|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | Hemophagocytic lymphohistiocytosis: Recent progress in the pathogenesis, diagnosis and treatment显示文摘Hemophagocytic lymphohistiocytosis(HLH) is a hyperinflammatory syndrome that develops as a primary(familial/hereditary) or secondary(non-familial/hereditary) disease characterized in the majority of the cases by hereditary or acquired impaired cytotoxic T-cell(CTL) and natural killer responses. The molecular mechanisms underlying impaired immune homeostasis have been clarified, particularly for primary diseases. Familial HLH(familial hemophagocytic lymphohistiocytosis type 2-5, Chediak-Higashi syndrome, Griscelli syndrome type 2, Hermansky-Pudlak syndrome type 2) develops due to a defect in lytic granule exocytosis, impairment of(signaling lymphocytic activation molecule)-associated protein, which plays a key role in CTL activity [e.g., X-linked lymphoproliferative syndrome(XLP) 1], or impairment of X-linked inhibitor of apoptosis, a potent regulator of lymphocyte homeostasis(e.g., XLP2). The development of primary HLH is often triggered by infections, but not in all. Secondary HLH develops in association with infection, autoimmune diseases/rheumatological conditions and malignancy. The molecular mechanisms involved in secondary HLH cases remain unknown and the pathophysiology is not the same as primary HLH. For either primary or secondary HLH cases, immunosuppressive therapy should be given to control the hypercytokinemia with steroids, cyclosporine A, or intravenous immune globulin, and if primary HLH is diagnosed, immunochemotherapy with a regimen containing etoposide or anti-thymocyte globulin should be started. Thereafter, allogeneic hematopoietic stem-cell transplantation is recommended for primary HLH or secondary refractory disease(especially EBVHLH). | Shinsaku Imashuku | 2014 | World Journal of Hematology2014，3，3： | 5 |
| 2 | The inflammatory micro-environment in tumor progression: The role of tumor-associated macrophages显示文摘 | Paola Allavena Antonio Sica Graziella Solinas Chiara Porta Alberto Mantovani | 2007 | Critical Reviews in Oncology and Hematology2007，，1： | 5 |
| 3 | Aspirin responsive platelet thrombophilia in essential thrombocythemia and polycythemia vera显示文摘Essential thrombocythemia(ET) and polycythemia vera(PV) frequently present with erythromelalgia and acrocyanotic complications, migraine-like microvascular cerebral and ocular transient ischemic attacks(MIAs) and/or acute coronary disease. The spectrum of MIAs in ET range from poorly localized symptoms of transient unsteadiness, dysarthria and scintillating scotoma to focal symptoms of transient monocular blindness, transient mono- or hemiparesis or both. The attacks all have a sudden onset, occur sequentially rather than simultaneously, last for a few seconds to several minutes and are usually associated with a dull, pulsatile or migraine-like headache. Increased hematocrit and blood viscosity in PV patients aggravate the microvascular ischemic syndrome of thrombocythemia to major arterial and venous thrombotic complications. Phlebotomy to correct hematocrit to normal in PV significantly reduces major arterial and venous thrombotic complications, but fails to prevent the platelet-mediated erythromelalgia and MIAs. Complete long-term relief of the erythromelalgic microvascular disturbances, MIAs and major thrombosis in ET and PV patients can be obtained with low dose aspirin and platelet reduction to normal, but not with anticoagulation. Skin punch biopsies from the erythromelalgic area show fibromuscular intimal proliferation of arterioles complicated by occlusive plateletrich thrombi leading to acrocyanotic ischemia. Symptomatic ET patients with erythromelalgic microvascular disturbances have shortened platelet survival, increased platelet activation markers β-thromboglobulin(β-TG), platelet factor 4(PF4) and thrombomoduline(TM), increased urinary thromboxane B2(TXB2) excretion, and no activation of the coagulation markers thrombin fragments F1+2 and fibrin degradation products. Inhibition of platelet cyclooxygenase(COX1) by aspirin is followed by the disappearance and no recurrence of microvascular disturbances, increase in platelet number, correction of the shortened platelet survival times to normal, and reduction of increased plasma levels of β-TG, PF4, TM and urinary TXB2 excretion to normal. These results indicate that platelet-mediated fibromuscular intimal proliferation and platelet-rich thrombi in the peripheral, cerebral and coronary end-arterial microvasculature are responsible for the erythromelalgic ischemic complica-tions, MIAs and splanchnic vein thrombosis. Baseline platelet P-selectin levels and arachidonic acid induced COX1 mediated platelet activation showed a highly significant increase of platelet P-selectin expression(not seen in ADP and collagen stimulated platelets), which was significantly higher in JAK2V617 F mutated compared to JAK2 wild type ET. | Jan Jacques Michiels Fibo WJ Ten Kate Peter J Koudstaal Perry JJ Van Genderen | 2013 | World Journal of Hematology2013，2，2： | 4 |
| 4 | CD4 + CD25 + Foxp3 + Regulatory T Cells in the Pathophysiology of Immune Thrombocytopenia显示文摘 | Tetsuya Nishimoto Masataka Kuwana | 2013 | Seminars in Hematology2013，，： | 4 |
| 5 | Vesical dysfunctions after radical hysterectomy for cervical cancer: a critical review显示文摘 | Marzio Angelo Zullo Natalina Manci Roberto Angioli Ludovico Muzii Pierluigi Benedetti Panici | 2003 | Critical Reviews in Oncology and Hematology2003，，3： | 4 |
| 6 | Derivation of multipotent progenitors from human circulating CD14 + monocytes显示文摘 | Noriyuki Seta Masataka Kuwana | 2010 | Experimental Hematology2010，，7： | 3 |
| 7 | European vs 2015-World Health Organization clinical molecular and pathological classification of myeloproliferative neoplasms显示文摘The BCR/ABL fusion gene or the Ph^1-chromosome in the t(9;22)(q34;q11)exerts a high tyrokinase acticity,which is the cause of chronic myeloid leukemia(CML).The1990 Hannover Bone Marrow Classification separated CML from the myeloproliferative disorders essential thrombocythemia(ET),polycythemia vera(PV)and chronic megakaryocytic granulocytic myeloproliferation(CMGM).The 2006-2008 European Clinical Molecular and Pathological(ECMP)criteria discovered 3variants of thrombocythemia:ET with features of PV(prodromal PV),'true'ET and ET associated with CMGM.The 2008 World Health Organization(WHO)-ECMP and 2014 WHO-CMP classifications defined three phenotypes of JAK2^(V617F)mutated ET:normocellular ET(WHO-ET),hypercelluar ET due to increased erythropoiesis(prodromal PV)and ET with hypercellular megakaryocytic-granulocytic myeloproliferation.The JAK2^(V617F)mutation load in heterozygous WHO-ET is low and associated with normal life expectance.The hetero/homozygous JAK2^(V617F)mutation load in PV and myelofibrosis is related to myeloproliferative neoplasm(MPN)disease burden in terms of symptomaticsplenomegaly,constitutional symptoms,bone marrow hypercellularity and myelofibrosis.JAK2 exon 12mutated MPN presents as idiopathic eryhrocythemia and early stage PV.According to 2014 WHO-CMP criteria JAK2 wild type MPL^(515)mutated ET is the second distinct thrombocythemia featured by clustered giant megakaryocytes with hyperlobulated stag-horn-like nuclei,in a normocellular bone marrow consistent with the diagnosis of'true'ET.JAK2/MPL wild type,calreticulin mutated hypercellular ET appears to be the third distinct thrombocythemia characterized by clustered larged immature dysmorphic megakaryocytes and bulky(bulbous)hyperchromatic nuclei consistent with CMGM or primary megakaryocytic granulocytic myeloproliferation. | Jan Jacques Michiels Fransje Valster Jenne Wielenga Katrien Schelfout Hendrik De Raeve | 2015 | World Journal of Hematology2015，4，3： | 3 |
| 8 | Priming with G-CSF effectively enhances low-dose Ara-C-induced in vivo apoptosis in myeloid leukemia cells显示文摘 | Amuguleng Bai Hiroshi Kojima Mitsuo Hori Nobuo Nara Takuya Komeno Yuichi Hasegawa Haruhiko Ninomiya Tsukasa Abe Toshiro Nagasawa | 1999 | Experimental Hematology1999，，2： | 3 |
| 9 | miR-320 targets transferrin receptor 1 (CD71) and inhibits cell proliferation显示文摘 | Dale G. Schaar Daniel J. Medina Dirk F. Moore Roger K. Strair Yi Ting | 2009 | Experimental Hematology2009，，2： | 3 |
| 10 | Rituximab: Mechanism of Action显示文摘 | George J. Weiner | 2010 | Seminars in Hematology2010，，2： | 3 |
| 11 | Retrospective analysis of primary gastric diffuse large B cell lymphoma in the rituximab era: a multicenter study of 95 patients in Japan显示文摘 | Tsutomu Tanaka Kazuyuki Shimada Kazuhito Yamamoto Yoshiki Hirooka Yasumasa Niwa Isamu Sugiura Kunio Kitamura Hiroshi Kosugi Tomohiro Kinoshita Hidemi Goto Shigeo Nakamura | 2012 | Annals of Hematology2012，，3： | 3 |
| 12 | Circulating microRNAs: Association with disease and potential use as biomarkers显示文摘 | Glen Reid Michaela B. Kirschner Nico van Zandwijk | 2010 | Critical Reviews in Oncology / Hematology2010，，2： | 3 |
| 13 | The cellular and molecular basis of hyperthermia显示文摘 | Bert Hildebrandt Peter Wust Olaf Ahlers Annette Dieing Geetha Sreenivasa Thoralf Kerner Roland Felix Hanno Riess | 2002 | Critical Reviews in Oncology and Hematology2002，，： | 3 |
| 14 | A concise, practical guide to diagnostic assessment for mast cell activation disease显示文摘As recognition of mast cell(MC) involvement in a range of chronic inflammatory disorders has increased, diagnosticians' suspicions of MC activation disease(MCAD) in their chronically mysteriously inflamed patients have similarly increased. It is now understood that the various forms of systemic mastocytosis- diseases of inappropriate activation and proliferation of MCs seemingly driven by a small set of rare, usually constitutively activating mutations in assorted MC regulatory elements-comprise merely the tip of the MCAD iceberg, whereas the far larger and far more clinically heterogeneous(and thus more difficult to recognize) bulk of the iceberg consists of assorted forms of MC activation syndrome(MCAS) which manifest little to no abnormal MC proliferation and may originate from a far more heterogeneous set of MC mutations. It is reasonable to suspect MCAD when symptoms and signs of MC activation are present and no other diagnosis better accounting for the full range of findings is present. Initial laboratory assessment should include not only routine blood counts and serum chemistries but also a serum total tryptase level, which helps direct further evaluation for mastocytosis vs MCAS. Appropriate tissue examinations are needed to diagnose mastocytosis, while elevated levels of relatively specific mast cell mediators are sought to support diagnosis of MCAS. Whether assessing for mastocytosis or MCAS, testing is fraught with potential pitfalls which can easily yield false negatives leading to erroneous rejection of diagnostic consideration of MCAD in spite of a clinical history highly consistent with MCAD. Efforts at accurate diagnosis of MCAD are worthwhile, as many patients then respond well to appropriately directed therapeutic efforts. | Lawrence B Afrin Gerhard J Molderings | 2014 | World Journal of Hematology2014，3，1： | 3 |
| 15 | First-line single-agent cetuximab in elderly patients with metastatic colorectal cancer. A phase II clinical and molecular study of the Spanish group for digestive tumor therapy (TTD)显示文摘 | J. Sastre E. Aranda C. Grávalos B. Massutí M. Varella-Garcia F. Rivera G. Soler A. Carrato J.L. Manzano E. Díaz-Rubio M. Hidalgo | 2009 | Critical Reviews in Oncology and Hematology2009，，1： | 2 |
| 16 | Reduced intensity conditioning and co-transplantation of unrelated peripheral stem cells combined with umbilical cord mesenchymal stem/stroma cells for young patients with refractory severe aplastic anemia显示文摘 | Yuewen Fu Qian Wang Jian Zhou Shengquan Liu Baijun Fang Xudong Wei Yongping Song | 2013 | International Journal of Hematology2013，，6： | 2 |
| 17 | High prevalence of occult hepatitis B virus infection in patients with B cell non-Hodgkin’s lymphoma显示文摘 | Ming-Huang Chen Liang-Tsai Hsiao Tzeon-Jye Chiou Jin-Hwang Liu Jyh-Pyng Gau Hao-Wei Teng Wei-Shu Wang Ta-Chung Chao Chueh-chuan Yen Po-Min Chen | 2008 | Annals of Hematology2008，，6： | 2 |
| 18 | Mesenchymal stem cells for the treatment and prevention of graft-versus-host disease: experiments and practice显示文摘 | Nayoun Kim Keon-Il Im Jung-Yeon Lim Eun-Joo Jeon Young-Sun Nam Eun-Jung Kim Seok-Goo Cho | 2013 | Annals of Hematology2013，，10： | 2 |
| 19 | Octreotide prevents l -asparaginase–induced pancreatic injury in rats显示文摘 | Mitsuyoshi Suzuki Toshiaki Shimizu Takahiro Kudo Hiromichi Shoji Yoshikazu Ohtsuka Yuichiro Yamashiro | 2008 | Experimental Hematology2008，，2： | 2 |
| 20 | CIK cells from recurrent or refractory AML patients can be efficiently expanded in vitro and used for reduction of leukemic blasts in vivo显示文摘 | Yao Wang Jian Bo Han-ren Dai Xue-chun Lu Hai-yan Lv Bo Yang Tao Wang Wei-dong Han | 2012 | Experimental Hematology2012，，： | 2 |
您所在的机构暂未开通此部分的功能，请联系管理员