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Andrea M McCollum,
Connie Austin,
John Nawrocki,
Julia Howland,
Julie Pryde,
Awais Vaid,
David Holmes,
M Ryan Weil,
Yu Li,
Kimberly Wilkins, Hui Zhao,
Scott K Smith,
Kevin Karem,
Mary G Reynolds,
Inger K Damon
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ABSTRACT: Cowpox virus is an Orthopoxvirus that can cause infections in humans and a variety of animals. Infections occur in Eurasia; infections in humans and animals have not been reported in the United States. This report describes the occurrence of the first known human case of laboratory-acquired cowpox virus infection in the United States and the ensuing investigation.
The patient and laboratory personnel were interviewed, and laboratory activities were reviewed. Real-time polymerase chain reaction (PCR) and serologic assays were used to test the patient's specimens. PCR assays were used to test specimens obtained during the investigation.
A specimen from the patient's lesion tested positive for cowpox virus DNA. Genome sequencing revealed a recombinant region consistent with a strain of cowpox virus stored in the research laboratory's freezer. Cowpox virus contamination was detected in 6 additional laboratory stocks of viruses. Orthopoxvirus DNA was present in 3 of 20 environmental swabs taken from laboratory surfaces.
The handling of contaminated reagents or contact with contaminated surfaces was likely the mode of transmission. Delays in recognition and diagnosis of this infection in a laboratory researcher underscore the importance of a thorough patient history-including occupational information-and laboratory testing in facilitating a prompt investigation and application of control and remediation measures.
The Journal of Infectious Diseases 04/2012; 206(1):63-8. · 6.41 Impact Factor
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Xiaolei Zhu,
Cong Chen,
Dan Ye,
Dening Guan,
Lan Ye,
Jiali Jin, Hui Zhao,
Yanting Chen,
Zhongyuan Wang,
Xin Wang,
Yun Xu
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ABSTRACT: Mitochondrial dysfunction is a hallmark of beta-amyloid (Aβ)-induced neurotoxicity in Alzheimer's disease (AD), and is considered an early event in AD pathology. Diammonium glycyrrhizinate (DG), the salt form of Glycyrrhizin, is known for its anti-inflammatory effects, resistance to biologic oxidation and membranous protection. In the present study, the neuroprotective effects of DG on Aβ(1-42)-induced toxicity and its potential mechanisms in primary cortical neurons were investigated. Exposure of neurons to 2 µM Aβ(1-42) resulted in significant viability loss and cell apoptosis. Accumulation of reactive oxygen species (ROS), decreased mitochondrial membrane potential, and activation of caspase-9 and caspase-3 were also observed after Aβ(1-42) exposure. All these effects induced by Aβ(1-42) were markedly reversed by DG treatment. In addition, DG could alleviate lipid peroxidation and partially restore the mitochondrial function in Aβ(1-42)-induced AD mice. DG also significantly increased the PGC-1α expression in vivo and in vitro, while knocking down PGC-1α partially blocked the protective effects, which indicated that PGC-1α contributed to the neuroprotective effects of DG. Furthermore, DG significantly decreased the escape latency and search distance and increased the target crossing times of Aβ(1-42)-induced AD mice in the Morris water maze test. Therefore, these results demonstrated that DG could attenuate Aβ(1-42)-induced neuronal injury by preventing mitochondrial dysfunction and oxidative stress and improved cognitive impairment in Aβ(1-42)-induced AD mice, indicating that DG exerted potential beneficial effects on AD.
PLoS ONE 01/2012; 7(4):e35823. · 4.09 Impact Factor
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Jianping Li,
Shaoguang Yang,
Shihong Lu, Hui Zhao,
Jianming Feng,
Wenqian Li,
Fengxia Ma,
Qian Ren,
Bin Liu,
Lei Zhang,
Yizhou Zheng,
Zhong Chao Han
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ABSTRACT: Aplastic anemia (AA) is generally considered as an immune-mediated bone marrow failure syndrome with defective hematopoietic stem cells (HSCs) and marrow microenvironment. Previous studies have demonstrated the defective HSCs and aberrant T cellular-immunity in AA using a microarray approach. However, little is known about the overall specialty of bone marrow mesenchymal stem cells (BM-MSCs). In the present study, we comprehensively compared the biological features and gene expression profile of BM-MSCs between AA patients and healthy volunteers. In comparison with healthy controls, BM-MSCs from AA patients showed aberrant morphology, decreased proliferation and clonogenic potential and increased apoptosis. BM-MSCs from AA patients were susceptible to be induced to differentiate into adipocytes but more difficult to differentiate into osteoblasts. Consistent with abnormal biological features, a large number of genes implicated in cell cycle, cell division, proliferation, chemotaxis and hematopoietic cell lineage showed markedly decreased expression in BM-MSCs from AA patients. Conversely, more related genes with apoptosis, adipogenesis and immune response showed increased expression in BM-MSCs from AA patients. The gene expression profile of BM-MSCs further confirmed the abnormal biological properties and provided significant evidence for the possible mechanism of the destruction of the bone marrow microenvironment in AA.
PLoS ONE 01/2012; 7(11):e47764. · 4.09 Impact Factor
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Jie Tao,
Ming Yang,
Zhong Chen,
Ying Huang,
Qinjun Zhao,
Jianhui Xu,
He Ren, Hui Zhao,
Zhenping Chen,
Qian Ren,
Renchi Yang
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ABSTRACT: DNA methylation is known to play an important role in gene transcription and alterations of methylation contribute to the development of certain disorders such as cancer and immunodeficiency. Recent years have found an increasing interest in the role of epigenetic modifications in the etiology of human autoimmune diseases, such as systemic lupus erythromatosus (SLE) and rheumatoid arthritis (RA). DNA methyltransferases (DNMTs) are involved in the epigenetic control of DNA methylation processes. S-adenosylmethionine (SAM) and S-adenosylhomocysteine (SAH), as the substrate and product of essential cellular methyltransferase reactions, have important indicator action of cellular methylation status. The aim of this study is to explore if DNA methylation plays a role in the pathogenesis of idiopathic thrombocytopenic purpura (ITP).
DNMT1, DNMT3A, and DNMT3B mRNA expression in peripheral blood mononuclear cells (PBMCs) of adult ITP patients were analyzed by real-time quantitative polymerase chain reaction. Plasma SAM and SAH levels were assayed with reversed-phase high performance liquid chromatography (HPLC).
DNMT3A and DNMT3B mRNA expressions were significantly lower in ITP patients than in healthy controls (p < 0.001), while DNMT1 mRNA expression was not significantly different between the two groups (p = 0.774). Plasma SAH concentration was significantly elevated in ITP patients than in healthy controls (p < 0.05), while the plasma SAM and SAM/SAH were not significantly different between the two groups (p = 0.133, p = 0.624 respectively).
Our observations suggest that aberrant DNA methylation status reflected by increased plasma SAH concentration and decreased mRNA expression levels of DNMT3A and 3B are possibly involved in the pathogenesis of ITP although the precise mechanisms need further study.
Journal of Clinical Immunology 10/2008; 28(5):432-9. · 3.08 Impact Factor
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ABSTRACT: There are very limited data reported about childhood acute promyelocytic leukemia (APL), especially with arsenic trioxide (As2O3) treatment. We review the clinical course and treatment outcome of 65 children APL.
Between January 1999 and December 2005, 65 children (<18 years) with newly diagnosed APL were treated.
Three groups of patients were identified according to the different induction regimens. Forty patients were given ATRA alone (group 1, G1), 8 patients were given As2O3 alone (group 2, G2), 15 patients (group 3, G3) were treated with combination of ATRA and As2O3. Two patients received cytosine arabinoside and died at days 2 and 4, respectively. The CR rate of G1 was 95% (38/40). The overall CR rate of G2+G3 was 91.3% (21/23). Toxicity of ATRA and As2O3 were minimal and recoverable during induction. Five children had a hematologic relapse and two developed molecular relapse. Five of them were successfully treated with ATRA alone or combined with As2O3. The 5-year estimate of EFS, DFS and OS between G1 and G2+G3 has no difference.
As2O3 is an effective and well tolerable therapy for children with APL and it may be used in those who have dose limiting side effects of ATRA, but also for those with newly diagnosed or relapsed APL.
Pediatric Blood & Cancer 08/2008; 51(2):210-5. · 1.89 Impact Factor
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Zhi-Bo Han,
He Ren, Hui Zhao,
Ying Chi,
Ke Chen,
Bin Zhou,
Yong-jun Liu,
Lei Zhang,
Bin Xu,
Bin Liu,
Renchi Yang,
Zhong-Chao Han
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ABSTRACT: Stem cell factor (SCF) plays important roles in tumor growth and angiogenesis. However, its regulatory mechanism remains largely undefined. Here, we report that hypoxia upregulated the expression of SCF in MCF-7 breast cancer cells in both messenger RNA and protein levels. When hypoxia-inducible factor (HIF)-1 alpha expression was knocked down by RNA interference, the MCF-7 cell expression of SCF was decreased significantly. Furthermore, the SCF receptor, c-kit phosphorylation was significantly strengthened by the condition culture media from hypoxic MCF-7 and MCF-7-c cells. The survival of A549 cells was more dependent on SCF under hypoxia. Analysis of SCF promoter 5'-flanking region revealed a potential hypoxia-response element (HRE; 5'-GCGTG-3') located at -68 to -64 relative to the transcriptional start site. Chromatin immunoprecipitation assay demonstrated that HIF-1 alpha directly bound to this region under normoxia, and this binding activity was significantly enhanced under hypoxia. Overexpression of HIF-1 alpha significantly upregulated the expression of luciferase reporter gene under control of the SCF promoters in both MCF-7 cells and human embryonic kidney 293 cells, but mutation of the HRE site completely blocked this effect. Epidermal growth factor was also able to enhance the SCF expression under normoxia in MCF-7 cells, which was dependent on HIF-1 alpha. Taken together, our data demonstrated that HIF-1 alpha was a key regulator of SCF expression in breast cancer cells. Hypoxia and epidermal growth factor receptor signal coexisted in the tumor microenvironment and might promote angiogenesis through HIF-1 alpha-mediated upregulation of SCF and other angiogenic factors.
Carcinogenesis 04/2008; 29(10):1853-61. · 5.70 Impact Factor
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ABSTRACT: The aim of this study was to explore the profile and function of CD4(+)CD25(+) regulatory T cells (Treg cells) in idiopathic thrombocytopenic purpura (ITP) patients.
Treg cell numbers were analyzed by flow cytometric analysis in peripheral blood mononuclear cells collected from healthy donors or patients with ITP. Quantification of cell proliferation was assayed by an enzyme-linked immunosorbent assay kit, based on the measurement of BrdU incorporation during DNA synthesis.
The percentage of Treg cells was significantly decreased in ITP patients in active and non-remission state(5.79 +/- 1.22%) when compared with the patients in remission(11.63 +/- 4.56%) and to healthy subjects(12.68 +/- 3.59%). The suppressive activity of Treg cells in ITP patients was also found to be impaired.
These results suggest that decreased number and function of Treg cells might be one of mechanisms that cause immune regulation dysfunction in ITP.
European Journal Of Haematology 03/2007; 78(2):139-43. · 2.61 Impact Factor
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ABSTRACT: Excision repair cross-complementation group 1 (ERCC1) is important in repairing DNA damage and genomic instability, and polymorphisms in ERCC1 may play a role in human tumors. In this study, the relationship of two ERCC1 polymorphisms, 8092C>A and 19007G>A, with susceptibility to acute lymphoblastic leukemia (ALL) was investigated in 183 childhood patients. For the ERCC1 8092C>A polymorphism, individuals carrying the ERCC1 8092CC genotype had a significantly higher risk when compared with those carrying at least one A allele gene (AA/AC). Analysis after stratification for sex showed that the males carrying ERCC1 8092CC genotype were associated with highly significant increased risk of ALL (1.94-fold) but not females. There was no association between ERCC1 19007G>A polymorphism and ALL risk when all patients as a group were analyzed. However, the males carrying ERCC119007A allele were associated with highly significant increased risk of ALL (2.36-fold). For the ERCC1 8092C>A polymorphism, individuals under 8 years old (median age) carrying CC genotype had significantly higher risk. However, the 19007G>A polymorphism was not associated with such age-related ALL risk. These results suggest that the ERCC1 8092C>A polymorphism may be related to the occurrence of childhood ALL in a Chinese population.
Leukemia Research 11/2006; 30(11):1341-5. · 2.92 Impact Factor
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He Ren, Hui Zhao,
Tingting Wang,
Yanhui Yang,
Zhibo Han,
Bin Liu,
Zida Wu,
Jie Tao,
Bin Zhou,
Lei Zhang,
Renchi Yang,
Zhong Chao Han
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ABSTRACT: Chronic idiopathic thrombocytopenic purpura (ITP) is an organ-specific autoimmune disease characterized by the production of antibodies against antigens on the membranes of platelets, resulting in enhanced destruction of the platelets by macrophages. Leptin, a cytokine-like hormone, plays a role in the pathogenesis of several autoimmune diseases. In this study, we observed significantly increased plasma leptin levels combined with decreased soluble leptin receptor (sOB-R) levels in 18 chronic ITP patients compared with 14 controls. We also demonstrated significantly elevated mRNA expression of long form leptin receptor (Ob-Rb) on peripheral blood mononuclear cells (PBMCs) from chronic ITP patients. Treatment with recombinant leptin or serum with high leptin levels enhanced in vitro secretion of IgG antiplatelet antibodies by splenocytes and PBMCs from patients with chronic ITP. After depletion of CD4(+) T cells from splenocytes, leptin lost this function. Further studies showed that leptin could increase platelet reactive T cells. These findings suggest that leptin may be involved in the pathogenesis of chronic ITP and might offer a potential target for the treatment of this disease.
Clinical Immunology 09/2006; 120(2):205-11. · 4.05 Impact Factor
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ABSTRACT: To explore the profiles of type 1 and type 2 T cells in chronic idiopathic thrombocytopenic purpura (ITP) patients.
Samples of peripheral blood were collected from 30 chronic ITP patients, 8 males and 22 females, aged 34, 20 being in the active stage, and 10 in the remission stage, and 20 healthy persons, 7 males and 13 females, aged 31. Peripheral blood mononuclear cells (PBMCs) were isolated, cultured, and activated with PMA/ionomycin. Flow cytometry was used to measure the intracellular cytokines interferon (IFN)-gamma and interleukin (IL)-4 in the PBMCs so as to identify the Th1 cells (IFN-gamma(+) IL-4(+) CD4(+) cells), Th2 cells (IFN-gamma(-) IL-4(+) CD4(+) cells), Tc1 cells (IFN-gamma+ IL-4(-) CD8(+) cells), and Tc2 cells (IFN-gamma(-) IL-4(+) CD8(+) cells). The ratios of Th2/Tc2, Th1/Th2, and Tc1/Tc2 were calculated. Samples of spleen tissue were collected from 8 patients with chronic ITP, 3 males and 5 females, aged 30, and 6 patients with hereditary spherocytosis (HS), 3 males and 3 females, aged 35, who underwent splenectomy. Splenocytes were isolated, cultured, and activated with PMA/ionomycin. Real-time PCR was used to detect the mRNA expression of T-bet and GATA-3 in the PBMCs and splenocytes.
The Th1/Th2 ratio of the patients in active stage was 25.62, significantly higher than those of the patients in remission stage (9.86) and the control (8.29, both P < 0.01), and the Tc1/Tc2 ratio of the patients in active stage was 30.23, significantly higher than those of the patients in remission stage (10.10) and the controls (12.58, both P < 0.01). The Th1/Th2 ratio of the splenocytes of the patients in active stage was 41.46, significantly higher than that of the controls (16.30, P < 0.01), and the Tc1/Tc2 ratio of the splenocytes of the active ITP patients was 35.80, not significantly higher than that of the controls (16.30, P = 0.082). The GATA-3 mRNA expression level of the PBMCs of the active ITP patients was one-fifth of that of the controls (P < 0.05) and the GATA-3 mRNA expression level of the splenocytes of the ITP patients was 0.34 of that of the HS patients (P < 0.05), however, there was no difference in the T-bet expression among the 3 groups. The T-bet/GATA-3 ratio of the PBMCs of the active ITP patients was 5.85 times that of the controls and the T-bet/GATA-3 ratio of the splenocytes of the active ITP patients was 2.68 times that of the controls (both P < 0.01).
ITP is a T1 cells (Th1 and Tc1) predominant disease. The T-bet/GATA-3 ratio may provide a surrogate marker of T1/T2 cytokine balance. Shifting the cytokine patterns from T1 to T2 may be a potential immunotherapy for ITP.
Zhonghua yi xue za zhi 04/2006; 86(10):669-73.
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ABSTRACT: We retrospectively analyzed the clinical characteristics and management of 472 Chinese children (age 1~14 years) with chronic idiopathic thrombocytopenic purpura (ITP). The distribution of cases by age showed a maximum at 4 years and more patients below 7 years old than between 7 and 14 years old had ITP (337, 71.4% vs. 135, 28.6%). Variable bleeding signs occurred in this series of patients. Steroids therapy was effective for Chinese children with chronic ITP whether as first- or second-line therapy. Traditional Chinese medicine was less effective than steroids.
Haematologica 07/2005; 90(6):860-1. · 6.42 Impact Factor
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ABSTRACT: Adult idiopathic thrombocytopenic purpura (ITP) is a chronic acquired organ-specific autoimmune hemorrhagic disease characterized by the production of antibodies against antigens on the membranes of platelet, resulting in enhanced Fc-mediated destruction of the platelets by macrophages in the reticuloendothelial system. Dysfunctional cellular immunity is considered important in the pathophysiology of ITP. The aim of this study was to explore the profile of type1 and type2 T cells in chronic ITP patients.
The balance of Th1/Th2 and Tc1/Tc2 was studied by simultaneous analysis of intracellular cytokines of peripheral blood mononuclear cells and splenocytes in short-term cultures activated with PMA/ionomycin as well as mRNA expression of T-bet and GATA-3 in peripheral blood mononuclear cells and splenocytes using real-time polymerase chain reaction.
Patients with active disease but not patients in remission had significant higher Th1/Th2 (p<0.01) and Tc1/Tc2 (p<0.01) ratios in peripheral blood (PB) and significant higher Th1/Th2 ratio in splenocytes (p<0.01) than those in the control group. The Tc1/Tc2 ratio in splenocytes in ITP patients was higher than that in control, but did not reach significant difference (p=0.082). GATA-3 mRNA expression in ITP patients was significantly lower both in PB (p<0.01) and in splenocytes (p<0.01) than in corresponding samples from controls while there was no difference in T-bet expression.
Our data indicate that ITP is a T1 cell (Th1 and Tc1) predominant disease although the precise mechanisms await further functional assay. The T-bet/GATA-3 ratio may provide a surrogate marker of T1/T2 cytokine balance. Shifting the cytokine patterns from T1 to T2 might be a potential immunotherapy for ITP.
Haematologica 07/2005; 90(7):914-23. · 6.42 Impact Factor
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ABSTRACT: Idiopathic thrombocytopenic purpura (ITP) is an organ-specific autoimmune disorder characterized by a low platelet count and mucocutaneous bleeding. The decrease of platelets is caused by increased autoantibodies against self-antigens, particularly IgG antibodies against GPIIb/IIIa. The production of these autoantibodies by B cells depends on a number of cellular mechanisms that form a network of modulation, with T cells playing a pivotal role in pathophysiology. Delineation of the dysfunction of cellular immunity has recently been attempted. This review will focus on these recent advances applicable to ITP and to highlight how these may translate into novel approaches to treatment in the future. Multi-dysfunction in these networks may include a failure of self-antigen recognition and tolerance, involvement of abnormal cell surface molecules, altered Th1/Th2 cytokine profiles, impaired megakaryocytopoiesis and impaired cell-mediated cytotoxicity. In ITP, multi-step dysfunctions in these networks may take place that finally lead to the occurrence of the disease. Therefore, unveiling these dysfunctions is vital in understanding the pathophysiology of ITP and will finally lead to the development of new therapies to fight the disease.
Critical Reviews in Oncology/Hematology 06/2005; 54(2):107-16. · 4.41 Impact Factor
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ABSTRACT: Adult chronic idiopathic thrombocytopenic purpura (ITP) is a common hematologic disease characterized by persistent thrombocytopenia. So far, there were only a few reports on adult Chinese patients with chronic ITP. This study aimed at defining the treatment outcome and prognostic factors for chronic ITP based on a large cohort of Chinese patients followed up for over 25 years at a single center.
The medical records of 1791 patients aged 14 years or older who were diagnosed as having chronic ITP at our hospital from 1974 to 1999 were retrospectively analyzed.
The female-to-male ratio was 2:1, with a median age of 34 years (ranging from 14 to 80 years), median platelet count of 38 x 10(9)/L [range (1-99) x 10(9)/L], and median follow-up of 36 months (range 1-220 months). Steroids were used in 689 patients, among them 209 (30.3%) achieved complete remission (CR). A splenectomy was performed in 124 patients, and response to steroid pre-splenectomy was not available in 14 patients. The CR rate after a splenectomy was lower in steroid nonresponders (29 of 90, 32.2%) than in those who relapsed after successful steroid treatment (12 of 20, 60.0%) (P < 0.05). In comparison with patients negative for antinuclear antibody (ANA), those who were ANA positive had similar responses to steroids, but a significantly shorter remission period after a splenectomy (P < 0.01).
Adult Chinese chronic ITP patients can have long-term remission after steroid therapy and splenectomies. Primary steroid refractoriness is a prognostic factor predicting poor subsequent response to a splenectomy.
Chinese medical journal 01/2005; 118(1):34-7. · 0.86 Impact Factor
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ABSTRACT: Essential thrombocythemia (ET) is a chronic myeloproliferative disorder with abnormal megakaryocyte/platelet production. Recent studies have found that Bcl-xL, as a member of the bcl-2 family of proteins that inhibit apoptosis, is essential in megakaryocytic differentiation. In this study the expression of Bcl-xL was evaluated during megakaryocytic differentiation in ET patients.
To study the role of Bcl-xL in megakaryocyte differentiation, we evaluated the effect of small interfering RNA (siRNA) on the expression of Bcl-xL. CD34+ cells from patients with ET, chronic myeloid leukemia (CML), polycythemia vera (PV) and normal individuals were cultured in serum-free medium supplemented with thrombopoietin (TPO). Immunocytochemical staining and flow cytometric analysis were used to evaluate the Bcl-xL expression during megakaryocytic differentiation of CD34+ cells.
When exposured to si-Bcl-xL, the percentage of K562 cells induced into megakaryocytes in 72 hours was lower than the corresponding percentage of control cells. CD41a+ cells from the three groups of patients and the control group were cultured. At day 10, the percentage of Bcl-xL- cells in CD41a+ cells from ET patients was 61.0+/-28.1%, which was significantly higher than that from patients with CML (2.5+/-20.9%), PV (33.6+/-10.0%) or control subjects (15.1+/-13.0%).]
These results demonstrate that Bcl-xL is down-regulated early during in vitro differentiation of megakaryocytes from ET patients; this might reflect an early entry of megakaryocytes into a degenerating mature stage.
Haematologica 11/2004; 89(10):1199-206. · 6.42 Impact Factor
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Chinese medical journal 07/2004; 117(6):953-5. · 0.86 Impact Factor
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ABSTRACT: The purpose of this study was to evaluate serum leptin levels in idiopathic thrombocytopenic purpura (ITP), in order to determine the influence of leptin on the pathogenesis of ITP.
Forty-six untreated patients with chronic ITP were compared with 40 healthy people of similar age, sex and body mass index (BMI). Serum leptin levels (ng/mL) were measured by enzyme-linked immunosorbent assay (ELISA).
We found that the mean serum leptin levels in patients with ITP (22.11 +/- 15.84 ng/mL) were significantly (P < 0.001) higher than that in healthy control volunteers (5.44 +/- 4.84 ng/mL). Furthermore, serum leptin levels in patients with ITP were inversely related (r = -0.86, P < 0.001) to the platelet counts and positively related to the platelet-associated IgG (PAIgG) levels (r = 0.7, P < 0.001). The levels of PAIgG and platelet counts were significantly different between leptin-positive (level greater than mean +/- 2 SD control value) and leptin-negative patients.
These findings suggest that leptin might play an important role in the pathogenesis of ITP.
European Journal Of Haematology 05/2004; 72(5):348-52. · 2.61 Impact Factor
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ABSTRACT: Transient pancytopenia preceding acute lymphoblastic leukemia (pre-ALL) is a rare occurrence usually affecting children with subsequent development of B lineage ALL. We report a case of pre-ALL characterized by a T cell immunophenotype and abnormal karyotype t (11; 14) (q10; q10). The patient achieved a transient complete remission after initial therapy, but relapsed within a few months and died of leukemic encephalopathy. To the best of our knowledge, this is the first report of T lineage pre-ALL.
Acta Haematologica 02/2004; 112(3):167-9. · 1.35 Impact Factor
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European Journal Of Haematology 04/2003; 70(3):196-7. · 2.61 Impact Factor
