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1.

001-es BibID:BIBFORM016513
Első szerző:Appenzeller, Silke
Cím:Autosomal-Dominant Striatal Degeneration Is Caused by a Mutation in the Phosphodiesterase 8B Gene / Silke Appenzeller, Anja Schirmacher, Hartmut Halfter, Sebastian Bäumer, Manuela Pendziwiat, Vincent Timmerman, Peter De Jonghe, Klára Fekete, Florian Stögbauer, Peter Lüdemann, Margret Hund, Elgar Susanne Quabius, E. Bernd Ringelstein, Gregor Kuhlenbäumer
Dátum:2010
Megjegyzések:Autosomal-dominant striatal degeneration (ADSD) is an autosomal-dominant movement disorder affecting the striatal part of the basalganglia. ADSD is characterized by bradykinesia, dysarthria, and muscle rigidity. These symptoms resemble idiopathic Parkinson disease,but tremor is not present. Using genetic linkage analysis, we have mapped the causative genetic defect to a 3.25 megabase candidateregion on chromosome 5q13.3-q14.1. A maximum LOD score of 4.1 (Q ? 0) was obtained at marker D5S1962. Here we show thatADSD is caused by a complex frameshift mutation (c.94G>Cc.95delT) in the phosphodiesterase 8B (PDE8B) gene, which resultsin a loss of enzymatic phosphodiesterase activity. We found that PDE8B is highly expressed in the brain, especially in the putamen,which is affected by ADSD. PDE8B degrades cyclic AMP, a second messenger implied in dopamine signaling. Dopamine is one ofthe main neurotransmitters involved in movement control and is deficient in Parkinson disease. We believe that the functionalanalysis of PDE8B will help to further elucidate the pathomechanism of ADSD as well as contribute to a better understanding of movementdisorders.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Acute Stroke
Organized Stroke Care
Stroke Care
Thrombolysis
Door-toneedle
Megjelenés:The American Journal of Human Genetics. - 86 : 1 (2010), p. 83-87. -
További szerzők:Schirmacher, Anja Halfter, Hartmut Bäumer, Sebastian Pendziwiat, Manuela Timmerman, Vincent De Jonghe, Peter Fekete Klára (1978-) (neurológus) Stögbauer, Florian Lüdemann, Peter Hund, Margret Quabius, Elgar Susanne Ringelstein, E. Bernd Kuhlenbäumer, Gregor
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2.

001-es BibID:BIBFORM091893
Első szerző:Bessenyei Beáta (molekuláris biológus)
Cím:Genetic investigation of the LIS1, DCX and TUBA1A genes in patients with lissencephaly / B. Bessenyei, A. Mokanszki, O. Nagy, K. Szakszon, A. Zimmermann, M. Zombor, E. Horvath, A. Ujfalusi, I. Balogh, L. Sztriha
Dátum:2019
Tárgyszavak:Orvostudományok Klinikai orvostudományok idézhető absztrakt
folyóiratcikk
Megjelenés:European Journal of Human Genetics. - 27 (2019), p. 286. -
További szerzők:Mokánszki Attila (1983-) (molekuláris biológus Ph.D hallgató) Nagy Orsolya (1990-) (PhD hallgató) Szakszon Katalin (1977-) (csecsemő- és gyermekgyógyász, klinikai genetikus) Zimmermann Alíz Zombor Melinda Horváth E. Ujfalusi Anikó (1968-) (gyermekorvos, laboratóriumi szakorvos) Balogh István (1972-) (molekuláris biológus, genetikus) Sztriha László
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3.

001-es BibID:BIBFORM119059
035-os BibID:(WoS)001147414902541
Első szerző:Csók Ádám (biológus)
Cím:Assessing the potential of miRNA biomarkers for the differential diagnosis of Wilms' tumor and diffuse hyperplastic perilobar nephroblastomatosis / Á. Csók, T. Micsik, Z. Magyar, T. Tornóczky, L. Kuthi, Y. Nishi, B. Soltész, K. Szirák, I. Balogh, G. Buglyó
Dátum:2024
ISSN:1018-4813
Tárgyszavak:Orvostudományok Elméleti orvostudományok idézhető absztrakt
folyóiratcikk
Megjelenés:European Journal Of Human Genetics. - 32 : S1 (2024), p. 553. -
További szerzők:Micsik Tamás Magyar Zsófia Tornóczky Tamás Kuthi Levente Nishi, Yumika Soltész Beáta (1987-) (molekuláris biológus) Szirák Krisztina (1973-) (molekuláris genetikus) Balogh István (1972-) (molekuláris biológus, genetikus) Buglyó Gergely (1980-) (genetikus)
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4.

001-es BibID:BIBFORM044276
Első szerző:Einarsdottir, Elisabet
Cím:Multiple independent variants in 6q21-22 associated with susceptibility to celiac disease in the Dutch, Finnish and Hungarian populations / Einarsdottir Elisabet, Bevova Marianna R., Zhernakova Alexandra, Monsuur Alienke, Koskinen Lotta L. E., van't Slot Ruben, Mulder Chris, Mearin M. Luisa, Korponay-Szabo Ilma R., Kaukinen Katri, Kurppa Kalle, Kere Juha, Mäki Markku, Wijmenga Cisca, Saavalainen Päivi
Dátum:2011
ISSN:1018-4813
Megjegyzések:Celiac disease is an inflammatory enteropathy caused by intolerance to gluten. Previous linkage studies in the Dutch, Finnish and Hungarian populations have revealed a locus on chromosome 6q21-22 conferring susceptibility to celiac disease. This locus has previously been implicated in susceptibility to other autoimmune diseases such as Crohn's disease and type 1 diabetes. We performed fine mapping on 446 independent individuals with celiac disease and 641 controls of Dutch origin, testing 872 tagging SNPs in a 22 Mb region of chromosome 6. The 12 most promising SNPs were followed up in 2071 individuals from 284 Finnish and 357 Hungarian celiac disease families to identify risk variants in this region. Multiple markers in the region were significantly associated with celiac disease in the Dutch material. Two SNPs, rs9391227 and rs4946111, were significantly associated with celiac disease in the Finnish population. The association to rs9391227 represents the strongest association signal found in the Finnish (P = 0.003, OR 0.66) as well as the combined Dutch, Finnish and Hungarian populations (P = 3.6 ? 10(-5), OR 0.76). The rs9391227 is situated downstream of the HECT domain and ankyrin repeat containing, E3 ubiquitin protein ligase 1 (HACE1) gene and is contained within a region of strong linkage disequilibrium enclosing HACE1. Two additional, independent, susceptibility variants in the 6q21-22 region were also found in a meta-analysis of the three populations. The 6q21-22 region was confirmed as a celiac disease susceptibility locus and harbors multiple independent associations, some of which may implicate ubiquitin-pathways in celiac disease susceptibility.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:European Journal Of Human Genetics. - 19 : 6 (2011), p. 682-686. -
További szerzők:Bevova, Marianna R. Zhernakova, Alexandra Monsuur, Alienke Koskinen, Lotta L. E. van't Slot, Ruben Mulder, Chris J. Mearin, Maria Luisa Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Kaukinen, Katri Kurppa, Kalle Kere, Juha Mäki, Markku Wijmenga, Cisca Saavalainen, Päivi
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5.

001-es BibID:bibEBI00021206
Első szerző:Hilgert, Nele
Cím:Phenotypic variability of patients homozygous for the GJB2 mutation 35delG cannot be explained by the influence of one major modifier gene / Hilgert N., Huentelman M.J., Thorburn A.Q., Fransen E., Dieltjens N., Mueller-Malesinska M., Pollak A., Skorka A., Waligora J., Ploski R., Castorina P., Primignani P., Ambrosetti U., Murgia A., Orzan E., Pandya A., Arnos K., Norris V., Seeman P., Janousek P., Feldmann D., Marlin S., Denoyelle F., Nishimura C.J., Janecke A., Nekahm-Heis D., Martini A., Mennucci E., Tóth T., Sziklai I., Del Castillo I., Moreno F., Petersen M.B., Iliadou V., Tekin M., Incesulu A., Nowakowska E., Bal J., Van de Heyning P., Roux A. F., Blanchet C., Goizet C., Lancelot G., Fialho G., Caria H., Liu X.Z., Xiaomei O., Govaerts P., Gronskov K., Hostmark K., Frei K., Dhooge I., Vlaeminck S., Kunstmann E., Van Laer L., Smith R.J., Van Camp G.
Dátum:2009
Megjegyzések:Hereditary hearing loss (HL) is a very heterogeneous trait, with 46 gene identifications for non-syndromic HL. Mutations in GJB2 cause up to half of all cases of severe-to-profound congenital autosomal recessive non-syndromic HL, with 35delG being the most frequent mutation in Caucasians. Although a genotype-phenotype correlation has been established for most GJB2 genotypes, the HL of 35delG homozygous patients is mild to profound. We hypothesise that this phenotypic variability is at least partly caused by the influence of modifier genes. By performing a whole-genome association (WGA) study on 35delG homozygotes, we sought to identify modifier genes. The association study was performed by comparing the genotypes of mild/moderate cases and profound cases. The first analysis included a pooling-based WGA study of a first set of 255 samples by using both the Illumina 550K and Affymetrix 500K chips. This analysis resulted in a ranking of all analysed single-nucleotide polymorphisms (SNPs) according to their P-values. The top 250 most significantly associated SNPs were genotyped individually in the same sample set. All 192 SNPs that still had significant P-values were genotyped in a second independent set of 297 samples for replication. The significant P-values were replicated in nine SNPs, with combined P-values between 3 x 10(-3) and 1 x 10(-4). This study suggests that the phenotypic variability in 35delG homozygous patients cannot be explained by the effect of one major modifier gene. Significantly associated SNPs may reflect a small modifying effect on the phenotype. Increasing the power of the study will be of greatest importance to confirm these results.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
connexin 26
35delG
hereditary hearing loss
association study
modifier gene
Megjelenés:European Journal of Human Genetics. - 17 : 4 (2009), p. 517-524. -
További szerzők:Huentelman, Matthew J. Thorburn, Ashley Q. Fransen, Erik Dieltjens, Nele Mueller-Malesinska, Malgorzata Pollak, Agnieszka Skorka, Agata Waligora, Jaroslaw Ploski, Rafal Castorina, Pierangela Primignani, Paola Ambrosetti, Umberto Murgia, Alessandra Orzan, Eva Pandya, Arti Arnos, Kathleen Norris, Virginia Seeman, Pavel Janousek, Petr Feldmann, Delphine Marlin, Sandrine Denoyelle, Francoise Nishimura, Carla J. Janecke, Andreas Nekahm-Heis, Doris Martini, Alessandro Mennucci, Elena Tóth Tímea (1974-) (fül-orr-gégész) Sziklai István (1954-) (fül-orr-gégész) Del Castillo, Ignacio Moreno, Felipe Petersen, Michael B. Iliadou, Vasiliki Tekin, Mustafa Incesulu, Armagan Nowakowska, Ewa Bal, Jerzy Heyning, Paul, van de Roux, Anne-Francoise Blanchet, Catherine Goizet, Cyril Lancelot, Guenaelle Fialho, Graca Caria, Helena Liu, Xue Zhoung Xiaomei, Ouyang Govaerts, Paul Gronskov, Karen Hostmark, Karianne Frei, Klemens Dhooge, Ingeborg Vlaeminck, Stephen Kunstmann, Erdmute Laer, L., Van Smith, Richard J. Camp, Guy, Van
Internet cím:DOI
elektronikus változat
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6.

001-es BibID:BIBFORM031514
Első szerző:Hoope, Richard R.
Cím:Dent Disease with mutations in OCRL1 / Richard R. Hoopes, Antony E. Shrimpton, Stephen J. Knohl, Paul Hueber, Bernd Hoppe, Janos Matyus, Ari Simckes, Velibor Tasic, Burkhard Toenshoff, Sharon F. Suchy, Robert L. Nussbaum, Steven J. Scheinman
Dátum:2005
Megjegyzések:Dent disease is an X-linked renal proximal tubulopathy associated with mutations in the chloride channel gene CLCN5. Lowe syndrome, a multisystem disease characterized by renal tubulopathy, congenital cataracts, and mental retardation, is associated with mutations in the gene OCRL1, which encodes a phosphatidylinositol 4,5-bisphosphate (PIP(2)) 5-phosphatase. Genetic heterogeneity has been suspected in Dent disease, but no other gene for Dent disease has been reported. We studied male probands in 13 families, all of whom met strict criteria for Dent disease but lacked mutations in CLCN5. Linkage analysis in the one large family localized the gene to a candidate region at Xq25-Xq27.1. Sequencing of candidate genes revealed a mutation in the OCRL1 gene. Of the 13 families studied, OCRL1 mutations were found in 5. PIP(2) 5-phosphatase activity was markedly reduced in skin fibroblasts cultured from the probands of these five families, and protein expression, measured by western blotting, was reduced or absent. Slit-lamp examinations performed in childhood or adulthood for all five probands showed normal results. Unlike patients with typical Lowe syndrome, none of these patients had metabolic acidosis. Three of the five probands had mild mental retardation, whereas two had no developmental delay or behavioral disturbance. These findings demonstrate that mutations in OCRL1 can occur with the isolated renal phenotype of Dent disease in patients lacking the cataracts, renal tubular acidosis, and neurological abnormalities that are characteristic of Lowe syndrome. This observation confirms genetic heterogeneity in Dent disease and demonstrates more-extensive phenotypic heterogeneity in Lowe syndrome than was previously appreciated. It establishes that the diagnostic criteria for disorders resulting from mutations in the Lowe syndrome gene OCRL1 need to be revised.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:American Journal of Human Genetics. - 76 : 2 (2005), p. 260-267. -
További szerzők:Shrimpton, Antony E. Knohl, Stephen J. Hueber, Paul Hoppe, Bernd Mátyus János (1957-) (belgyógyász, nephrológus) Simckes, Ari Tasic, Velibor Toenshoff, Burkhard Suchy, Sharon F. Nussbaum, Robert L. Scheinman, Steven J.
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7.

001-es BibID:BIBFORM016245
Első szerző:Kellermayer, Richard
Cím:A novel IL2RG mutation associated with maternal T lymphocyte engraftment in a patient with severe combined immunodeficiency / Richard Kellermayer, Amy P. Hsu, József Stankovics, Péter Balogh, Kinga Hadzsiev, Ágnes Vojcek, László Maródi, Pál Kajtár, György Kosztolányi, Jennifer M. Puck
Dátum:2006
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal of Human Genetics. - 51 : 5 (2006), p. 495-497. -
További szerzők:Hsu, Amy P. Stankovics József Balogh Péter (Pécs) Hadzsiev Kinga Vojcek Ágnes Maródi László (1949-) (gyermekgyógyász infektológus, immunológus) Kajtár Pál Kosztolányi György Puck, Jennifer M.
Pályázati támogatás:T 49017
OTKA
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8.

001-es BibID:BIBFORM073381
035-os BibID:(cikkazonosító)E-P18.36 (WoS)000489312608202
Első szerző:Keserű Judit (molekuláris genetikus)
Cím:Determination of miR-196a Single Nucleotide Polymorphism (SNP) with melting-curve analysis in the population of patients with ovarian cancer / J. S. Keserű, J. Lukács, B. Soltész, K. Szirák, Z. Birkó, A. Penyige, B. Nagy, R. Póka
Dátum:2018
ISSN:1018-4813 1476-5438
Megjegyzések:Introduction: miRNA molecules are short, non-coding sequences regulating gene expression after transcription. They are important in the development, progression and treatability of tumours. Single Nucleotide Polymorphism (SNP) is the most frequent type of genetic polymorphism. That is true also for miRNAs and their polymorphisms can cause alterations in the gene expression profile. miR-196a was also linked to the genesis of different tumours.Aim: Search for correlation between miR-196a polymorphism and development of ovarian cancer.Materials and Methods: 75 patients with ovarian cancer and 75 healthy persons were investigated. 15-16 mL blood anticoagulated with EDTA was drawn. DNA was isolated with silica absorption method and the melting curve of PCR products generated with LightSnip kit (TibMolbiol, Berlin, Germany) developed for miR-196a (rs11614913) SNP was determined by LightCycler 96 equipment. Allele and genotype frequencies were specified and Student t-test was applied for statistical analysis of data.Results: The Tm of PCR products were 55.5?C for T allele and 62.6?C for C allele with melting-curve analysis. T allele occurred in 32.66% in population of patients and in 40.66% in control group. Genotypes among control persons were 18.66% for TT, 44.0% for TC, and 37.33% CC, while in case of patients these frequencies were 12.0%, 41.33%, and 46.66%, respectively (p=0.3815).Conclusion: miR-196a influences the expression of 684 genes, it requires further complex investigation, whether it is involved in the development of ovarian cancer.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idézhető absztrakt
folyóiratcikk
ovarian cancer
miR-196a
SNP
Megjelenés:European Journal of Human Genetics. - 26 : Suppl. (2018), p. 1. -
További szerzők:Lukács János (1975-) (szülész-nőgyógyász, genetikus) Soltész Beáta (1987-) (molekuláris biológus) Szirák Krisztina (1973-) (molekuláris genetikus) Hádáné Birkó Zsuzsanna (1971-) (molekuláris genetikus) Penyige András (1954-) (molekuláris genetikus) Nagy Bálint (1956-) (molekuláris genetikus) Póka Róbert (1960-) (szülész-nőgyógyász, klinikai onkológus)
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9.

001-es BibID:BIBFORM073492
035-os BibID:(WoS)000436456100005 (Scopus)85045735086
Első szerző:Pös, Ondrej (biológus)
Cím:Circulating cell-free nucleic acids : characteristics and applications / Ondrej Pös, Orsolya Biró, Tomas Szemes, Bálint Nagy
Dátum:2018
ISSN:1018-4813
Megjegyzések:Liquid biopsy is becoming a very popular sample obtaining procedure, replacing the invasive sampling methods for the diagnostic protocols. The advantages of this method include the possibility to isolate cell-free nucleic acids (cfNAs) for diagnostic or screening purposes. A comprehensive review combining all current and perspective applications of cell-free nucleic acids is missing. Published articles are dealing with one type of cfNAs, or discuss them from the perspective of single disorder. We collected here all known types of cfNAs which are known to be present in biological fluids and could be involved in further studies to find out the exact biological role of them in normal physiological and pathological conditions. Beyond doubt cfNAs will have a tremendous effect in future screening, diagnosis, prognosis, follow-up, and treatment of cardiovascular diseases, cancer, diabetes and other diseases.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
cell-free nucleic acids
liquid biopsy
application
Megjelenés:European Journal of Human Genetics. - 26 : 7 (2018), p. 937-945. -
További szerzők:Biró Orsolya (molekuláris biológus) Szemes, Tomas (1980-) (biológus) Nagy Bálint (1956-) (molekuláris genetikus)
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DOI
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10.

001-es BibID:BIBFORM040456
Első szerző:Snoeckx, Rikkert L
Cím:GJB2 Mutations and Degree of Hearing Loss : a Multicenter Study / Snoeckx R. L., Huygen P. L. M., Feldmann D., Marlin S., Denoyelle F., Waligora J., Mueller-Malesinska M., Pollak A., Ploski R., Murgia A., Orzan E., Castorina P., Ambrosetti U., Nowakowska-Szyrwinska E., Bal J., Wiszniewski W., Janecke A. R., Nekahm-Heis D., Seeman P., Bendova O., Kenna M. A., Frangulov A., Rehm H. L., Tekin M., Incesulu A., Dahl H. H. M., du Sart D., Jenkins L., Lucas D., Bitner-Glindzicz M., Avraham K. B., Brownstein Z., del Castillo I., Moreno F., Blin N., Pfister M., Sziklai I., Toth T., Kelley P. M., Cohn E. S., Van Maldergem L., Hilbert P., Roux A. F., Mondain M., Hoefsloot L. H., Cremers C. W., Löppönen T., Löppönen H., Parving A., Gronskov K., Schrijver I., Roberson J., Gualandi F., Martini A., Lina-Granade G., Pallares-Ruiz N., Correia C., Fialho G., Cryns K., Hilgert N., Van de Heyning P., Nishimura C. J., Smith R. J., Van Camp G.
Dátum:2005
ISSN:0002-9297
Megjegyzések:Hearing impairment (HI) affects 1 in 650 newborns, which makes it the most common congenital sensory impairment. Despite extraordinary genetic heterogeneity, mutations in one gene, GJB2, which encodes the connexin 26 protein and is involved in inner ear homeostasis, are found in up to 50% of patients with autosomal recessive nonsyndromic hearing loss. Because of the high frequency of GJB2 mutations, mutation analysis of this gene is widely available as a diagnostic test. In this study, we assessed the association between genotype and degree of hearing loss in persons with HI and biallelic GJB2 mutations. We performed cross-sectional analyses of GJB2 genotype and audiometric data from 1,531 persons, from 16 different countries, with autosomal recessive, mild-to-profound nonsyndromic HI. The median age of all participants was 8 years; 90% of persons were within the age range of 0-26 years. Of the 83 different mutations identified, 47 were classified as nontruncating, and 36 as truncating. A total of 153 different genotypes were found, of which 56 were homozygous truncating (T/T), 30 were homozygous nontruncating (NT/NT), and 67 were compound heterozygous truncating/nontruncating (T/NT). The degree of HI associated with biallelic truncating mutations was significantly more severe than the HI associated with biallelic nontruncating mutations (P<.0001). The HI of 48 different genotypes was less severe than that of 35delG homozygotes. Several common mutations (M34T, V37I, and L90P) were associated with mild-to-moderate HI (median 25-40 dB). Two genotypes--35delG/R143W (median 105 dB) and 35delG/dela(GJB6-D13S1830) (median 108 dB)--had significantly more-severe HI than that of 35delG homozygotes.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:American Journal Of Human Genetics. - 77 : 6 (2005), p. 945-957. -
További szerzők:Huygen, Patrick L. M. Feldmann, Delphine Marlin, Sandrine Denoyelle, Francoise Waligora, Jaroslaw Mueller-Malesinska, Malgorzata Pollak, Agnieszka Ploski, Rafal Murgia, Alessandra Orzan, Eva Castorina, Pierangela Ambrosetti, Umberto Nowakowska-Szyrwinska, Ewa Bal, Jerzy Wiszniewski, Wojciech Janecke, Andreas Nekahm-Heis, Doris Seeman, Pavel Bendova, Olga Kenna, Margaret A. Frangulov, Anna Rehm, Heidi L. Tekin, Mustafa Incesulu, Armagan Dahl, Hans-Henrik M. du Sart, Desirée Jenkins, Lucy Lucas, Deirdre Bitner-Glindzicz, Maria Avraham, Karen B. Brownstein, Zippora Del Castillo, Ignacio Moreno, Felipe Blin, Nikolaus Pfister, Markus Sziklai István (1954-) (fül-orr-gégész) Tóth Tímea (1974-) (fül-orr-gégész) Kelley, Philip M. Cohn, Edward S. Van Maldergem, Lionel Hilbert, Pascale Roux, Anne-Francoise Mondain, Michel Hoefsloot, Lies H. Cremers, Cor W.R.J. Löppönen, Tuija Löppönen, Heikki Parving, Agnete Gronskov, Karen Schrijver, Iris Roberson, Joseph Gualandi, Francesca Martini, Alessandro Lina-Granade, Geneviéve Pallares-Ruiz, Nathalie Correia, Céu Fialho, Graca Cryns, Kim Hilgert, Nele Heyning, Paul, van de Nishimura, Carla J. Smith, Richard J. Camp, Guy, Van
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