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| 1 | Clinical use of dendritic cells for cancer therapy显示文摘 | Sébastien Anguille Evelien L Smits Eva Lion Viggo F van Tendeloo Zwi N Berneman | 2014 | Lancet Oncology2014，，7： | 3 |
| 2 | Dendritic cells in the pathogenesis and treatment of human diseases: a Janus Bifrons?显示文摘 | Nathalie Cools Annacarmen Petrizzo Evelien Smits Franco M Buonaguro Maria L Tornesello Zwi Berneman Luigi Buonaguro | 2011 | Immunotherapy2011，，10： | 2 |
| 3 | Regulatory T Cells and Human Disease显示文摘 | Nathalie Cools Peter Ponsaerts Viggo F. I. Van Tendeloo Zwi N. Berneman Yang Liu | 2008 | Clinical and Developmental Immunology2008，，： | 1 |
| 4 | Modulation of phenotype,cytokine production and stimulatory function of CD34+-derived DC by NiCI and SDS显示文摘 | De Smedt A C Van Den Heuvel R L Zwi Berneman N | 2001 | Toxicol In Vitro2001，15，45： | 1 |
| 5 | Apoptosis: mechanisms and relevance in cancer显示文摘 | Katrien Vermeulen Dirk R. Bockstaele Zwi N. Berneman | 2005 | Annals of Hematology2005，，10： | 1 |
| 6 | Apoptosis: mechanisms and relevance in cancer显示文摘 | Katrien Vermeulen Dirk R. Bockstaele Zwi N. Berneman | 2005 | Annals of Hematology2005，，10： | 1 |
| 7 | PVSG and WHO vs European Clinical,Molecular and Pathological Criteria for prefibrotic myeloproliferative neoplasms显示文摘The Polycythemia Vera Study Group(PVSG),World Health Organization(WHO) and European Clinical,Molecular and Pathological(ECMP) classifications agree upon the diagnostic criteria for polycythemia vera(PV) and advanced primary myelofibrosis(MF). Essential thrombocythemia(ET) according to PVSG and 2007/2008 WHO criteria comprises three variants of JAK2V617 F mutated ET when the ECMP criteria are applied. These include normocellular ET,hypercellular ET with features of early PV(prodromal PV),and hypercellular ET due to megakaryocytic,granulocytic myeloprolifera-tion(ET.MGM). Evolution of prodromal PV into overt PV is common. Development of MF is rare in normocellular ET(WHO-ET) but rather common in hypercellular ET.MGM. The JAK2V617 F mutation burden in heterozygous mutated normocellular ET and in heterozygous/homozygous or homozygous mutated PV and ET.MGM is of major prognostic significance. JAK2/MPL wild type ET associated with prefibrotic primary megakaryocytic and granulocytic myeloproliferation(PMGM) is characterized by densely clustered immature dysmorphic megakaryocytes with bulky(bulbous) hyperchromatic nuclei,which are never seen in JAK2V617 F mutated ET,and PV and also not in MPL515 mutated normocellular ET(WHO-ET). JAK2V617 mutation burden,spleen size,LDH,circulating CD34+ cells,and pre-treatment bone marrow histopathology are mandatory to stage the myeloproliferative neoplasms ET,PV,PMGM for proper prognosis assessment and therapeutic implications. MF itself is not a disease because reticulin fibrosis and reticulin/collagen fibrosis are secondary responses of activated polyclonal fibroblasts to cytokines released from the clonal myeloproliferative granulocytic and megakaryocytic progenitor cells in ET.MGM,PV and PMGM. | Jan Jacques Michiels Zwi Berneman Wilfried Schroyens King H Lam Hendrik De Raeve | 2013 | World Journal of Hematology2013，2，3： | 1 |
| 8 | Apoptosis: mechanisms and relevance in cancer显示文摘 | Katrien Vermeulen Dirk R. Bockstaele Zwi N. Berneman | 2005 | Annals of Hematology2005，，10： | 1 |
| 9 | Cell cycleand apoptosis显示文摘 | Katrien V Zwi N Berneman DR | 2003 | Cell Prolif2003，36，： | 1 |
| 10 | Modulation of phenotype, cytokine production and stimulatory function of CD34^+ - derived DC by NiC1 (2) and SDS显示文摘 | De Smedt A C Van Den Heuvel R L Zwi Berneman N | 2001 | Toxicol In Vitro2001，15，45： | 1 |
| 11 | Pseudohemophilia of Erik von Willebrand caused by homozygous one nucleotide deletion in exon 18 of the VW-factor gene显示文摘The original description of a novel severe bleeding disorder as'Hereditary Pseudohemophilia'by Erik von Willebrand can currently be labelled as von Willebrand disease(VWD)type 3.VWD type 3 is autosomal recessive caused by homozygous or double heterozygous null mutations in the von Willebrand factor(VWF)gene and typically characterized by prolonged bleeding time and APTT,FⅧ:C levels below 2%,undetectable VWF:Ag,VWF:RCo and VWF:CB and absence of ristocetin induced platelet aggregation(RIPA).Autosomal recessive von Willebrand disease type 3 VWD with virtual complete VWF deficiency are homozygous or compound heterozygous for two null alleles(gene deletions,stop codons,frame shift mutations,splice site mutations,and absence of m RNA).Reports on severerecessive VWD compound heterozygous for a null allele and a missense mutation and homozygous or double heterozygous for missense mutations are associated with very low but measurable FⅧand VWF:Ag and should be reclassified as severe recessive type 1 VWD.Homozygous missense or compound missense/null mutations related to recessive severe type 1 VWD have been indentified in the VWF prosequence D1 and D2domains,the D4,B1-3,C1-2 domains,and only a very few in the dimmerization site(D3 domain).The detection of even tiny amounts of VWF:Ag after desmopressin acetate(DDAVP)or in hidden sites like platelets allows the differentiation between patients with VWD type 3 and homozygous or double heterozygous recessive severe type 1.Carriers of a null allele related to VWD type 3 or a missense mutation related with severe recessive type 1 VWD may present with mild VWD with low penetrance of bleeding in particular when associated with blood group O.Heterozygous obligatory carriers(OC)of a null mutation or a missense mutation related to recessive VWD type 3 or severe type 1both present with asymptomatic or mild VWD type 1 in particular when associated with blood group O.The response to DDAVP of OC of either a nonsense or a missense mutation appears to be abnormal and diagnostic with a 3-times higher response of FⅧ:C as compared to VWF:Ag.In contrast,the responses to DDAVP of FⅧ:C and VWF:Ag are equally good in individuals with low VWF levels related to blood group O and a normal VWF gene and protein(pseudo-VWD).These observations are completely in line with and extend the original observations of von Willebrand in a large family with VWD type 3 and asymptomatic or mild true type1 VWD in OC. | Alain Gadisseur Zwi Berneman Wilfried Schroyens Jan Jacques Michiels | 2013 | World Journal of Hematology2013，2，4： | 0 |
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