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3. Corrigendum: SPOCK1 promotes the development of hepatocellular carcinoma

Author

Váncza, Lóránd, primary, Karászi, Katalin, additional, Péterfia, Bálint, additional, Turiák, Lilla, additional, Dezső, Katalin, additional, Sebestyén, Anna, additional, Reszegi, Andrea, additional, Petővári, Gábor, additional, Kiss, András, additional, Schaff, Zsuzsanna, additional, Baghy, Kornélia, additional, and Kovalszky, Ilona, additional

Published
2023
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10. SPOCK1 Promotes the Development of Hepatocellular Carcinoma

Author

Váncza, Lóránd, primary, Karászi, Katalin, additional, Péterfia, Bálint, additional, Turiák, Lilla, additional, Dezső, Katalin, additional, Sebestyén, Anna, additional, Reszegi, Andrea, additional, Petővári, Gábor, additional, Kiss, András, additional, Schaff, Zsuzsanna, additional, Baghy, Kornélia, additional, and Kovalszky, Ilona, additional

Published
2022
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14. Additional file 1: of Gene promoter and exon DNA methylation changes in colon cancer development – mRNA expression and tumor mutation alterations

Author

Molnár, Béla, Galamb, Orsolya, Péterfia, Bálint, Wichmann, Barnabás, Csabai, István, Bodor, András, Kalmár, Alexandra, Szigeti, Krisztina, Barták, Barbara, Nagy, Zsófia, Valcz, Gábor, Patai, Árpád, Igaz, Péter, and Tulassay, Zsolt

Abstract

Table S1A. Top50 hypermethylated DMRs in CRC versus NAT comparison. Table S1B. Top50 hypomethylated DMRs in CRC versus NAT comparison. Table S1C. Top50 hypermethylated DMRs in adenoma tissue compared to NAT samples. Table S1D. Top50 hypomethylated DMRs in adenoma tissue compared to NAT samples. (DOC 253 kb)

Published
2018
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15. Additional file 2: of Gene promoter and exon DNA methylation changes in colon cancer development – mRNA expression and tumor mutation alterations

Author

Molnár, Béla, Galamb, Orsolya, Péterfia, Bálint, Wichmann, Barnabás, Csabai, István, Bodor, András, Kalmár, Alexandra, Szigeti, Krisztina, Barták, Barbara, Nagy, Zsófia, Valcz, Gábor, Patai, Árpád, Igaz, Péter, and Tulassay, Zsolt

Abstract

Figure S1. Box plots of significant DMRs in TP53 pathway gene promoters between CRC and NAT samples. Figure S2. DNA methylation pattern of top50 hypermethylated DMRs on an independent set of samples. Figure S3. DNA methylation profiles of the overlapping regions on methyl capture sequencing and EpiTect array results. (DOC 902 kb)

Published
2018
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18. Elsődleges genetikai vizsgálat Prader–Willi-szindróma igazolására

Author

Ács, Orsolya Dóra, primary, Péterfia, Bálint, additional, Hollósi, Péter, additional, Haltrich, Irén, additional, Sallai, Ágnes, additional, Luczay, Andrea, additional, Buiting, Karin, additional, Horsthemke, Bernhard, additional, Török, Dóra, additional, Szabó, András, additional, and Fekete, György, additional

Published
2018
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19. Colorectal adenoma and cancer detection based on altered methylation pattern of SFRP1, SFRP2, SDC2, and PRIMA1 in plasma samples

Author

Barták, Barbara Kinga, primary, Kalmár, Alexandra, additional, Péterfia, Bálint, additional, Patai, Árpád V., additional, Galamb, Orsolya, additional, Valcz, Gábor, additional, Spisák, Sándor, additional, Wichmann, Barnabás, additional, Nagy, Zsófia Brigitta, additional, Tóth, Kinga, additional, Tulassay, Zsolt, additional, Igaz, Péter, additional, and Molnár, Béla, additional

Published
2017
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20. Additional file 5: Figure S2. of DNA hypermethylation and decreased mRNA expression of MAL, PRIMA1, PTGDR and SFRP1 in colorectal adenoma and cancer

Author

Kalmár, Alexandra, Péterfia, Bálint, Hollósi, Péter, Galamb, Orsolya, Spisák, Sándor, Wichmann, Barnabás, Bodor, András, Tóth, Kinga, Patai, Árpád, Valcz, Gábor, Nagy, Zsófia, Kubák, Vivien, Tulassay, Zsolt, Kovalszky, Ilona, and Molnár, Béla

Abstract

Box plot representation of DNA methylation alterations of analysed genes in biopsies and macrodissected specimens of NAT (n = 10), AD (n = 10), and CRC (n = 10) and in LCM epithelial cells of NAT (n = 5), AD (n = 5) and CRC (n = 5). Red dots are individual DNA methylation percent values, box plots represent median and standard deviation of the data. Asterisk (*) represents significance (p

Published
2015
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21. Additional file 1: Table S1. of DNA hypermethylation and decreased mRNA expression of MAL, PRIMA1, PTGDR and SFRP1 in colorectal adenoma and cancer

Author

Kalmár, Alexandra, Péterfia, Bálint, Hollósi, Péter, Galamb, Orsolya, Spisák, Sándor, Wichmann, Barnabás, Bodor, András, Tóth, Kinga, Patai, Árpád, Valcz, Gábor, Nagy, Zsófia, Kubák, Vivien, Tulassay, Zsolt, Kovalszky, Ilona, and Molnár, Béla

Abstract

Clinical data of the analysed gene expression datasets (GSE4183, GSE37364, GSE10714 and GSE15960). (DOC 249 kb)

Published
2015
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22. Additional file 3: Figure S1. of DNA hypermethylation and decreased mRNA expression of MAL, PRIMA1, PTGDR and SFRP1 in colorectal adenoma and cancer

Author

Kalmár, Alexandra, Péterfia, Bálint, Hollósi, Péter, Galamb, Orsolya, Spisák, Sándor, Wichmann, Barnabás, Bodor, András, Tóth, Kinga, Patai, Árpád, Valcz, Gábor, Nagy, Zsófia, Kubák, Vivien, Tulassay, Zsolt, Kovalszky, Ilona, and Molnár, Béla

Abstract

Gene expression of the selected marker set in normal (n = 49), adenoma (n = 49), and tumour (n = 49) biopsy samples. Results are represented as pairwise box plots showing single gene expession in the biopsy and in the laser microdissected epithelial cells from normal (n = 6), adenoma (n = 6), and tumour (n = 6). Red dots are normalised gene expression values, box plots represent median and standard deviation of the data. Asterisk (*) represents significance (p

Published
2015
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23. Additional file 2: Table S2. of DNA hypermethylation and decreased mRNA expression of MAL, PRIMA1, PTGDR and SFRP1 in colorectal adenoma and cancer

Author

Kalmár, Alexandra, Péterfia, Bálint, Hollósi, Péter, Galamb, Orsolya, Spisák, Sándor, Wichmann, Barnabás, Bodor, András, Tóth, Kinga, Patai, Árpád, Valcz, Gábor, Nagy, Zsófia, Kubák, Vivien, Tulassay, Zsolt, Kovalszky, Ilona, and Molnár, Béla

Abstract

Clinical data of patients involved in the study. (DOCX 24 kb)

Published
2015
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24. Construction of a multiplex mutation hot spot PCR panel: the first step towards colorectal cancer genotyping on the GS Junior platform

Author

Péterfia, Bálint, primary, Kalmár, Alexandra, additional, Patai, Árpád V., additional, Csabai, István, additional, Bodor, András, additional, Micsik, Tamás, additional, Wichmann, Barnabás, additional, Egedi, Krisztina, additional, Hollósi, Péter, additional, Kovalszky, Ilona, additional, Tulassay, Zsolt, additional, and Molnár, Béla, additional

Published
2017
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26. Comprehensive DNA Methylation and Mutation Analyses Reveal a Methylation Signature in Colorectal Sessile Serrated Adenomas

Author

Patai, Árpád V., primary, Barták, Barbara Kinga, additional, Péterfia, Bálint, additional, Micsik, Tamás, additional, Horváth, Réka, additional, Sumánszki, Csaba, additional, Péter, Zoltán, additional, Patai, Árpád, additional, Valcz, Gábor, additional, Kalmár, Alexandra, additional, Tóth, Kinga, additional, Krenács, Tibor, additional, Tulassay, Zsolt, additional, and Molnár, Béla, additional

Published
2016
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27. Aberrant DNA methylation of WNT pathway genes in the development and progression of CIMP-negative colorectal cancer

Author

Galamb, Orsolya, primary, Kalmár, Alexandra, additional, Péterfia, Bálint, additional, Csabai, István, additional, Bodor, András, additional, Ribli, Dezső, additional, Krenács, Tibor, additional, Patai, Árpád V., additional, Wichmann, Barnabás, additional, Barták, Barbara Kinga, additional, Tóth, Kinga, additional, Valcz, Gábor, additional, Spisák, Sándor, additional, Tulassay, Zsolt, additional, and Molnár, Béla, additional

Published
2016
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29. DNA hypermethylation and decreased mRNA expression of MAL, PRIMA1, PTGDR and SFRP1 in colorectal adenoma and cancer

Author

Kalmár, Alexandra, primary, Péterfia, Bálint, additional, Hollósi, Péter, additional, Galamb, Orsolya, additional, Spisák, Sándor, additional, Wichmann, Barnabás, additional, Bodor, András, additional, Tóth, Kinga, additional, Patai, Árpád V., additional, Valcz, Gábor, additional, Nagy, Zsófia Brigitta, additional, Kubák, Vivien, additional, Tulassay, Zsolt, additional, Kovalszky, Ilona, additional, and Molnár, Béla, additional

Published
2015
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30. Comprehensive DNA Methylation Analysis Reveals a Common Ten-Gene Methylation Signature in Colorectal Adenomas and Carcinomas

Author

Patai, Árpád V., primary, Valcz, Gábor, additional, Hollósi, Péter, additional, Kalmár, Alexandra, additional, Péterfia, Bálint, additional, Patai, Árpád, additional, Wichmann, Barnabás, additional, Spisák, Sándor, additional, Barták, Barbara Kinga, additional, Leiszter, Katalin, additional, Tóth, Kinga, additional, Sipos, Ferenc, additional, Kovalszky, Ilona, additional, Péter, Zoltán, additional, Miheller, Pál, additional, Tulassay, Zsolt, additional, and Molnár, Béla, additional

Published
2015
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32. Myofibroblast-Derived SFRP1 as Potential Inhibitor of Colorectal Carcinoma Field Effect

Author

Valcz, Gábor, primary, Patai, Árpád V., additional, Kalmár, Alexandra, additional, Péterfia, Bálint, additional, Fűri, István, additional, Wichmann, Barnabás, additional, Műzes, Györgyi, additional, Sipos, Ferenc, additional, Krenács, Tibor, additional, Mihály, Emese, additional, Spisák, Sándor, additional, Molnár, Béla, additional, and Tulassay, Zsolt, additional

Published
2014
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35. Syndecan-1 Enhances Proliferation, Migration and Metastasis of HT-1080 Cells in Cooperation with Syndecan-2

Author

Péterfia, Bálint, primary, Füle, Tibor, additional, Baghy, Kornélia, additional, Szabadkai, Krisztina, additional, Fullár, Alexandra, additional, Dobos, Katalin, additional, Zong, Fang, additional, Dobra, Katalin, additional, Hollósi, Péter, additional, Jeney, András, additional, Paku, Sándor, additional, and Kovalszky, Ilona, additional

Published
2012
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36. Colorectal adenoma and cancer detection based on altered methylation pattern of SFRP1, SFRP2, SDC2, and PRIMA1in plasma samples

Author

Barták, Barbara Kinga, Kalmár, Alexandra, Péterfia, Bálint, Patai, Árpád V., Galamb, Orsolya, Valcz, Gábor, Spisák, Sándor, Wichmann, Barnabás, Nagy, Zsófia Brigitta, Tóth, Kinga, Tulassay, Zsolt, Igaz, Péter, and Molnár, Béla

Abstract

ABSTRACTAberrant methylation is one of the most frequent epigenetic alterations that can contribute to tumor formation. Cell-free DNA can originate from tumor tissue; therefore, the evaluation of methylation markers in cell-free DNA can be a promising method for cancer screening. Our aim was to develop a panel of biomarkers with altered methylation along the colorectal adenoma-carcinoma sequence in both colonic tissue and plasma. Methylation of selected CpG sites in healthy colonic (n = 15), adenoma (n = 15), and colorectal cancer (n = 15) tissues was analyzed by pyrosequencing. MethyLight PCR was applied to study the DNA methylation of SFRP1, SFRP2, SDC2,and PRIMA1gene promoters in 121 plasma and 32 biopsy samples. The effect of altered promoter methylation on protein expression was examined by immunohistochemistry. Significantly higher (P< 0.05) DNA methylation levels were detected in the promoter regions of all 4 markers, both in CRC and adenoma tissues compared with healthy controls. Methylation of SFRP1, SFRP2, SDC2,and PRIMA1promoter sequences was observed in 85.1%, 72.3%, 89.4%, and 80.9% of plasma samples from patients with CRC and 89.2%, 83.8%, 81.1% and 70.3% from adenoma patients, respectively. When applied as a panel, CRC patients could be distinguished from controls with 91.5% sensitivity and 97.3% specificity [area under the curve (AUC) = 0.978], while adenoma samples could be differentiated with 89.2% sensitivity and 86.5% specificity (AUC = 0.937). Immunohistochemical analysis indicated decreasing protein levels of all 4 markers along the colorectal adenoma-carcinoma sequence. Our findings suggest that this methylation biomarker panel allows non-invasive detection of colorectal adenoma and cancer from plasma samples.

Published
2017
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37. Initial Genomics of the Human Nucleolus

Author

Németh, Attila, primary, Conesa, Ana, additional, Santoyo-Lopez, Javier, additional, Medina, Ignacio, additional, Montaner, David, additional, Péterfia, Bálint, additional, Solovei, Irina, additional, Cremer, Thomas, additional, Dopazo, Joaquin, additional, and Längst, Gernot, additional

Published
2010
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38. Lack of Matrilin-2 Favors Liver Tumor Development via Erk1/2 and GSK-3β Pathways In Vivo.

Author

Fullár, Alexandra, Baghy, Kornélia, Deák, Ferenc, Péterfia, Bálint, Zsák, Yvonne, Tátrai, Péter, Schaff, Zsuzsa, Dudás, József, Kiss, Ibolya, and Kovalszky, Ilona

Subjects
LIVER regeneration, MATRILINS, EXTRACELLULAR matrix, ADAPTOR proteins, RETINOBLASTOMA protein, GASTROINTESTINAL tumors
Abstract

Matrilin-2 (Matn2) is a multidomain adaptor protein which plays a role in the assembly of extracellular matrix (ECM). It is produced by oval cells during stem cell-driven liver regeneration. In our study, the impact of Matn2 on hepatocarcinogenesis was investigated in Matn2-/- mice comparing them with wild-type (WT) mice in a diethylnitrosamine (DEN) model. The liver tissue was analyzed macroscopically, histologically and immunohistochemically, at protein level by Proteome Profiler Arrays and Western blot analysis. Matn2-/- mice exhibited higher susceptibility to hepatocarcinogenesis compared to wild-type mice. In the liver of Matn2-/- mice, spontaneous microscopic tumor foci were detected without DEN treatment. After 15 μg/g body weight DEN treatment, the liver of Matn2-/- mice contained macroscopic tumors of both larger number and size than the WT liver. In contrast with the WT liver, spontaneous phosphorylation of EGFR, Erk1/2 GSK-3α/β and retinoblastoma protein (p-Rb), decrease in p21/CIP1 level, and increase in β-Catenin protein expression were detected in Matn2-/- livers. Focal Ki-67 positivity of these samples provided additional support to our presumption that the lack of Matn2 drives the liver into a pro-proliferatory state, making it prone to tumor development. This enhanced proliferative capacity was further increased in the tumor nodules of DEN-treated Matn2-/- livers. Our study suggests that Matn2 functions as a tumor suppressor in hepatocarcinogenesis, and in this process activation of EGFR together with that of Erk1/2, as well as inactivation of GSK-3β, play strategic roles. [ABSTRACT FROM AUTHOR]

Published
2014
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40. Lack of Matrilin-2 Favors Liver Tumor Development via Erk1/2 and GSK-3β Pathways In Vivo.

Author

Fullár, Alexandra, Baghy, Kornélia, Deák, Ferenc, Péterfia, Bálint, Zsák, Yvonne, Tátrai, Péter, Schaff, Zsuzsa, Dudás, József, Kiss, Ibolya, and Kovalszky, Ilona

Subjects
*LIVER regeneration, *MATRILINS, *EXTRACELLULAR matrix, *ADAPTOR proteins, *RETINOBLASTOMA protein, *GASTROINTESTINAL tumors
Abstract

Matrilin-2 (Matn2) is a multidomain adaptor protein which plays a role in the assembly of extracellular matrix (ECM). It is produced by oval cells during stem cell-driven liver regeneration. In our study, the impact of Matn2 on hepatocarcinogenesis was investigated in Matn2-/- mice comparing them with wild-type (WT) mice in a diethylnitrosamine (DEN) model. The liver tissue was analyzed macroscopically, histologically and immunohistochemically, at protein level by Proteome Profiler Arrays and Western blot analysis. Matn2-/- mice exhibited higher susceptibility to hepatocarcinogenesis compared to wild-type mice. In the liver of Matn2-/- mice, spontaneous microscopic tumor foci were detected without DEN treatment. After 15 μg/g body weight DEN treatment, the liver of Matn2-/- mice contained macroscopic tumors of both larger number and size than the WT liver. In contrast with the WT liver, spontaneous phosphorylation of EGFR, Erk1/2 GSK-3α/β and retinoblastoma protein (p-Rb), decrease in p21/CIP1 level, and increase in β-Catenin protein expression were detected in Matn2-/- livers. Focal Ki-67 positivity of these samples provided additional support to our presumption that the lack of Matn2 drives the liver into a pro-proliferatory state, making it prone to tumor development. This enhanced proliferative capacity was further increased in the tumor nodules of DEN-treated Matn2-/- livers. Our study suggests that Matn2 functions as a tumor suppressor in hepatocarcinogenesis, and in this process activation of EGFR together with that of Erk1/2, as well as inactivation of GSK-3β, play strategic roles. [ABSTRACT FROM AUTHOR]

Published
2014
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41. [Rapid first-tier genetic diagnosis in patients with Prader-Willi syndrome].

Author

Ács OD, Péterfia B, Hollósi P, Haltrich I, Sallai Á, Luczay A, Buiting K, Horsthemke B, Török D, Szabó A, and Fekete G

Subjects
Child, Child, Preschool, Chromosomes, Human, Pair 15 genetics, Female, Genotype, Humans, Male, Prader-Willi Syndrome genetics, Nucleic Acid Amplification Techniques methods, Polymerase Chain Reaction methods, Prader-Willi Syndrome diagnosis
Abstract

Introduction: According to the international literature, DNA methylation analysis of the promoter region of SNRPN locus is the most efficient way to start genetic investigation in patients with suspected Prader-Willi syndrome., Aim: Our aim was to develop a simple, reliable first-tier diagnosis to confirm Prader-Willi syndrome, therefore to compare our self-designed simple, cost-efficient high-resolution melting analysis and the most commonly used methylation-specific multiplex ligation-dependent probe amplification to confirm Prader-Willi syndrome., Method: We studied 17 clinically suspected Prader-Willi syndrome children and their DNA samples. With self-designed primers, bisulfite-sensitive polymerase chain reaction, high-resolution melting analysis and, as a control, methylation-specific multiplex ligation-dependent probe amplification were performed., Results: Prader-Willi syndrome was genetically confirmed in 6 out of 17 clinically suspected Prader-Willi syndrome patients. The results of high-resolution melting analysis and methylation-specific multiplex ligation-dependent probe amplification were equivalent in each case., Conclusion: Using our self-designed primers and altered bisulfite-specific PCR conditions, high-resolution melting analysis appears to be a simple, fast, reliable and effective method for primarily proving or excluding clinically suspected Prade-Willi syndrome cases. Orv Hetil. 2018; 159(2): 64-69.

Published
2018
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42. [Role of syndecan-1 proteoglycan in the invasiveness of HT-1080 fibrosarcoma].

Author

Péterfia B, Hollósi P, Szilák L, Timár F, Paku S, Jeney A, and Kovalszky I

Subjects
Animals, Cell Line, Tumor, Fibrosarcoma metabolism, Immunohistochemistry, Lung Neoplasms secondary, Mice, Neoplasm Invasiveness, Phenotype, Sarcoma, Experimental metabolism, Syndecan-1, Syndecans, Transfection, Fibrosarcoma pathology, Membrane Glycoproteins metabolism, Proteoglycans metabolism, Sarcoma, Experimental pathology
Abstract

Syndecan-1 is a transmembrane heparan sulfate proteoglycan which plays pivotal role in cell-cell and cell-extracellular matrix interactions. However, its implication in the establishment of malignant phenotype is still controversial. Its expression indicates differentiated phenotype in certain tumors, while it confers invasive nature for others. For the better understanding of the role of syndecan-1 in cancer we transfected HT-1080 fibrosarcoma cell line with the full and a truncated construct of syndecan-1 and established stable cell lines with them. We studied the in vitro and in vivo growth capacity and metastatic potential of the transfectants in comparison with the cell line bearing only the EGFP expression vector. Our results showed that the growth rate of syndecan transfectants increased and they developed more lung metastases than the control cells. As local growth of the full transfectant was faster than that of the 78sig we presume that the full protein and maybe the shedding is needed for the local development of the tumor, but the intracellular and transmembrane domain is sufficient to promote metastasis formation.

Published
2006
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