Josef T Prchal

University of Utah, Salt Lake City, Utah, United States

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Publications (324)2391.91 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: The causative genetic mutations of inherited giant platelet disorders (IGPD) encompass genes coding for the platelet glycoprotein Ib-IX complex (Bernard Soulier syndrome and its variants), myosin heavy chain 9 (MYH9 gene mutated in May-Hegglin anomaly and other IGPDs), GATA-01 (GATA-related thrombocytopenia), TUBB-1, ITGA2, ITGAB3, FLNA and some others. IGPDs are frequently associated with other disorders including renal disease, sensorineural deafness, and leukocyte inclusion bodies. Most are accompanied with variable degrees of bleeding diathesis, while others, like TUBB1 IGPD, do not have any bleeding manifestations. Harris platelet syndrome (HPS), previously called asymptomatic constitutional macrothrombocytopenia, is an autosomal dominant disorder characterized by low-normal to severe thrombocytopenia IGPD and absence of bleeding. HPS has also been observed in healthy blood donors from the northeastern part of India (Bengal) and some areas of Bangladesh, Bhutan and Nepal. We describe a high prevalence of an autosomal dominantly inherited form of IGPD with mild to severe thrombocytopenia in the Muslim population in Kashmir Valley in the northern Indian subcontinent. 830 voluntary, healthy, male blood donors from Kashmir Valley were included in the study. They were aged 15-55 years (median 31 years) and underwent ancillary screening as follows; CBC, peripheral smear, HBV, HCV, HIV, ANA and Anti-H pylori antibodies. 15% of the donors had thrombocytopenia (mean platelet count 109.6 compared to 189.9 in controls; p=<0.0001). No differences were noted in age between the 2 groups. The mean platelet volume (MPV) in thrombocytopenic subjects was higher (12.53 + 0.78 vs 9.52 + 1.03 fl). The red cell distribution width (RDW) in thrombocytopenic subjects was higher than in those with normal counts (15.6 + 1.61 Vs 13. 22 + 1.36, p=<0.001). Hematocrit and other red cell indices were not different in the 2 groups. None of the participants had a history of bleeding, renal disease, sensorineural deafness, or leukocyte inclusion bodies. Peripheral blood platelet morphology revealed large platelets in all subjects. In a pilot study of 7 families, Kashmiri thrombocytopenia was compatible with autosomal dominant inheritance affecting both genders. The congenital nature of Kashmiri thrombocytopenia was demonstrated by analyses of 34 consecutive neonates born in Sher-i-Kashmir Institute Hospital; among 20 girls and 19 boys, we found 18% (2 male and 5 female) to have low platelet count, the mean platelet count of the affected group when compared to unaffected group were 102.6 vs 234 (p=<0.001) respectively. We then searched for a causative mutation using the following approaches. We sequenced the MYH9 gene and no mutation was found. We then employed SNP array analyses using Shared Genome Segment (SGS) and Whole Genome Association Study (WGAS). We were able to exclude all previously reported IGPD-causing genes. SGS that overlapped with WGAS narrowed the target into 3 chromosome regions in Chr. 5 (rs6872531-rs100072476), Chr. 9 (rs11999541-rs12682912) and Chr. 10 (rs11013452-rs7083349). The performed SNP analyses included large genomic segments as candidates for a Kashmiri thrombocytopenia-causative gene. To further narrow down the cause of this disorder, we recruited 3 TRIO families (an affected parent and a child) for stronger linkage analysis and next-generation sequencing to continue the search for the cause of the Kashmiri thrombocytopenia.
    American Society of Hematology, San Francisco, California, USA; 12/2014
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    ABSTRACT: Anemia is common in older persons and is associated with substantial morbidity and mortality. One third of anemic older adults have unexplained anemia of the elderly (UAE). We carried out a randomized, wait list control trial in outpatients with UAE and serum ferritin levels between 20 and 200 ng/mL. Intravenous iron sucrose was given as a 200-mg weekly dose for 5 weeks either immediately after enrollment (immediate intervention group) or following a 12-week wait list period (wait list control group). The primary outcome measure was changed in 6-minute walk test (6MWT) distances from baseline to 12 weeks between the two groups. Hematologic, physical, cognitive, and quality of life parameters were also assessed. The study was terminated early after 19 subjects enrolled. The distance walked in the 6MWT increased a mean 8.05 ± 55.48 m in the immediate intervention group and decreased a mean 11.45 ± 49.46 m in the wait list control group (p = 0.443). The hemoglobin increased a mean 0.39 ± 0.46 g/dL in the immediate intervention group and declined a mean 0.39 ± 0.85 g/dL in the wait list control group (p = 0.026). Thus, a subgroup of adults with UAE may respond to intravenous iron. Enrollment of subjects into this type of study remains challenging.
    Blood Cells Molecules and Diseases 12/2014; · 2.26 Impact Factor
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    ABSTRACT: Abstract Myeloproliferative neoplasms (MPNs) are clonal disorders of hematopoiesis characterized by a high frequency of genetic alterations and include chronic myeloid leukemia (CML) and the BCR-ABL1-negative MPNs. Herein we summarize recent advances and controversies in our understanding of the biology and therapy of these disorders, as discussed at the 8th post-American Society of Hematology CML-MPN workshop. The principal areas addressed include the breakthrough discovery of CALR mutations in JAK2/MPL wild type MPN patients, candidate therapies based on novel genetic findings in leukemic transformation and new therapeutic targets in MPNs, an appraisal of bone marrow histopathology in MPNs with a focus on the potential new clinical entity of 'masked' polycythemia vera, an update on clinical trials of JAK inhibitors is presented as well as current understanding regarding the definitions and mechanisms of resistance to JAK inhibitors and updated information on the safety and efficacy of discontinuation of tyrosine kinase inhibitors in CML patients.
    Leukemia & lymphoma. 10/2014;
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    ABSTRACT: We evaluated a neonate with severe jaundice but a negative family history. Spherocytes were present and suspected hereditary spherocytosis was confirmed by osmotic fragility and eosin-5-maleimide erythrocyte staining. We found he was a compound heterozygote for two pathogenic mutations in the gene encoding α-spectrin: a previously reported α(LEPRA) inherited from his asymptomatic mother, and a novel α-spectrin mutation in intron 45 +1 disrupting the consensus splice site, from his asymptomatic father. © 2014 S. Karger AG, Basel.
    Neonatology 10/2014; 106(4):355-357. · 2.57 Impact Factor
  • Blood 09/2014; 124(10):1691-2. · 9.78 Impact Factor
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    ABSTRACT: Tibetans do not exhibit increased hemoglobin concentration at high altitude. We describe a high-frequency missense mutation in the EGLN1 gene, which encodes prolyl hydroxylase 2 (PHD2), that contributes to this adaptive response. We show that a variant in EGLN1, c.[12C>G; 380G>C], contributes functionally to the Tibetan high-altitude phenotype. PHD2 triggers the degradation of hypoxia-inducible factors (HIFs), which mediate many physiological responses to hypoxia, including erythropoiesis. The PHD2 p.[Asp4Glu; Cys127Ser] variant exhibits a lower Km value for oxygen, suggesting that it promotes increased HIF degradation under hypoxic conditions. Whereas hypoxia stimulates the proliferation of wild-type erythroid progenitors, the proliferation of progenitors with the c.[12C>G; 380G>C] mutation in EGLN1 is significantly impaired under hypoxic culture conditions. We show that the c.[12C>G; 380G>C] mutation originated ~8,000 years ago on the same haplotype previously associated with adaptation to high altitude. The c.[12C>G; 380G>C] mutation abrogates hypoxia-induced and HIF-mediated augmentation of erythropoiesis, which provides a molecular mechanism for the observed protection of Tibetans from polycythemia at high altitude.
    Nature Genetics 08/2014; · 35.21 Impact Factor
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    ABSTRACT: From 2007 to 2011, 66 patients with primary myelofibrosis (PMF) or MF preceded by essential thrombocythemia or polycythemia vera were enrolled into a prospective phase II clinical trial of reduced intensity allogeneic hematopoietic stem cell transplantation (AHSCT), Myeloproliferative Disorder Research Consortium -101 trial. The study included patients with sibling donors (n=32) receiving fludarabine/melphalan (FluMel) as a preparative regimen and patients with unrelated donors (n=34) receiving conditioning with FluMel+anti-thymocyte globulin (rATG). Patient characteristics in the two cohorts were similar. Engraftment occurred in 97% of siblings and 76% unrelated transplants, while secondary graft failure occurred in 3% and 12%, respectively. With a median follow-up of 25 months for patients alive, the overall survival was 75% in the sibling (median not reached) and 32% in the unrelated group (median OS: 6 months, 95% CI:3,25) (HR 3.9, 95% CI: 1.8,8.9) (p<0.001). Non-relapse-mortality was 22% in siblings and 59% in unrelated AHSCT. Survival correlated with type of donor, but not with the degree of histocompatibility match, age or JAK2(V617F)-status. In patients with myelofibrosis with sibling donors AHSCT is an effective therapeutic option while AHSCT from unrelated donors with FluMel+ATG conditioning led to high rate of graft failure and limited survival. This study was registered at clinicaltrials.gov, identifier: 00572897.
    Blood 06/2014; · 9.78 Impact Factor
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    ABSTRACT: A fraction of polycythemia vera (PV) and essential thrombocythemia (ET) cases will, in time, undergo myelofibrotic transformation. In such cases, fibrosis may mask the diagnostic histologic features of the original underlying myeloproliferative neoplasm. Thus, confidently differentiating postfibrotic PV/ET from primary myelofibrosis (PMF) histologically may not be possible. It is controversial whether post-PV/ET myelofibrosis (MF) differs clinicopathologically from PMF, or whether these entities are biologically, clinically, and prognostically indistinguishable. To answer this question, we compared multiple candidate biological, morphologic, and prognostic parameters between 19 postfibrotic ET/PV individuals and 18 PMF individuals. The postfibrotic ET/PV and PMF cases did not differ with regard to clinical outcome, cytogenetic abnormalities, serum lactate dehydrogenase level, peripheral blast count, bone marrow morphology, or grade of reticulin fibrosis. Only JAK2 allele burden, which was higher in the postfibrotic PV/ET population (P=0.011), differed between the 2 groups. Cardinal morphologic features of PMF (ie, marrow cellularity, intrasinusoidal hematopoiesis, osteosclerosis, etc.) were commonly observed in post-PV/ET MF marrow biopsies, and only a minority of post-PV/ET MF marrow biopsies the retained diagnostic features of the primary myeloproliferative neoplasm (panmyelosis in PV and megakaryocytic hyperplasia in ET). Our study indicates that PMF and post-PV/ET MF are clinically and biologically indistinguishable.
    06/2014;
  • Haematologica 06/2014; 99(6):945-949. · 5.94 Impact Factor
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    ABSTRACT: von Hippel-Lindau (VHL) protein is the principal negative regulator of hypoxia sensing mediated by transcription factors. Mutations in exon 3 of the VHL gene lead to Chuvash (VHLR200W) and Croatian (VHLH191D) polycythemias. Here, we describe an infant of Bangladesh ethnicity with a novel homozygous VHLD126N mutation with congenital polycythemia and dramatically elevated erythropoietin (EPO) levels, who developed severe fatal pulmonary hypertension. In contrast to Chuvash polycythemia, erythroid progenitors (BFU-Es) did not reveal a marked EPO hypersensitivity. Further, NF-E2 and RUNX1 transcripts that correlate with BFU-Es EPO hypersensitivity in polycythemic mutations were not elevated. Pediatr Blood Cancer © 2014 Wiley Periodicals, Inc.
    Pediatric Blood & Cancer 04/2014; · 2.35 Impact Factor
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    ABSTRACT: We postulated that the hypoxic response in sickle cell disease (SCD) contributes to altered gene expression and pulmonary hypertension, a complication associated with early mortality. To identify genes regulated by the hypoxic response and not other effects of chronic anemia, we compared expression variation in peripheral blood mononuclear cells from 13 SCD subjects with hemoglobin SS genotype and 15 Chuvash polycythemia subjects (VHL(R200W) homozygotes with constitutive up-regulation of hypoxia inducible factors in the absence of anemia or hypoxia). At 5% false discovery rate, 1040 genes exhibited >1.15 fold change in both conditions; 297 were up-regulated and 743 down-regulated including MAPK8 encoding a mitogen-activated protein kinase important for apoptosis, T-cell differentiation and inflammatory responses. Association mapping with a focus on local regulatory polymorphisms in 61 SCD patients identified expression quantitative trait loci (eQTL) for 103 of these hypoxia response genes. In a University of Illinois SCD cohort the A allele of a MAPK8 eQTL, rs10857560, was associated with pre-capillary pulmonary hypertension defined as mean pulmonary artery pressure ≥25 and pulmonary capillary wedge pressure ≤15 mm Hg at right heart catheterization (allele frequency=0.66; OR=13.8, P=0.00036, n=238). This association was confirmed in an independent Walk-PHaSST cohort (allele frequency=0.65; OR=11.3, P=0.0025, n=519). The homozygous AA genotype of rs10857560 was associated with decreased MAPK8 expression and present in all 14 identified pre-capillary pulmonary hypertension cases among the combined 757 patients. Our study demonstrates a prominent hypoxic transcription component in SCD and a MAPK8 eQTL associated with pre-capillary pulmonary hypertension.
    Circulation 02/2014; · 15.20 Impact Factor
  • Leukemia: official journal of the Leukemia Society of America, Leukemia Research Fund, U.K 01/2014; · 10.16 Impact Factor
  • Leukemia: official journal of the Leukemia Society of America, Leukemia Research Fund, U.K 01/2014; · 10.16 Impact Factor
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    ABSTRACT: High altitude exerts selective evolutionary pressure primarily due to its hypoxic environment, resulting in multiple adaptive responses. High hemoglobin–oxygen affinity is postulated to be one such adaptive change, which has been reported in Sherpas of the Himalayas. Tibetans have lived on the Qinghai–Tibetan plateau for thousands of years and have developed unique phenotypes, such as protection from polycythemia which has been linked to PDH2 mutation, resulting in the downregulation of the HIF pathway. In order to see if Tibetans also developed high hemoglobin–oxygen affinity as a part of their genetic adaptation, we conducted this study assessing hemoglobin–oxygen affinity and their fetal hemoglobin levels in Tibetan subjects from 3 different altitudes. We found normal hemoglobin–oxygen affinity in all subjects, fetal hemoglobin levels were normal in all except one and no hemoglobin variants in any of the subjects. We conclude that increased hemoglobin–oxygen affinity or increased fetal hemoglobin are not adaptive phenotypes of the Tibetan highlanders.
    Blood Cells Molecules and Diseases 01/2014; · 2.26 Impact Factor
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    ABSTRACT: Constitutive heterozygous GATA2 mutation is associated with deafness, lymphedema, mononuclear cytopenias, infection, myelodysplasia (MDS) and AML. Here we describe a cross-sectional analysis of 24 patients and 6 relatives with 14 different frameshift or substitution mutations of GATA2. A pattern of mononuclear cytopenia (DCML deficiency) with elevated Flt3 ligand (Flt3L) was observed in all 20 patients phenotyped, including patients with Emberger's syndrome, monoMAC, and MDS. Four unaffected relatives had a normal phenotype indicating that cellular deficiency may evolve over time or is incompletely penetrant, while 2 developed subclinical cytopenias or elevated Flt3L. Patients with GATA2 mutation maintained higher hemoglobin, neutrophils and platelets and were younger than controls with acquired MDS and wild-type GATA2. Frame-shift mutations were associated with earlier age of clinical presentation than substitution mutations. Elevated Flt3L, loss of bone marrow progenitors and clonal myelopoiesis were early signs of disease evolution. Clinical progression was associated with increasingly elevated Flt3L, depletion of transitional B cells, CD56(bright) NK cells and naïve T cells and accumulation of terminally differentiated NK and CD8(+) memory T cells. These studies provide a framework for clinical and laboratory monitoring of patients with GATA2 mutation and may inform therapeutic decision making.
    Blood 12/2013; · 9.78 Impact Factor
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    ABSTRACT: Overexpression of transcription factors RUNX1 and NF-E2 was reported in granulocytes of patients with polycythemia vera and other myeloproliferative neoplasms (MPN). Further, a transgenic mouse overexpressing the NF-E2 transgene was reported to be a model of MPN. We hypothesized that increased transcripts of RUNX1 and NF-E2 might characterize other polycythemic states with primary polycythemic features, i.e., those with exaggerated erythropoiesis due to augmented erythropoietin (EPO) sensitivity. We tested the expression of RUNX1 and NF-E2 in polycythemic patients of diverse phenotypes and molecular causes. We report that RUNX1 and NF-E2 overexpression is not specific for MPN; these transcripts were also significantly elevated in polycythemias with augmented hypoxia-inducible factor activity whose erythroid progenitors were hypersensitive to EPO. RUNX1 and NF-E2 overexpression was not detected in patients with EPO receptor (EPOR) gain-of-function, suggesting distinct mechanisms by which erythroid progenitors in polycythemias with defects of hypoxia sensing and EPOR mutations exert their EPO-hypersensitivity.
    Blood 12/2013; · 9.78 Impact Factor
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    ABSTRACT: We cared for a term male infant born to Burmese immigrants. At about 24 hours a total serum bilirubin (TSB) was 9.3 mg/dL, and phototherapy was begun. It was stopped 48 hours later, with a TSB of 10.9 mg/dL, and he was discharged from the hospital with an appointment for a repeat TSB check 48 hours later. A few hours before the appointment he became listless and apneic, and his parents took him to the emergency department of the regional children's hospital, where sepsis was suspected. The TSB was 41 mg/dL. He died 4 hours later, despite intensive care efforts, with opisthotonus and refractory hypotension. Blood drawn before the exchange transfusion had low glucose-6-phosphate dehydrogenase (G6PD) enzymatic activity, and sequencing of the G6PD gene revealed the G6PD Mahidol mutation (c.487G>A). Cultures and postmortem examination did not demonstrate an infectious process, but kernicterus was present. Acute kernicterus can mimic septic shock.
    PEDIATRICS 11/2013; · 4.47 Impact Factor
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    ABSTRACT: We cared for a neonate who had problematic hyperbilirubinemia born into a family where nine first-degree relatives had hereditary elliptocytosis (HE). As neonates, the nine relatives did not have any significant jaundice or anemia that was recognizable. Blood films on the proband suggested a diagnosis of pyropoikilocytosis. Analysis of the α-spectrin gene (SPTA1) in the proband revealed two previously reported low-frequency heterozygous polymorphisms of unknown clinical significance and the α(LELY) allele. In addition, a novel heterozygous mutation was identified in exon 2 of the β-spectrin gene SPTB. No mutations were identified in ANK1 (ankyrin-1), SLC4A1 (band 3), EPB41 (band 4.1), or EPB42 (band 4.2). © 2013 S. Karger AG, Basel.
    Neonatology 10/2013; 105(1):1-4. · 2.57 Impact Factor
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    ABSTRACT: Ruxolitinib, a Janus kinase 1 and 2 inhibitor, demonstrated improvements in spleen volume, symptoms, and survival over placebo and best available therapy in intermediate-2 or high-risk myelofibrosis patients with baseline platelet counts ≥100 ×109/L in phase III studies. The most common adverse events were dose-dependent anemia and thrombocytopenia, which were anticipated because thrombopoietin and erythropoietin signal through JAK2. These events were manageable, rarely leading to treatment discontinuation. Because approximately one-quarter of MF patients have platelet counts <100 ×109/L consequent to their disease, ruxolitinib was evaluated in this subset of patients using lower initial doses. Interim results of a phase II study of ruxolitinib in myelofibrosis patients with baseline platelet counts of 50-100 ×109/L are reported. Ruxolitinib was initiated at a dose of 5 mg twice daily (BID), and doses could be increased by 5 mg once daily every 4 weeks to 10 mg BID if platelet counts remained adequate. Additional dosage increases required evidence of suboptimal efficacy. Assessments included measurement of spleen volume by MRI, MF symptoms by MF Symptom Assessment Form v2.0 Total Symptom Score [TSS]), Patient Global Impression of Change (PGIC); EORTC QLQ-C30, and safety/tolerability. By week 24, 62% of patients achieved stable doses ≥ 10 mg BID. Median reductions in spleen volume and TSS were 24.2% and 43.8%, respectively. Thrombocytopenia necessitating dose reductions and dose interruptions occurred in 12 and 8 patients, respectively, and occurred mainly in patients with baseline platelet counts ≤75 ×109/L. Seven patients experienced platelet count increases ≥15 ×109/L. Mean hemoglobin levels remained stable over the treatment period. Two patients discontinued for adverse events: 1 for grade 4 retroperitoneal hemorrhage secondary to multiple and suspected pre-existing renal artery aneurysms and 1 for grade 4 thrombocytopenia. Results suggest that a low starting dose of ruxolitinib with escalation to 10 mg BID may be appropriate in myelofibrosis patients with low platelet counts.
    Journal of Hematology & Oncology 10/2013; 6(1):81. · 4.46 Impact Factor
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    ABSTRACT: Abstract β-Thalassemia (β-thal) is a public health problem in the Gaza Strip, Palestine, where about 320 patients are currently managed through blood transfusions and iron chelation. Within the restrictive environment of the Gaza Strip, no advanced molecular analysis [sequencing, real-time polymerase chain reaction (real-time PCR)] technology is currently available for developing a premarital screening protocol and providing couples at risk with prenatal diagnosis. Therefore, genetic identification of samples with indicators of β-thal is delayed for weeks before the samples can be sequenced outside the country. As nine causative mutations have been identified in the majority of β-thal cases in the Gaza Strip, a basic genetic screening strategy was designed to improve timeliness in mutation identification and reduce costs to the Palestinian health system. In the present study, we developed a reliable method for the detection of nine Mediterranean β-thal mutations common to the Palestinian population using a panel of restriction enzyme digests. This strategy utilizes standard instrumentation (thermocycler and agarose gel electrophoresis) that would be available in any basic molecular genetics or biochemical laboratory and provides a reliable method of genetic screening and counseling for patients at risk for β-thal.
    Hemoglobin 10/2013; · 0.89 Impact Factor

Publication Stats

7k Citations
2,391.91 Total Impact Points

Institutions

  • 2006–2014
    • University of Utah
      • • Division of Hematology
      • • School of Medicine
      • • Division of Pediatric Hematology and Oncology
      Salt Lake City, Utah, United States
    • Ospedali Riuniti di Bergamo
      • Department of Hematology
      Bergamo, Lombardy, Italy
  • 2013
    • National Institutes of Health
      Maryland, United States
  • 2005–2013
    • University of Illinois at Chicago
      • • Comprehensive Sickle Cell Center
      • • Section of Hematology and Oncology
      Chicago, IL, United States
    • Universität Basel
      Bâle, Basel-City, Switzerland
  • 2012
    • Children's National Medical Center
      • Division of Cardiology
      Washington, D. C., DC, United States
    • Al-Azhar University - Gaza
      Ghazzah, Gaza Strip, Palestinian Territory
  • 2011
    • The Children's Hospital of Philadelphia
      • Center for Applied Genomics
      Philadelphia, PA, United States
  • 2005–2011
    • Howard University
      • • Department of Medicine
      • • Center for Sickle Cell Disease
      Washington, WV, United States
  • 2010
    • Johns Hopkins University
      Baltimore, Maryland, United States
  • 2009–2010
    • Institute of Hematology and Blood Transfusion
      Praha, Praha, Czech Republic
    • Arup
      Londinium, England, United Kingdom
  • 2008–2009
    • University of Texas MD Anderson Cancer Center
      • Department of Leukemia
      Houston, TX, United States
    • Russian Children's Clinical Hospital
      Moskva, Moscow, Russia
  • 1978–2009
    • University of Alabama at Birmingham
      • • Department of Medicine
      • • Division of Nephrology
      • • Division of Hematology / Oncology
      • • Department of Ophthalmology
      • • Division of Laboratory Medicine
      Birmingham, AL, United States
  • 2007
    • Stanford University
      • Department of Medicine
      Stanford, CA, United States
    • Charles University in Prague
      • Institute of Pathological Physiology (Pilsen)
      Praha, Praha, Czech Republic
  • 2001–2007
    • Baylor College of Medicine
      • • Department of Medicine
      • • Section of Hematology/Oncology
      Houston, Texas, United States
  • 2003
    • Texas Children's Cancer and Hematology Centers
      Houston, Texas, United States
    • Universitätsspital Basel
      Bâle, Basel-City, Switzerland
  • 1997
    • Chuvash State University
      Cheboksar’, Chuvashia, Russia
  • 1988–1997
    • St. Elizabeth's Medical Center
      Boston, Massachusetts, United States
    • City of Hope National Medical Center
      Duarte, California, United States
    • The University of Calgary
      Calgary, Alberta, Canada
  • 1995
    • Brigham and Women's Hospital
      • Department of Medicine
      Boston, MA, United States
  • 1994
    • Cooper Hospital
      Birmingham, Alabama, United States
  • 1985
    • University of Alabama
      Tuscaloosa, Alabama, United States