Hans-Ulrich Schulz
Hans-Ulrich Schulz has a total of 9 co-authors. Here are the top co-authors by number of shared publications:
- Albert Roessner
Institute of Pathology, Otto-von-Guericke University, 39120 Magdeburg, Germany
1 shared publication - Antal Csepregi
Department of Gastroenterology, Hepatology, and Infectious Diseases, Otto-von-Guericke University, 39120 Magdeburg, Germany
1 shared publication - Christoph Röcken
Department of Pathology, University Hospital Schleswig-Holstein, Kiel, Germany
1 shared publication Hans Lippert
Otto von Guericke University of Magdeburg
1 shared publication- Juliane Hoffmann
Institute of Clinical Chemistry and Pathobiochemistry, Otto-von-Guericke-University, 39120 Magdeburg, Germany
1 shared publication - Matthias P. A. Ebert
Department of Gastroenterology, Hepatology, and Infectious Diseases, Otto-von-Guericke University, 39120 Magdeburg, Germany
1 shared publication
Latest Publications
- 14 November 2012
- Published by Springer Nature
- p. 65-77
Basic Chapter
- Open Access
- 22 June 2010
- Published by Springer Nature in BMC Cancer
- Vol. 10 (1) , 317
Promoter methylation of CDKN2A and lack of p16 expression characterize patients with hepatocellular carcinoma
The product of CDKN2A, p16 is an essential regulator of the cell cycle controlling the entry into the S-phase. Herein, we evaluated CDKN2A promoter methylation and p16 protein expression for the differentiation of hepatocellular carcinoma (HCC) from other liver tumors. Tumor and corresponding non-tumor liver tissue samples were obtained from 85 patients with liver tumors. CDKN2A promoter methylation was studied using MethyLight technique and methylation-specific PCR (MSP). In the MethyLight analysis, samples with ≥ 4% of PMR (percentage of methylated reference) were regarded as hypermethylated. p16 expression was evaluated by immunohistochemistry in tissue sections (n = 148) obtained from 81 patients using an immunoreactivity score (IRS) ranging from 0 (no expression) to 6 (strong expression). Hypermethylation of the CDKN2A promoter was found in 23 HCCs (69.7%; mean PMR = 42.34 ± 27.8%), six (20.7%; mean PMR = 31.85 ± 18%) liver metastases and in the extralesional tissue of only one patient. Using MSP, 32% of the non-tumor (n = 85), 70% of the HCCs, 40% of the CCCs and 24% of the liver metastases were hypermethylated. Correspondingly, nuclear p16 expression was found immunohistochemically in five (10.9%, mean IRS = 0.5) HCCs, 23 (92%; mean IRS = 4.9) metastases and only occasionally in hepatocytes of non-lesional liver tissues (mean IRS = 1.2). The difference of CDKN2A-methylation and p16 protein expression between HCCs and liver metastases was statistically significant (p < 0.01, respectively). Promoter methylation of CDKN2A gene and lack of p16 expression characterize patients with HCC.
- 22 June 2010
- Published by Springer Nature in BMC Cancer
- Vol. 10 (1) , 317
Open AccessPromoter methylation of CDKN2A and lack of p16 expression characterize patients with hepatocellular carcinoma
The product of CDKN2A, p16 is an essential regulator of the cell cycle controlling the entry into the S-phase. Herein, we evaluated CDKN2A promoter methylation and p16 protein expression for the differentiation of hepatocellular carcinoma (HCC) from other liver tumors. Tumor and corresponding non-tumor liver tissue samples were obtained from 85 patients with liver tumors. CDKN2A promoter methylation was studied using MethyLight technique and methylation-specific PCR (MSP). In the MethyLight analysis, samples with ≥ 4% of PMR (percentage of methylated reference) were regarded as hypermethylated. p16 expression was evaluated by immunohistochemistry in tissue sections (n = 148) obtained from 81 patients using an immunoreactivity score (IRS) ranging from 0 (no expression) to 6 (strong expression). Hypermethylation of the CDKN2A promoter was found in 23 HCCs (69.7%; mean PMR = 42.34 ± 27.8%), six (20.7%; mean PMR = 31.85 ± 18%) liver metastases and in the extralesional tissue of only one patient. Using MSP, 32% of the non-tumor (n = 85), 70% of the HCCs, 40% of the CCCs and 24% of the liver metastases were hypermethylated. Correspondingly, nuclear p16 expression was found immunohistochemically in five (10.9%, mean IRS = 0.5) HCCs, 23 (92%; mean IRS = 4.9) metastases and only occasionally in hepatocytes of non-lesional liver tissues (mean IRS = 1.2). The difference of CDKN2A-methylation and p16 protein expression between HCCs and liver metastases was statistically significant (p < 0.01, respectively). Promoter methylation of CDKN2A gene and lack of p16 expression characterize patients with HCC.