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Our PhD researches include brownfield revitalization,1 the application of the methods of interim utilizations on greeneries,2 and the formation background and potential of community gardens.3 We compared our systems of criteria in hope of extensive research conclusions. In order to trace the urban development possibilities in Budapest, we analysed brownfield revitalizations where the interim utilizations included allotment gardens, too. We concluded that such developments are likely to create environmental and social added value. Early results of the valorization process are important by themselves, but the perpetuation of interim land utilization holds even greater values.

Somatic insertions/deletions in the calreticulin gene have recently been discovered to be causative alterations in myeloproliferative neoplasms. A combination of qualitative and quantitative allele-specific polymerase chain reaction, fragment-sizing, high resolution melting and Sanger-sequencing was applied for the detection of three driver mutations (in Janus kinase 2, calreticulin and myeloproliferative leukemia virus oncogene genes) in 289 cases of essential thrombocythemia and 99 cases of primary myelofibrosis. In essential thrombocythemia, 154 (53%) Janus kinase 2 V617F, 96 (33%) calreticulin, 9 (3%) myeloproliferative leukemia virus oncogene gene mutation-positive and 30 triple-negative (11%) cases were identified, while in primary myelofibrosis 56 (57%) Janus kinase 2 V617F, 25 (25%) calreticulin, 7 (7%) myeloproliferative leukemia virus oncogene gene mutation-positive and 11 (11%) triple-negative cases were identified. Patients positive for the calreticulin mutation were younger and had higher platelet counts compared to Janus kinase 2 mutation-positive counterparts. Calreticulin mutation-positive patients with essential thrombocythemia showed a lower risk of developing venous thrombosis, but no difference in overall survival. Calreticulin mutation-positive patients with primary myelofibrosis had a better overall survival compared to that of the Janus kinase 2 mutation-positive (P=0.04) or triple-negative cases (P=0.01). Type 2 calreticulin mutation occurred more frequently in essential thrombocythemia than in primary myelofibrosis (P=0.049). In essential thrombocythemia, the calreticulin mutational load was higher than the Janus kinase 2 mutational load (P

Sipos Andrea. Sportsmedical follow up of the Hungarian Sydney 2000 triathlon team. In: Les Cahiers de l'INSEP, n°24, 1999. 2e Congrès international de triathlon de l’INSEP – 2nd INSEP international triathlon Congress pp. 310-313.

Sipos Andrea. New Supporting Systems for Junior Athletes in Hungary. In: Les Cahiers de l'INSEP, n°24, 1999. 2e Congrès international de triathlon de l’INSEP – 2nd INSEP international triathlon Congress pp. 69-72.

Sipos Andrea. Suivi médico-sportif de l'équipe olympique hongroise de triathlon. In: Les Cahiers de l'INSEP, n°24, 1999. 2e Congrès international de triathlon de l’INSEP – 2nd INSEP international triathlon Congress pp. 306-309.

Background Prognostic risk stratification according to acquired or inherited genetic alterations has received increasing attention in acute myeloid leukemia in recent years. A germline Janus kinase 2 haplotype designated as the 46/1 haplotype has been reported to be associated with an inherited predisposition to myeloproliferative neoplasms, and also to acute myeloid leukemia with normal karyotype. The aim of this study was to assess the prognostic impact of the 46/1 haplotype on disease characteristics and treatment outcome in acute myeloid leukemia. Design and Methods Janus kinase 2 rs12343867 single nucleotide polymorphism tagging the 46/1 haplotype was genotyped by LightCycler technology applying melting curve analysis with the hybridization probe detection format in 176 patients with acute myeloid leukemia under 60 years diagnosed consecutively and treated with curative intent. Results The morphological subtype of acute myeloid leukemia with maturation was less frequent among 46/1 carriers than among non-carriers (5.6% versus 17.2%, P =0.018, cytogenetically normal subgroup: 4.3% versus 20.6%, P =0.031), while the morphological distribution shifted towards the myelomonocytoid form in 46/1 haplotype carriers (28.1% versus 14.9%, P =0.044, cytogenetically normal subgroup: 34.0% versus 11.8%, P =0.035). In cytogenetically normal cases of acute myeloid leukemia, the 46/1 carriers had a considerably lower remission rate (78.7% versus 94.1%, P =0.064) and more deaths in remission or in aplasia caused by infections (46.8% versus 23.5%, P =0.038), resulting in the 46/1 carriers having shorter disease-free survival and overall survival compared to the 46/1 non-carriers. In multivariate analysis, the 46/1 haplotype was an independent adverse prognostic factor for disease-free survival ( P =0.024) and overall survival ( P =0.024) in patients with a normal karyotype. Janus kinase 2 46/1 haplotype had no impact on prognosis in the subgroup with abnormal karyotype. Conclusions Janus kinase 2 46/1 haplotype influences morphological distribution, increasing the predisposition towards an acute myelomonocytoid form. It may be a novel, independent unfavorable risk factor in acute myeloid leukemia with a normal karyotype.

Somatic gain-of-function mutation of the Janus kinase (JAK2) gene (NM_004972.2: c.1849G>T transversion resulting in V617F) has been identified in BCR–ABL-negative chronic myeloproliferative neoplasms (MPNs) (in >95% of polycythaemia vera (PV), and in 40–60% of essential thrombocythaemia (ET) and primary myelofibrosis (PMF)). The inherited genetic background of an individual patient has been long predicted to influence disease susceptibility and phenotype in MPN. Recent studies have demonstrated that the presence of JAK2 V617F is associated with an inherited JAK2 haplotype designated as ‘46/1’ haplotype.1, 2, 3 Carriers of the 46/1 haplotype have higher risk of acquiring JAK2 V617F mutation, but the role of 46/1 haplotype as a predisposition factor for V617F-negative MPN is still remained controversial. Only a few studies4, 5 investigated the potential role of the 46/1 haplotype as a MPN phenotype modifier in the context of the frequency of complications affecting life expectancy, such as thrombosis and myelofibrotic or leukaemic transformation. To extend these observations, the aims of our study were the following: (a) to examine and confirm associations of MPN and the presence of the JAK2 46/1 haplotype in Hungarian V617F-positive and -negative MPN patients; (b) to examine associations of the 46/1 haplotype with distinct clinical characteristics of MPN, (c) to test the haplotype frequency among JAK2 V617F-negative acute myeloid leukemia (AML) patients.

Sipos Andrea. Les nouveaux systèmes d'aide pour les triathlètes juniors en Hongrie. In: Les Cahiers de l'INSEP, n°24, 1999. 2e Congrès international de triathlon de l’INSEP – 2nd INSEP international triathlon Congress pp. 64-68.

Common HFE gene point mutations (C282Y, H63D and S65C) are responsible for hemochromatosis type 1 in homozygous or compound heterozygous states. Although HFE-related hemochromatosis is inherited in a recessive manner, heterozygous carriers were shown to have higher iron parameters (serum iron and ferritin levels, transferrin saturation) without progressive iron overload. Heterozygous HFE carriership has been implicated as a genetic modifier of several diseases, where iron homeostasis play an important role in disease susceptibility or disease progression (porphyria cutanea tarda, myelodyslasia). We investigated 336 unrelated patients with chronic myeloproliferative disease (CMPD) [176 patients with polycythemia vera (PV), 131 patients with essential thrombocythemia (ET) and 29 patients with chronic idiopathic myelofibrosis (CIMF)] and 171 first time blood donors as controls for allele frequencies (AFs) of HFE mutations by Light Cycler allele discrimination method. The presence of the acquired JAK2 V617F mutation in CMPD was investigated by allele specific PCR. Laboratory (hemoglobin, white blood cell and platelet count) and clinical features (sex, age at diagnosis, splenomegaly, presence of thrombotic, myelofibrotic or leukemic transformation) were recorded in the patient group. Compared to controls (4.7 +/− 2.3%), decreased HFE C282Y AF was found in patient group (1.8 +/− 1.0%; p=0.02; OR=0.38 [0.17–0.85]). Decreased HFE C282Y AFs were detected in all patient subgroups according to diagnosis (PV, ET, CIMF) and according to JAK2 V617F mutational status, but the difference remained significant only in the patient group with PV or with JAK2 V617F positive CMPD (PV:1.7 +/− 1.4%; p=0.04; JAK2 V617F positive patients: 1.6+/− 1.1%). H63D and S65C mutational status did not differ significantly between control (12.0+/−3.5% and 1.3+/−1.8%) and patient groups (13.1+/−2.6% and 0.5+/−0.5%). JAK2 V617F frequency was 86.9% (153/176) in PV, 60.3% (79/131) in ET, and 72.4% (21/29) in CIMF. We found significantly elevated hemoglobin levels and WBC values (measured at the time of diagnosis) in the V617F-positive PV (and ET patient groups compared to V617F-negative patients. The incidence of vascular complications (arterial and venous thrombosis or bleeding) was higher in JAK2 V617F CMPD. The age of CMPD onset and the rate of different complications were not altered by HFE mutational status. Our data confirm earlier observations that JAK2 V617F-positive ET shares clinical features (elevated hemoglobin) with PV. We found that HFE C282Y mutation may be associated with a protective role against CMPD (also CMPD associated with JAK2 positivity). Chronic iron deficiency or latent anemia may trigger disease susceptibility for CMPD, and HFE C282Y positivity can play a protective role against chronic iron deficiency.