2024-03-29T06:43:20Zhttp://repository.helmholtz-hzi.de/oai/requestoai:repository.helmholtz-hzi.de:10033/1254482019-08-30T11:27:09Zcom_10033_107102com_10033_6799col_10033_107103
Helmholtz Zentrum für Infektionsforschung Repository
author
Klawonn, Frank
author
Wüstefeld, T.
author
Zender, Lars
department
Helmholtz Center for Infection Research, Inhoffenstr. 7, D-38124 Braunschweig, Germany
2011-03-23T15:24:15Z
2011-03-23T15:24:15Z
03029743
http://hdl.handle.net/10033/125448
Lecture Notes in Computer Science (including subseries Lecture Notes in Artificial Intelligence and Lecture Notes in Bioinformatics)
null
Statistical modelling for data from experiments with short hairpin RNAs
Article
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URL
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oai:repository.helmholtz-hzi.de:10033/2106692019-08-30T11:29:17Zcom_10033_107102com_10033_6799col_10033_107103
Helmholtz Zentrum für Infektionsforschung Repository
author
Sirma, Hüseyin
author
Kumar, Mukesh
author
Meena, Jitendra K
author
Witt, Britta
author
Weise, Julia M
author
Lechel, Andre
author
Ande, Satyanarayana
author
Sakk, Vadim
author
Guguen-Guillouzo, Christiane
author
Zender, Lars
author
Rudolph, Karl-Lenhard
author
Günes, Cagatay
department
Heinrich-Pette-Institute, Hamburg, Germany.
2012-02-14T10:14:50Z
2011-07
The promoter of human telomerase reverse transcriptase is activated during liver regeneration and hepatocyte proliferation. 2011, 141 (1):326-37, 337.e1-3 Gastroenterology
1528-0012
21447332
10.1053/j.gastro.2011.03.047
http://hdl.handle.net/10033/210669
Gastroenterology
Telomerase activity has not been detected in healthy human liver biopsy samples, but it is up-regulated in most human liver tumors. It is not clear whether telomerase is activated in response to acute or chronic liver injury. Telomerase activity is closely associated with expression of its catalytic subunit, telomerase reverse transcriptase (TERT). We analyzed the activity of the human TERT (hTERT) promoter during liver regeneration in vivo and hepatocyte proliferation in vitro.
en
The promoter of human telomerase reverse transcriptase is activated during liver regeneration and hepatocyte proliferation.
Article
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URL
https://hzi.openrepository.com/bitstream/10033/210669/1/Sirma%20et%20al_final.pdf
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URL
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oai:repository.helmholtz-hzi.de:10033/2422972019-08-30T11:27:46Zcom_10033_107102com_10033_6799col_10033_107103
Helmholtz Zentrum für Infektionsforschung Repository
author
Hoenicke, Lisa
author
Zender, Lars
department
Helmholtz Centre for Infection Research, Braunschweig, Germany.
2012-09-10T13:45:39Z
2012-06
Immune surveillance of senescent cells--biological significance in cancer- and non-cancer pathologies. 2012, 33 (6):1123-6 Carcinogenesis
1460-2180
22470164
10.1093/carcin/bgs124
http://hdl.handle.net/10033/242297
Carcinogenesis
Cellular senescence, a state of stable growth arrest, can occur in response to various stress stimuli such as telomere shortening, treatment with chemotherapeutic drugs or the aberrant activation of oncogenes. Senescent cells communicate with their environment by secreting various cytokines and growth factors, and it has become clear that this 'secretory phenotype' can have pro- as well as anti-tumorigenic effects. Recent work from our laboratory showed that premalignant, senescent hepatocytes are recognized and cleared through an antigen-specific immune response and that this immune response, designated as 'senescence surveillance' is crucial for tumor suppression in the liver [(Kang,T.W. et al. (2011) Senescence surveillance of pre-malignant hepatocytes limits liver cancer development. Nature, 479, 547-551]. It is an emerging concept that immune responses against senescent cells have a broader biological significance in cancer- as well as non-cancer pathologies and current data suggest that distinct immune responses are engaged to clear senescent cells in different disease settings. In this review article, we will discuss different examples how immune responses against senescent cells are involved to restrict disease progression in cancer- and non-cancer pathologies.
en
Archived with thanks to Carcinogenesis
Immune surveillance of senescent cells--biological significance in cancer- and non-cancer pathologies.
Article
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URL
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oai:repository.helmholtz-hzi.de:10033/2712922019-08-30T11:26:13Zcom_10033_107102com_10033_6799col_10033_107103
Helmholtz Zentrum für Infektionsforschung Repository
author
Xue, Wen
author
Kitzing, Thomas
author
Roessler, Stephanie
author
Zuber, Johannes
author
Krasnitz, Alexander
author
Schultz, Nikolaus
author
Revill, Kate
author
Weissmueller, Susann
author
Rappaport, Amy R
author
Simon, Janelle
author
Zhang, Jack
author
Luo, Weijun
author
Hicks, James
author
Zender, Lars
author
Wang, Xin Wei
author
Powers, Scott
author
Wigler, Michael
author
Lowe, Scott W
department
Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.
2013-03-06T09:03:42Z
2012-05-22
A cluster of cooperating tumor-suppressor gene candidates in chromosomal deletions. 2012, 109 (21):8212-7 Proc. Natl. Acad. Sci. U.S.A.
1091-6490
22566646
10.1073/pnas.1206062109
http://hdl.handle.net/10033/271292
Proceedings of the National Academy of Sciences of the United States of America
The large chromosomal deletions frequently observed in cancer genomes are often thought to arise as a "two-hit" mechanism in the process of tumor-suppressor gene (TSG) inactivation. Using a murine model system of hepatocellular carcinoma (HCC) and in vivo RNAi, we test an alternative hypothesis, that such deletions can arise from selective pressure to attenuate the activity of multiple genes. By targeting the mouse orthologs of genes frequently deleted on human 8p22 and adjacent regions, which are lost in approximately half of several other major epithelial cancers, we provide evidence suggesting that multiple genes on chromosome 8p can cooperatively inhibit tumorigenesis in mice, and that their cosuppression can synergistically promote tumor growth. In addition, in human HCC patients, the combined down-regulation of functionally validated 8p TSGs is associated with poor survival, in contrast to the down-regulation of any individual gene. Our data imply that large cancer-associated deletions can produce phenotypes distinct from those arising through loss of a single TSG, and as such should be considered and studied as distinct mutational events.
en
Archived with thanks to Proceedings of the National Academy of Sciences of the United States of America
A cluster of cooperating tumor-suppressor gene candidates in chromosomal deletions.
Article
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oai:repository.helmholtz-hzi.de:10033/5954122019-08-30T11:27:46Zcom_10033_107102com_10033_6799col_10033_107103
Helmholtz Zentrum für Infektionsforschung Repository
author
Schäfer, Martin
author
Lkhagvasuren, Otgonzul
author
Klein, Hans-Ulrich
author
Elling, Christian
author
Wüstefeld, Torsten
author
Müller-Tidow, Carsten
author
Zender, Lars
author
Koschmieder, Steffen
author
Dugas, Martin
author
Ickstadt, Katja
department
Helmholtz Centre for infection research, Inhoffenstr. 7, D-38124 Braunschweig, Germany.
2016-02-02T15:52:19Z
2012
Integrative analyses for omics data: a Bayesian mixture model to assess the concordance of ChIP-chip and ChIP-seq measurements. 2012, 75 (8-10):461-70 J. Toxicol. Environ. Health Part A
1528-7394
22686305
10.1080/15287394.2012.674914
http://hdl.handle.net/10033/595412
Journal of toxicology and environmental health. Part A
The analysis of different variations in genomics, transcriptomics, epigenomics, and proteomics has increased considerably in recent years. This is especially due to the success of microarray and, more recently, sequencing technology. Apart from understanding mechanisms of disease pathogenesis on a molecular basis, for example in cancer research, the challenge of analyzing such different data types in an integrated way has become increasingly important also for the validation of new sequencing technologies with maximum resolution. For this purpose, a methodological framework for their comparison with microarray techniques in the context of smallest sample sizes, which result from the high costs of experiments, is proposed in this contribution. Based on an adaptation of the externally centered correlation coefficient ( Schäfer et al. 2009 ), it is demonstrated how a Bayesian mixture model can be applied to compare and classify measurements of histone acetylation that stem from chromatin immunoprecipitation combined with either microarray (ChIP-chip) or sequencing techniques (ChIP-seq) for the identification of DNA fragments. Here, the murine hematopoietic cell line 32D, which was transduced with the oncogene BCR-ABL, the hallmark of chronic myeloid leukemia, was characterized. Cells were compared to mock-transduced cells as control. Activation or inhibition of other genes by histone modifications induced by the oncogene is considered critical in such a context for the understanding of the disease.
en
Integrative analyses for omics data: a Bayesian mixture model to assess the concordance of ChIP-chip and ChIP-seq measurements.
Article
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