, P, Bigas, A, Biondi, A, Bohonek, M, Bonnet, D, Borchmann, P, Borregaard, N, Brækkan, S, Van Den Brink, M, Brodin, E, Bullinger, L, Buske, C, Butzeck, B, Cammenga, J, Campo, E, Carbone, A, Cervantes, F, Cesaro, S, Charbord, P, Claas, F, Cohen, H, Conard, J, Coppo, P, Vives Corron, J, Da Costa, L, Davi, F, Delwel, R, Dianzani, I, Domanović, D, Donnelly, P, Drnovšek, T, Dreyling, M, Du, M, Dufour, C, Durand, C, Efremov, D, Eleftheriou, A, Elion, J, Emonts, M, Engelhardt, M, Ezine, S, Falkenburg, F, Favier, R, Federico, M, Fenaux, P, Fitzgibbon, J, Flygare, J, Foà, R, Forrester, L, Galacteros, F, Garagiola, I, Gardiner, C, Garraud, O, Van Geet, C, Geiger, H, Geissler, J, Germing, U, Ghevaert, C, Girelli, D, Godeau, B, Gökbuget, N, Goldschmidt, H, Goodeve, A, Graf, T, Graziadei, G, Griesshammer, M, Gruel, Y, Guilhot, F, Von Gunten, S, Gyssens, I, Halter, J, Harrison, C, Harteveld, C, Hellström Lindberg, E, Hermine, O, Higgs, D, Hillmen, P, Hirsch, H, Hoskin, P, Huls, G, Inati, A, Johnson, P, Kattamis, A, Kiefel, V, Kleanthous, M, Klump, H, Krause, D, Hovinga, J, Lacaud, G, Lacroix Desmazes, S, Landman Parker, J, Legouill, S, Lenz, G, Von Lilienfeld Toal, M, Von Lindern, M, Lopez Guillermo, A, Lopriore, E, Lozano, M, Macintyre, E, Makris, M, Mannhalter, C, Martens, J, Mathas, S, Matzdorff, A, Medvinsky, A, Menendez, P, Migliaccio, A, Miharada, K, Mikulska, M, Minard, V, Montalbán, C, De Montalembert, M, Montserrat, E, Morange, P, Mountford, J, Muckenthaler, M, Müller Tidow, C, Mumford, A, Nadel, B, Navarro, J, El Nemer, W, Noizat Pirenne, F, O’Mahony, B, Oldenburg, J, Olsson, M, Oostendorp, R, Palumbo, A, Passamonti, F, Patient, R, De Latour, R, Pflumio, F, Pierelli, L, Piga, A, Pollard, D, Raaijmakers, M, Radford, J, Rambach, R, Koneti Rao, A, Raslova, H, Rebulla, P, Rees, D, Ribrag, V, Rijneveld, A, Rinalducci, S, Robak, T, Roberts, I, Rodrigues, C, Rosendaal, F, Rosenwald, A, Rule, S, Russo, R, Saglio, G, Sanchez, M, Scharf, R, Schlenke, P, Semple, J, Sierra, J, So Osman, C, Soria, J, Stamatopoulos, K, Stegmayr, B, Stunnenberg, H, Swinkels, D, Barata, J, Taghon, T, Taher, A, Terpos, E, Thachil, J, Tissot, J, Touw, I, Toye, A, Trappe, R, Traverse Glehen, A, Unal, S, Vaulont, S, Viprakasit, V, Vitolo, U, Van Wijk, R, Wójtowicz, A, Zeerleder, S, Zieger, B, Andreas Engert, Carlo Balduini, Anneke Brand, Bertrand Coiffier, Catherine Cordonnier, Hartmut Döhner, Thom Duyvené de Wit, Sabine Eichinger, Willem Fibbe, Tony Green, Fleur de Haas, Achille Iolascon, Thierry Jaffredo, Francesco Rodeghiero, Gilles Salles, Jan Jacob Schuringa, the other authors of the EHA Roadmap for European Hematology Research, Anna Rita Migliaccio, EHA Roadmap for European Hematology, Research, Engert, A., Balduini, C., Brand, A., Coiffier, B., Cordonnier, C., Döhner, H., de Wit TD., Eichinger, S., Fibbe, W., Green, T., de Haas, F., Iolascon, A., Jaffredo, T., Rodeghiero, F., Salles, G., Schuringa, JJ., André, M., Andre-Schmutz, I., Bacigalupo, A., Bochud, PY., Boer, Md., Bonini, C., Camaschella, C., Cant, A., Cappellini, MD., Cazzola, M., Celso, CL., Dimopoulos, M., Douay, L., Dzierzak, E., Einsele, H., Ferreri, A., De Franceschi, L., Gaulard, P., Gottgens, B., Greinacher, A., Gresele, P., Gribben, J., de Haan, G., Hansen, JB., Hochhaus, A., Kadir, R., Kaveri, S., Kouskoff, V., Kühne, T., Kyrle, P., Ljungman, P., Maschmeyer, G., Méndez-Ferrer£££Simón£££ S., Milsom, M., Mummery, C., Ossenkoppele, G., Pecci, A., Peyvandi, F., Philipsen, S., Reitsma, P., Ribera, JM., Risitano, A., Rivella, S., Ruf, W., Schroeder, T., Scully, M., Socie, G., Staal, F., Stanworth, S., Stauder, R., Stilgenbauer, S., Tamary, H., Theilgaard-Mönch, K., Thein, SL., Tilly, H., Trneny, M., Vainchenker, W., Vannucchi, AM., Viscoli, C., Vrielink, H., Zaaijer, H., Zanella, A., Zolla, L., Zwaginga, JJ., Martinez, PA., van den Akker, E., Allard, S., Anagnou, N., Andolfo, I., Andrau, JC., Angelucci, E., Anstee, D., Aurer, I., Avet-Loiseau, H., Aydinok, Y., Bakchoul, T., Balduini, A., Barcellini, W., Baruch, D., Baruchel, A., Bayry, J., Bento, C., van den Berg, A., Bernardi, R., Bianchi, P., Bigas, A., Biondi, A., Bohonek, M., Bonnet, D., Borchmann, P., Borregaard, N., Brækkan, S., van den Brink, M., Brodin, E., Bullinger, L., Buske, C., Butzeck, B., Cammenga, J., Campo, E., Carbone, A., Cervantes, F., Cesaro, S., Charbord, P., Claas, F., Cohen, H., Conard, J., Coppo, P., Corrons, JL., Costa, Ld., Davi, F., Delwel, R., Dianzani, I., Domanović, D., Donnelly, P., Drnov?ek£££Tadeja Dovč£££ TD., Dreyling, M., Du, MQ., Dufour, C., Durand, C., Efremov, D., Eleftheriou, A., Elion, J., Emonts, M., Engelhardt, M., Ezine, S., Falkenburg, F., Favier, R., Federico, M., Fenaux, P., Fitzgibbon, J., Flygare, J., Foà, R., Forrester, L., Galacteros, F., Garagiola, I., Gardiner, C., Garraud, O., van Geet, C., Geiger, H., Geissler, J., Germing, U., Ghevaert, C., Girelli, D., Godeau, B., Gökbuget, N., Goldschmidt, H., Goodeve, A., Graf, T., Graziadei, G., Griesshammer, M., Gruel, Y., Guilhot, F., von Gunten, S., Gyssens, I., Halter, J., Harrison, C., Harteveld, C., Hellström-Lindberg, E., Hermine, O., Higgs, D., Hillmen, P., Hirsch, H., Hoskin, P., Huls, G., Inati, A., Johnson, P., Kattamis, A., Kiefel, V., Kleanthous, M., Klump, H., Krause, D., Hovinga, JK., Lacaud, G., Lacroix-Desmazes, S., Landman-Parker, J., LeGouill, S., Lenz, G., von Lilienfeld-Toal, M., von Lindern, M., Lopez-Guillermo, A., Lopriore, E., Lozano, M., MacIntyre, E., Makris, M., Mannhalter, C., Martens, J., Mathas, S., Matzdorff, A., Medvinsky, A., Menendez, P., Migliaccio, AR., Miharada, K., Mikulska, M., Minard, V., Montalbán, C., de Montalembert, M., Montserrat, E., Morange, PE., Mountford, J., Muckenthaler, M., Müller-Tidow, C., Mumford, A., Nadel, B., Navarro, JT., Nemer, We., Noizat-Pirenne, F., O'Mahony, B., Oldenburg, J., Olsson, M., Oostendorp, R., Palumbo, A., Passamonti, F., Patient, R., Peffault, R., Pflumio, F., Pierelli, L., Piga, A., Pollard, D., Raaijmakers, M., Radford, J., Rambach, R., Rao, AK., Raslova, H., Rebulla, P., Rees, D., Ribrag, V., Rijneveld, A., Rinalducci, S., Robak, T., Roberts, I., Rodrigues, C., Rosendaal, F., Rosenwald, A., Rule, S., Russo, R., Saglio, G., Sanchez, M., Scharf, RE., Schlenke, P., Semple, J., Sierra, J., So-Osman, C., Soria, JM., Stamatopoulos, K., Stegmayr, B., Stunnenberg, H., Swinkels, D., Barata£££João Pedro Taborda£££ JP., Taghon, T., Taher, A., Terpos, E., Thachil, J., Tissot, JD., Touw, I., Toye, A., Trappe, R., Traverse-Glehen, A., Unal, S., Vaulont, S., Viprakasit, V., Vitolo, U., van Wijk, R., Wójtowicz, A., Zeerleder, S., Zieger, B., Stem Cell Aging Leukemia and Lymphoma (SALL), and Çocuk Sağlığı ve Hastalıkları

Subjects
0301 basic medicine, Cancer Research, diagnosis, Health Services for the Aged, ACUTE PROMYELOCYTIC LEUKEMIA, Medizin, [SDV.IMM.II]Life Sciences [q-bio]/Immunology/Innate immunity, EHA Roadmap for European Hematology Research, Antineoplastic Agent, 0302 clinical medicine, European Hematology Association Roadmap, Germany, PERIPHERAL T-CELL, Medicine and Health Sciences, Hematopoiesi, genetics, Molecular Targeted Therapy, [SDV.IMM.ALL]Life Sciences [q-bio]/Immunology/Allergology, ComputingMilieux_MISCELLANEOUS, Hematology, Genome, Hematopoietic Stem Cell Transplantation, Anemia, Awareness, Supply & distribution, Combined Modality Therapy, 3. Good health, Europe, THROMBOPOIETIN-RECEPTOR AGONISTS, Blood Disorder, Italy, Austria, haematology, Medicine, France, Immunotherapy, Infection, [SDV.IMM.ALL] Life Sciences [q-bio]/Immunology/Allergology, Human, medicine.medical_specialty, Thrombopoietin Receptor Agonists, Consensus, Patients, Immunology, Antineoplastic Agents, Blood Coagulation, Gene Expression Profiling, Genetic Therapy, Genome, Human, Hematologic Diseases, Hematopoiesis, Humans, Consensu, [SDV.CAN]Life Sciences [q-bio]/Cancer, ACUTE MYELOID-LEUKEMIA, 1102 Cardiovascular Medicine And Haematology, Genetic therapy, methods, 03 medical and health sciences, blood, Internal medicine, medicine, Hematologi, THROMBOTIC THROMBOCYTOPENIC PURPURA, [SDV.IMM.II] Life Sciences [q-bio]/Immunology/Innate immunity, ACUTE LYMPHOBLASTIC-LEUKEMIA, therapy, business.industry, CHRONIC LYMPHOCYTIC-LEUKEMIA, supply & distribution, STEM-CELL TRANSPLANTATION, economics, Hematologic Disease, Opinion Article, Transplantation, 030104 developmental biology, Family medicine, therapeutic use, drug effects, RANDOMIZED-CONTROLLED-TRIAL, HEMOLYTIC-UREMIC SYNDROME, pathology, business, chemical synthesis, 030215 immunology, Stem Cell Transplantation, transplantation
Abstract

WOS: 000379156300012, PubMed ID: 26819058, The European Hematology Association (EHA) Roadmap for European Hematology Research highlights major achievements in diagnosis and treatment of blood disorders and identifies the greatest unmet clinical and scientific needs in those areas to enable better funded, more focused European hematology research. Initiated by the EHA, around 300 experts contributed to the consensus document, which will help European policy makers, research funders, research organizations, researchers, and patient groups make better informed decisions on hematology research. It also aims to raise public awareness of the burden of blood disorders on European society, which purely in economic terms is estimated at (sic)23 billion per year, a level of cost that is not matched in current European hematology research funding. In recent decades, hematology research has improved our fundamental understanding of the biology of blood disorders, and has improved diagnostics and treatments, sometimes in revolutionary ways. This progress highlights the potential of focused basic research programs such as this EHA Roadmap. The EHA Roadmap identifies nine 'sections' in hematology: normal hematopoiesis, malignant lymphoid and myeloid diseases, anemias and related diseases, platelet disorders, blood coagulation and hemostatic disorders, transfusion medicine, infections in hematology, and hematopoietic stem cell transplantation. These sections span 60 smaller groups of diseases or disorders. The EHA Roadmap identifies priorities and needs across the field of hematology, including those to develop targeted therapies based on genomic profiling and chemical biology, to eradicate minimal residual malignant disease, and to develop cellular immunotherapies, combination treatments, gene therapies, hematopoietic stem cell treatments, and treatments that are better tolerated by elderly patients., Biotechnology and Biological Sciences Research CouncilBiotechnology and Biological Sciences Research Council (BBSRC) [BB/L023776/1, BB/I00050X/1, BB/K021168/1]; Cancer Research UKCancer Research UK [11831]; Medical Research CouncilMedical Research Council UK (MRC) [G1000801a]; Novo Nordisk FondenNovo Nordisk [NNF12OC1015986]; British Heart FoundationBritish Heart Foundation [FS/09/039/27788]; Cancer Research UKCancer Research UK [12765]; Medical Research CouncilMedical Research Council UK (MRC) [MR/L022982/1, MC_UU_12009/8, MC_U137981013, MC_PC_12009]

Published
2016

9. Association of plasminogen activator inhibitor (PAI)-1 (SERPINE1) SNPs with myocardial infarction, plasma PAI-1, and metabolic parameters: the HIFMECH study

Author

Anders Hamsten, S.E. Humphries, John S Yudkin, G. Di Minno, Irène Juhan-Vague, Pierre Morange, Marie-Christine Alessi, Maurizio Margaglione, David-Alexandre Trégouët, Noémie Saut, Morange, Pe, Saut, N, Alessi, Mc, Yudkin, J, Margaglione, M, DI MINNO, Giovanni, Hamsten, A, Humphries, Se, Tregouet, Da, and JUHAN VAGUE, I.

Subjects
Male, medicine.medical_specialty, medicine.medical_treatment, PAI-1, Single-nucleotide polymorphism, Polymorphism, Single Nucleotide, Risk Assessment, Linkage Disequilibrium, White People, Body Mass Index, chemistry.chemical_compound, Gene Frequency, Risk Factors, Internal medicine, Genetic variation, Plasminogen Activator Inhibitor 1, medicine, Humans, Insulin, Genetic Predisposition to Disease, Risk factor, Promoter Regions, Genetic, Metabolic Syndrome, business.industry, Haplotype, Smoking, Middle Aged, medicine.disease, Europe, Endocrinology, Phenotype, myocardial infarction, chemistry, Haplotypes, Plasminogen activator inhibitor-1, Case-Control Studies, Metabolic syndrome, Cardiology and Cardiovascular Medicine, business, Plasminogen activator, SERPINE1
Abstract

Objective— The purpose of this study was to investigate the effects of plasminogen activator inhibitor-1 (PAI-1) gene (SERPINE1) single nucleotide polymorphisms (SNPs) on the risk of myocardial infarction (MI), on PAI-1 levels, and factors related to the metabolic syndrome. Methods and Results— Eleven SNPs capturing the common genetic variation of the SERPINE1 gene were genotyped in the HIFMECH study. In the 510 male cases and their 543 age-matched controls, a significant gene-smoking interaction was observed. In nonsmokers, the rs7242-G allele was more frequent in cases than in controls (0.486 versus 0.382, P =0.013) whereas the haplotype derived from the rs2227631 (−844A>G)-G and rs2227683-A alleles was ≈3-fold lower in cases than in controls (0.042 versus 0.115, P =0.006). SERPINE1 haplotypes explained 3.5% ( P =0.007) of the variability of PAI-1 levels, which was attributable to the combined effects of 3 SNPs, −844A>G, rs2227666, and rs2227694. The rs6092 (Ala15Thr) and rs7242 SNPs acted additively to explain 4.4% of the variability of plasma insulin levels and 1.6% of the variability of BMI ( P −3 and P =0.023, respectively). Conclusions— SERPINE1 haplotypes are mildly associated with plasma levels of PAI-1 and with the risk of MI in nonsmokers. They are also associated with insulin levels and BMI.

Published
2007

10. Interaction between the C-260T polymorphism of the CD14 gene and the plasma IL-6 concentration on the risk of myocardial infarction: the HIFMECH study

Author

Morange, P.E., Saut, N., Alessi, M.C., Frere, C., Hawe, E., Yudkin, J.S., Tremoli, E., Margaglione, M., Di Minno, G., Hamsten, A., Humphries, S.E., Juhan Vague, I., HIFMECH Study Group, Morange, Pe, Saut, N, Alessi, Mc, Frere, C, Hawe, E, Yudkin, J, Tremoli, E, Margaglione, M, DI MINNO, Giovanni, Hamsten, A, Humphries, Se, Juhan Vague, I, and HIFMECH Study, Group

Subjects
Male, medicine.medical_specialty, Genotype, Arteriosclerosis, CD14, Lipopolysaccharide Receptors, Pathogenesis, myocardial infarction, immune system, inflammation, Risk Factors, Internal medicine, medicine, Humans, Genetic Predisposition to Disease, Myocardial infarction, Allele, Promoter Regions, Genetic, Interleukin 6, Polymorphism, Genetic, biology, Interleukin-6, business.industry, C-reactive protein, Case-control study, Middle Aged, medicine.disease, Endocrinology, Case-Control Studies, biology.protein, Settore BIO/14 - Farmacologia, Cardiology and Cardiovascular Medicine, business
Abstract

Experimental and clinical observations suggest that innate immunity plays a major role in the pathogenesis and progression of atherosclerosis. A common C-260T polymorphism in the promoter of the CD14 gene, the trans-membrane receptor of lipopolysaccharides, has been inconsistently associated with coronary heart disease. Our objective was to evaluate the contribution of the CD14 polymorphism to the inflammatory response and to the risk of myocardial infarction (MI). We used an European case-control study, the HIFMECH study, comparing 533 men with MI and 575 sex- and age-matched controls. Associations between genotype and disease outcome, according to interleukin-6 (IL-6) and C-reactive protein (CRP) levels, were assessed using conditional logistic regression. The CD14/C-260T polymorphism was associated with plasma IL-6 levels, T/T subjects having higher plasma levels than C/C in cases but not in controls (mean ± S.D.: 2.04 ± 1.37 versus 1.70 ± 1.15, p = 0.01; 1.20 ± 0.75 versus 1.35 ± 0.88, p = 0.31, respectively). Overall, the CD14/C-260T polymorphism was not associated with the risk of MI. However, in individuals with IL-6 plasma levels in the highest tertile, T allele carriers had a higher risk of MI than C/C (OR: 1.85; CI 95 1.05–3.25). IL-6 increased the risk of MI in carriers of the T allele (OR for first versus third IL-6 tertile: 4.02; CI 95 2.24–7.21), but not in C/C (OR: 0.75; CI 95 0.32–1.74, p = 0.004 for interaction). The data indicate a role for CD14/C-260T in MI. The risk mediated by the polymorphism is highly dependent on IL-6 plasma levels. © 2004 Published by Elsevier Ireland Ltd.

Published
2005

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