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E Balogh

Publications and source records attributed to E Balogh.

At least 19 recordsLinked to original sources
PubMed2006

Robot-assisted needle placement in open-MRI: system architecture, integration and validation.

This work describes an integrated system for planning and performing percutaneous procedures-such as prostate biopsy-with robotic assistance under MRI-guidance. The physician interacts with a planning interface in order to specify the set of desired needle trajectories, based on anatomical structures and lesions observed in the patient's MR images. All image-space coordinates are automatically computed, and used to position a needle guide by means of an MRI-compatible robotic manipulator, thus avoiding the limitations of the traditional fixed needle template. Direct control of real-time imaging aids visualization of the needle as it is manually inserted through the guide. Results from in-scanner phantom experiments are provided.

Biopsy, Needle↗
PubMed2001

[Genetics of renal tumors].

The quintessence of malignant transformation is the genetic alteration of the tumor progenitor cell, i.e. somatic mutation. The genetic change appearing at chromosome and/or gene level results in the disturbance of the balance of cell proliferation and differentiation. In solid tumors, including renal tumors, the basic genetic mechanism proved to be the loss of function of a specific gene pair caused by loss of the particular chromosome or chromosomal region (monosomy, deletion) or by mutation of the gene. In the well studied Wilms' tumor-aniridia-syndrome the distal part of 11p13 region is deleted. The responsible gene is the WT-1 tumor suppressor gene, a Zn finger type transcription factor. In the majority of cases the mutation of this gene leads to the tumor formation without cytogenetically detectable deletion. For manifestation of the tumor the functional damage of both alleles is needed. In other histological types of renal tumors a great variation of chromosome losses and gains, as well as translocations can be identified. In Wilms tumor of embryonic origin, tumor suppressor genes located on the short arms of chromosomes 16 and 17 play a role in the pathogenesis. Besides, the significance of abnormal genomic imprinting of IGF2 and H19 genes located on 11p15 has also been confirmed. If a part of the embryonic cells do not regress, they may develop to papillary carcinoma together with the appearance of trisomies of chromosomes 7 and 17 and loss of Y. In the transformation process from papillary adenoma to carcinoma, duplication of several chromosomal regions is involved (3q+, +8, +12, +16, +20). The origin of renal carcinoma developing from normal nephron cells is associated with a deletion of 3p and 5q+, while during the progression of the disease further variable chromosome losses appear (6q-, 8p-, 14q-, -9). Tumor-specific cytogenetic and molecular genetic changes confirm the morphological classification of epithelial renal tumors pointing at the relation of the various entities or their independence. Based on cytogenetic alterations, a sequential predictive model of renal tumors can be developed. Individual types, together with joining and sequential appearance of aberrations are in line with the multistep mechanism of carcinogenesis. At the same time, the specific cytogenetic and molecular genetic changes confirm the diagnosis, provide further information about the histological type and progression of the disease. In hereditary cases, the members of the family at risk can be identified by recognizing the possibly associating clinical symptoms and/or by detecting the constitutional mutation of the gene using molecular genetic methods. Consequently, the genetic study of renal tumors plays important role not only in diagnosis and choosing adequate therapy but also in prevention of the disease.

Adenoma↗
PubMed2001

Effect of myelopoietic and pleiotropic cytokines on colony formation by blast cells of children with acute lymphoblastic leukemia.

The aim of this study was to see whether pleiotropic or myeloid hematopoietic growth factors, which do not stimulate normal lymphoid cells, can induce proliferation of blast cells of the acute lymphoid leukemia (ALL) of childhood. Bone marrow cells of 13 children with untreated ALL (nine common ALL, two myeloid antigen positive ALL and two early T-cell ALL) formed colonies of leukemic blast cells in primary methylcellulose cultures. Spontaneous growth was observed in three of 13 cases, whereas phytohemagglutinin-stimulated leukocyte conditioned medium (PHA-LCM), a conventional source of various natural human cytokines, induced colony formation in ten of 13 cases. A similar rate of responsiveness was seen with recombinant human granulocyte colony-stimulating factor (G-CSF), granulocyte-macrophage colony-stimulating factor (GM-CSF) and stem cell factor (SCF); a combination of these three cytokines induced colony formation in all cases studied. The effect of these growth factors on colony formation seemed to be dose-dependent in some cases. Of the stimuli studied, GM-CSF induced the smallest number of colonies, whereas the effects of G-CSF, SCF and PHA-LCM were similar in this respect. Combination of cytokines proved to be even more efficient in inducing clonal proliferation of leukemic lymphoblasts. In double combinations, G-CSF and GM-CSF as well as G-CSF and SCF were able to potentiate each other's effects. Triple combination of these cytokines mediated the most potent growth stimulus. Our results demonstrate that myeloid and pleiotropic cytokines are able to stimulate clonal proliferation of pediatric leukemic lymphoblasts. This may present a potential hazard to children with ALL while on adjuvant therapy with hematopoietic growth factors. In vitro colony assays performed prior to or in parallel with the administration of hematopoietic growth factors to ALL patients may help to forecast their possible effects on leukemic cells in vivo.

Adolescent↗
PubMed2000

[Fluorescence in situ hybridization in the diagnosis and follow-up of chronic myelogenous leukemia].

Chronic myelogenous leukaemia is a clonal myeloproliferative stem cell disease. Its cytogenetical hallmark is the Philadelphia chromosome (Ph) or the BCR/ABL fusion gene. Their identification is important both in the diagnosis and the follow-up of the disease. In our department we have investigated the BCR/ABL gene arrangement in 21 patients with fluorescence in situ hybridization. The aim of the analysis in freshly suspected patients without any previous therapy was to confirm diagnosis and mapping the ratio of Philadelphia positive cells. In contrast to the 95-100% Ph-positivity of mononuclear cells by classical cytogenetical examinations we found BCR/ABL gene arrangement only in various but always lower proportions. Therefore the latter examination gives a better representation of residual normal hemopoesis. Out of 9 patients who had received interferon treatment for at least 6 months, 4 gave a major, 4 a minor cytogenetical answer and in 1 case there was no cytogenetical response. Seven patients reached a complete and 2 a partial hematological remission. Among 5 other patients receiving interferon treatment, in 2 cases with double Ph-positivity we found a rapid progression. The data of 3 patients had to be excluded from the evaluation due to the so far short following time.

Diagnosis, Differential↗
PubMed2000

Prevalence of iodine deficiency and goitre during pregnancy in east Hungary.

OBJECTIVE: To assess the iodine nutritional status and the prevalence of goitre during pregnancy in a region of Hungary that appeared to be iodine sufficient in previous studies. DESIGN: A cross-sectional voluntary screening study was organized in which 313 pregnant women participated. METHODS: Urine iodine concentration and the volume of the thyroid gland were measured in every woman. In the presence of low urinary iodine concentrations, goitre, or both, thyroid function tests were performed. RESULTS: Iodine deficiency was found in 57.1% of the pregnant women, and was severe in 15.6%. The volume of the thyroid gland was enlarged in 19.2% of individuals. Nodular goitre was found in 17 women (5.4%). The frequency of goitre and the mean thyroid volume were increased in the group of iodine-deficient women. In the 89 cases of iodine deficiency or goitre, thyrotrophin concentrations were in the normal range; however, the free triiodothyronine:free throxine ratio was increased in 97% of them, indicating that the thyroid gland was in a stimulated state in these individuals. CONCLUSIONS: Iodine deficiency with high prevalence of goitre was recognized among pregnant women in an area that previously appeared to be iodine sufficient. An unexpected mild iodine deficiency was also noted in the non-pregnant control group. Reassessment and continuous monitoring of iodine nutritional status is warranted even in populations that are apparently considered to be 'at no risk' of iodine deficiency, especially in pregnant women. Regular administration of iodine, starting at preconception or in early pregnancy and continuing during the period of nursing, is recommended in these regions.

Adult↗
PubMed2000

Alterations of P53 and RB genes and the evolution of the accelerated phase of chronic myeloid leukemia.

Using the single-strand conformation polymorphism and heteroduplex analyses, the P53 and RB genes were analyzed in cell samples from twenty-eight patients with chronic myeloid leukemia (CML) both at diagnosis and at the onset of accelerated phase (AP) of the disease. No alterations of the P53 or RB genes were found in any of the chronic phase (CP) samples. Structural abnormalities of the P53 gene were observed in ten of twenty-eight AP samples within exons 4, 5, 7 and 9. Of the ten cases of AP disease with altered P53 genes, five patients also suffered from the deletion of the other allele. Alterations of the RB gene could be detected in six AP samples, and aberrant band patterns were found in the analysis of exons 2, 3, 4, 6, 7, 13, 14, 17, 21 and 26. Among the six AP samples with structural abnormalities of the RB gene, two showed the loss of the other allele. It is of note that alterations of both P53 and RB genes were observed in two AP samples. Our data strongly suggest that abnormalities of the P53 and RB genes and acceleration of CML are linked events in some cases of AP.

Adult↗
PubMed1999

Biclonal chromosomal aberrations in a child with myelodysplastic syndrome.

Hematological malignancies and premalignant diseases are generally of monoclonal origin. The prognostic and therapeutic significance of finding two genetically independent clones remains to be determined. We followed a case of childhood myelodysplastic syndrome showing biclonal chromosomal abnormalities (+8, -7) by conventional cytogenetic examination and double target fluorescence in situ hybridization (FISH). A 7-year-old girl presented with Plaut-Vincent angina and leukopenia. The cytogenetic aberration of +8 was the first sign to suggest MDS. Serial bone marrow controls, prompted by a progressive clinical course detected myelodysplastic changes and a new clonal aberration (-7). The presence of -7 and +8 in two independent clones was verified by double-target FISH. While at diagnosis and during cytokine treatment more cells showed +8, after successful all-trans retinoic acid (ATRA) therapy, the clone with -7 predominated. Following allogeneic bone marrow transplantation the patient displayed donor-derived hematopoesis. Our data stress the significance of cytogenetic and FISH examinations in detecting specific genetic abnormalities and progressive clonal changes as an indicator and guideline for therapy. Different cell clones characterized by different genetic changes might be associated with different biologic features reflected in their response to treatment.

Angina Pectoris↗
PubMed1999

Examination of the polymorphism of piroxicam in connection with the preparation of a new "soft-patch" type pharmaceutical dosage form.

The influence of different solvents (propylene glycol, glycerol, ethanol), as well as different technological procedures (melting, rapid and slow cooling), on the formation of polymorphous piroxicam modifications was examined in the course of the elaboration of a "soft-patch" type of semisolid pharmaceutical dosage form. The thermodynamical behavior, some physicochemical properties (such as melting point, dissolution rate), and infrared (IR) spectrum of the formed (needle and cubic) crystal modifications were studied, and the possibilities of their formation and their avoidance were examined.

Administration, Cutaneous↗
PubMed1998

Fluorescence in situ hybridization reveals trisomy 2q by insertion into 9p in hepatoblastoma.

Cytogenetics and fluorescence in situ hybridization (FISH) of a hepatoblastoma are presented. The results of standard chromosome analysis were as follows: 47,XY,+2,add(4)(q35),-9,+20[10]. FISH with the use of whole-chromosome paints revealed partial trisomy of the long arm of chromosome 2 by insertion into chromosome 9. Comparison of the G-banded metaphases with metaphase FISH led to a reinterpretation of the karyotype as: 47,XY,add(4)(q35),der(9)ins(9;2)(p22;q?21q?25),+20. This case supports previous observations that the critical region of trisomy 2 lies between 2q21 and 2qter and shows how partial trisomy 2q may evade detection in G-banded metaphases.

Child, Preschool↗
PubMed1998

Changes in oncogene expression implicated in evolution of chronic granulocytic leukemia from its chronic phase to acceleration.

Expression of nine oncogenes was investigated in cell samples from fifteen patients with Philadelphia chromosome (Ph)-positive chronic granulocytic leukemia (CGL) both at diagnosis and at the onset of accelerated phase (AP) of the disease. The bcr-abl fusion gene, the H-ras gene and the c-myb gene were universally expressed. In comparison with the chronic phase (CP) of the disease, an increase in the levels of bcr-abl-, c-myb- and H-ras-related transcripts was found in three, two and three AP samples, respectively. Elevation of the bcr-abl-related message was associated with duplication of the Ph chromosome and amplification of the bcr-abl fusion gene in one AP sample. No CP samples were positive for c-myc or c-sis expression. On the contrary, c-myc and c-sis were expressed in three and four AP samples, respectively. The presence of c-myc-related transcript was associated with trisomy 8 with or without amplification of the c-myc oncogene in leukemia cells of two patients with CGL in AP. No changes of oncogene expression were found in four AP samples. However, we observed deletions of chromosome 13 and 17 or i(17q) in three of them, suggesting that tumor suppressor gene alterations may also be responsible for the development of AP of CGL. Our data indicate that heterogeneous alterations in oncogenes and tumor suppressor genes accompany the evolution of CGL-CP to the AP of the disease.

Acute-Phase Reaction↗
PubMed1997

[2q21-qter trisomy in hepatoblastoma].

Cytogenetic findings and fluorescens in situ hybridization results of a hepatoblastoma of a boy of two and half years of age are presented. Cytogenetic analysis and fluorescens in situ hybridization technique were performed using tumor tissue obtained by biopsy. The direct culture was harvested after 16 hour colcemid treatment. The results of G-banding were as follows: 47,XY,add(4) (q26),-9,+20. There were considerable variation in the degree of condensation and hence in the number of visible G-bands both between metaphases and between homologous chromosomes in the same metaphases. Fluorescens in situ hybridisation were carried out by whole chromosome painting probes: 2,3,4, and 20. The karyotype of the malignant cells was adjusted accordingly: 47,XY,der(4)(q35),dir ins(9;2)(p22;q?21q?25),+20. The results confirm the most common primary chromosome abnormalities in hepatoblastoma are the following: trisomy 2, trisomy 20 and 4q structural rearrangement. Fluorescens in situ hybridization confirms the importance of trisomy 2q21-qter in hepatoblastoma. Authors recommend the use of fluorescens in situ hybridization to correct any tumor karyotype with difficult or ambiguous chromosome morphology.

Biopsy↗
PubMed1997

Diagnostic and prognostic significance of chromosome abnormalities in childhood acute lymphoblastic leukemia.

Current intensive chemotherapies cure about 70% of the children with ALL. On the other hand a significant number of the children are not cured despite intensive treatment. At the same time some highly curable patients are treated too intensively and suffer from unnecessary side effects of the chemo- and radiotherapy applied. In order to further improve the therapeutic results in this disease, we have to distinguish between the cases with a better and a worse prognosis. The initial karyotype (both numerical and structural chromosome abnormalities) proved to be one of the most reliable prognostic parameters, leading to the suggestion of developing genotype-specific therapies. Although the prognosis in patients with pseudodiploid karyotype is usually unfavorable, a significantly better prognosis can be observed in those with more than 50 chromosomes. Because the latter patients can achieve remission on a metabolite-based therapy, the toxic effects of more aggressive chemotherapy with anthracyclines and genotoxic agents can be avoided; thus, the reliable and accurate identification of patients with > 50 chromosomes is of particular importance. For this purpose three methods: chromosome analysis, DNA flow cytometry, and fluorescence in situ hybridization can be used. In 1993 it was decided to develop a comprehensive nationwide project in order to perform the initial genetic analysis of all ALL children diagnosed in the hematological/oncological centers of Hungary. Here the data obtained on 187 ALL patients diagnosed in the period from 1993 to 1995 are presented. In about 75% of patients (in 140 of 187) chromosome analysis was performed, in 78 cases (55.7%) successfully. The proportion of patients with abnormal karyotype was 36 of 78 (46.1%), and hyperdiploidy with more than 50 chromosomes was detected in 13 of 78 (16.6%) children. The lower ratio of hyperdiploid cases in our patients as compared to the data in the literature may be due to technical difficulties and the small number of patients studied, but it may reflect real geographic characteristics. Using flow cytometry, seven of 31 patients investigated (22.5%) proved to be hyperdiploid with a DNA index above 1.16. A higher ratio of hyperdiploid patients in this study calls attention to the significance of simultaneous application of the two methods. Taken together, 16 of 80 (20.0%) successfully studied patients proved to be hyperdiploid (> 50 chromosomes and/or DNA index above 1.16). The pattern of chromosome involvement in our study determined by chromosome analysis and/or FISH technique proved also to be different from the data of large international series. In addition to trisomies of chromosomes 4, 6, 10, 14, 17, 18, 21, and X, which are known to be the most frequently involved chromosomes, trisomies of chromosomes 3, 8, 11, and 13 were also observed with a high frequency. Comparison of survival curves of various cytogenetic subgroups showed a significant difference between diploid-pseudodiploid and diploid-hyperdiploid A (with 47-50 chromosomes) subgroups. No favorable prognosis of hyperdiploid patients (> 50 chromosomes) could be proved. Because of the small number of patients studied, prognostic differences of cytogenetic subgroups need further confirmation. The clinical and genetic differences observed, however, call attention to the necessity for further genetic studies of ALL patients in Hungary, because these differences may reflect real geographic characteristics and may be related to different environmental mutagen/carcinogen effects of the given geographic area. It is essential to determine whether or not these differences really exist and if they do to reveal the causes leading to these differences. In our view this is one of the routes by which the therapeutic results in childhood ALL can be further improved simultaneously with the avoidance of early and late toxicity of chemotherapy.

Child↗
PubMed1997

Idiopathic scoliosis--new surgical methods or search for the reasons.

Idiopathic scoliosis (IS) is a deformity of the spine whose aetiology is unknown despite of extensive clinical and basic research work. The significance of this disease lies in the consequences of a spine deformity (deformation of the chest, compromise of the cardio-pulmonar function, compression of the neurological elements, severe somatic and psychological sufferings). According to statistical data, one third of the idiopathic scoliotic cases progress and need surgical intervention. Cotrel and Dubousset introduced the three dimensional correction surgical method for the treatment of spine deformities in 1983 (CD method). The authors report on the application of the CD method for the treatment of IS from 1991 to date. After the operation of 36 patients they give an account of good results and report on the modifications of the surgical technique on the basis of their experiences. Aware of the late consequences of the surgical treatment of IS the authors started with the investigation of the aetiology of the disease in order to introduce a causal treatment. As for the aetiological background of IS, data on the role of heritable factors were relevant only. They gave a hint to start with studies aimed at the investigation of genetic determinants of the syndrome. I aberration of chromosome #10 [karyotype: inv(10)(p11q26)]. In one of the cases there was a multiple familial occurrence of the syndrome coupled with the same anomaly of the karyotype. The probands' father and grandfather all had the same pattern of scoliotic deformity and the same aberrant karyotype of chromosome #10 was found both in the proband and his father. Preparation of genomial DNA from peripheral blood of the patients was started. Fragment length polymorphism (RFLP) examination with PCR technique using oligonucleotide primers specific for chromosome #10 and for regulatory genes of left-right body assymetry is underway.

Chromosome Aberrations↗
PubMed1996

Special features of childhood and juvenile thyroid carcinomas.

A retrospective analysis was conducted on 36 patients who underwent surgery for childhood or juvenile thyroid cancers and who were regularly followed up during the course of 30 years. The biological properties and late prognosis of these patients were assessed, and the clinical and morphological characteristics of the tumors were examined. The distribution of the DNA content in the tumor cells was compared with that in adult tumor cells, and the results of cytogenetic tests performed on mothers operated on for thyroid tumors and their children are also discussed.

Adenocarcinoma, Follicular↗
PubMed1992

Autocrine regulation of murine B lymphocyte growth by an IgM antibody.

Culture supernatants of LPS-stimulated murine B lymphocytes are able to inhibit the growth of freshly isolated splenic B cells via an IgM antibody. The binding specificity of this IgM is not yet defined, but appears to be a B lymphocyte surface structure distinct from membrane immunoglobulin, MHC class II antigen, transferrin and Fc gamma receptors, and B220. The regulatory autoantibody allows the normal progression of early, but not late steps in the cycle of polyclonally-stimulated B lymphocytes and does not affect the increased antigen-presenting capacity of activated B cells. Therefore, this autoregulatory cycle is apparently ubiquitous and may be a major component of B lymphocyte homeostasis under physiological, as well as pathological conditions. Moreover, these findings bring into focus a possible regulating role of B lymphocytes in the humoral immune response.

Animals↗
PubMed1991

Burkitt's lymphoma with 3;14 and 2;8 translocations simultaneously.

Burkitt's lymphoma of a ten-year-old boy with specific 8;14 and variant 2;8 translocations is reported. The post mortem diagnosis of Burkitt's lymphoma was based on histological picture and the cytogenetic findings of the tumor biopsy. The child died four days after clinical admission. Because of the rapid progression of the disease immunological and serological investigations could not be performed. Therefore several questions remained unclarified. It is supposed that in the patient's B-lymphocytes multiple transformation events occurred leading to the development of the polyclonal lymphoma, similarly to that described in transplant-associated lymphoproliferations.

Burkitt Lymphoma↗