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Book ; Online ; Thesis: Ursprünge epigenetischer Veränderungen in tumorartigen neuroendokrinen Zellen

Lahtz, Christoph

2010

Author's details	vorgelegt von Christoph Lahtz
Language	German
Size	Online-Ressource
Document type	Book ; Online ; Thesis
Thesis / German Habilitation thesis	Gießen, Univ., Diss., 2010
Database	Library catalogue of the German National Library of Science and Technology (TIB), Hannover

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Book ; Online ; Thesis: Ursprünge epigenetischer Veränderungen in tumorartigen neuroendokrinen Zellen

Lahtz, Christoph [Verfasser]

2010

Author's details	vorgelegt von Christoph Lahtz
Keywords	Biowissenschaften, Biologie ; Life Science, Biology
Subject code	sg570
Language	German
Document type	Book ; Online ; Thesis
Database	Digital theses on the web

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Article ; Online: Epigenetic changes of DNA repair genes in cancer.

Lahtz, Christoph / Pfeifer, Gerd P

Journal of molecular cell biology

2011 Volume 3, Issue 1, Page(s) 51–58

Abstract: Every Hour Hurts, The Last One Kills'. That is an old saying about getting old. Every day, thousands of DNA damaging events take place in each cell of our body, but efficient DNA repair systems have evolved to prevent that. However, our DNA repair ... ...

Abstract	'Every Hour Hurts, The Last One Kills'. That is an old saying about getting old. Every day, thousands of DNA damaging events take place in each cell of our body, but efficient DNA repair systems have evolved to prevent that. However, our DNA repair system and that of most other organisms are not as perfect as that of Deinococcus radiodurans, for example, which is able to repair massive amounts of DNA damage at one time. In many instances, accumulation of DNA damage has been linked to cancer, and genetic deficiencies in specific DNA repair genes are associated with tumor-prone phenotypes. In addition to mutations, which can be either inherited or somatically acquired, epigenetic silencing of DNA repair genes may promote tumorigenesis. This review will summarize current knowledge of the epigenetic inactivation of different DNA repair components in human cancer.
MeSH term(s)	Animals ; DNA/genetics ; DNA Damage ; DNA Repair/genetics ; Epigenesis, Genetic ; Humans ; Neoplasms/genetics
Chemical Substances	DNA (9007-49-2)
Language	English
Publishing date	2011-01-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2500949-7
ISSN	1759-4685 ; 1674-2788
ISSN (online)	1759-4685
ISSN	1674-2788
DOI	10.1093/jmcb/mjq053
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Potent antitumor effects of cell-penetrating peptides targeting STAT3 axis.

Aftabizadeh, Maryam / Li, Yi-Jia / Zhao, Qianqian / Zhang, Chunyan / Ambaye, Nigus / Song, Jieun / Nagao, Toshikage / Lahtz, Christoph / Fakih, Marwan / Ann, David K / Yu, Hua / Herrmann, Andreas

JCI insight

2021 Volume 6, Issue 2

Abstract: To date, there are no inhibitors that directly and specifically target activated STAT3 and c-Myc in the clinic. Although peptide-based inhibitors can selectively block activated targets, their clinical usage is limited because of low cell penetration and/ ...

Abstract	To date, there are no inhibitors that directly and specifically target activated STAT3 and c-Myc in the clinic. Although peptide-based inhibitors can selectively block activated targets, their clinical usage is limited because of low cell penetration and/or serum stability. Here, we generated cell-penetrating acetylated (acet.) STAT3, c-Myc, and Gp130 targeting peptides by attaching phosphorothioated (PS) polymer backbone to peptides. The cell-penetrating peptides efficiently penetrated cells and inhibited activation of the intended targets and their downstream genes. Locally or systemically treating tumor-bearing mice with PS-acet.-STAT3 peptide at low concentrations effectively blocked STAT3 in vivo, resulting in significant antitumor effects in 2 human xenograft models. Moreover, PS-acet.-STAT3 peptide penetrated and activated splenic CD8+ T cells in vitro. Treating immune-competent mice bearing mouse melanoma with PS-acet.-STAT3 peptide inhibited STAT3 in tumor-infiltrating T cells, downregulating tumor-infiltrating CD4+ T regulatory cells while activating CD8+ T effector cells. Similarly, systemic injections of the cell-penetrating c-Myc and Gp130 peptides prevented pancreatic tumor growth and induced antitumor immune responses. Taken together, we have developed therapeutic peptides that effectively and specifically block challenging cancer targets, resulting in antitumor effects through both direct tumor cell killing and indirectly through antitumor immune responses.
MeSH term(s)	Acetylation ; Animals ; Antineoplastic Agents/chemistry ; Antineoplastic Agents/pharmacology ; Cell Line, Tumor ; Cell-Penetrating Peptides/chemistry ; Cell-Penetrating Peptides/pharmacology ; Cytokine Receptor gp130/chemistry ; Drug Design ; HCT116 Cells ; Humans ; Lymphocytes, Tumor-Infiltrating/drug effects ; Lymphocytes, Tumor-Infiltrating/immunology ; Melanoma, Experimental/drug therapy ; Melanoma, Experimental/immunology ; Melanoma, Experimental/metabolism ; Mice ; Mice, Inbred C57BL ; Pancreatic Neoplasms/drug therapy ; Peptide Fragments/chemistry ; Peptide Fragments/pharmacology ; Protein Multimerization ; Proto-Oncogene Proteins c-myc/chemistry ; Proto-Oncogene Proteins c-myc/pharmacology ; STAT3 Transcription Factor/antagonists & inhibitors ; STAT3 Transcription Factor/chemistry ; Xenograft Model Antitumor Assays
Chemical Substances	Antineoplastic Agents ; Cell-Penetrating Peptides ; MYC protein, human ; Peptide Fragments ; Proto-Oncogene Proteins c-myc ; STAT3 Transcription Factor ; STAT3 protein, human ; Stat3 protein, mouse ; Cytokine Receptor gp130 (133483-10-0)
Language	English
Publishing date	2021-01-25
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.136176
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: An effective cell-penetrating antibody delivery platform.

Herrmann, Andreas / Nagao, Toshikage / Zhang, Chunyan / Lahtz, Christoph / Li, Yi-Jia / Yue, Chanyu / Mülfarth, Ronja / Yu, Hua

JCI insight

2019 Volume 4, Issue 14

Abstract: Despite their well-recognized success in the clinic, antibodies generally do not penetrate cellular membranes to target intracellular molecules, many of which underlie incurable diseases. Here we show that covalently conjugating phosphorothioated DNA ... ...

Abstract	Despite their well-recognized success in the clinic, antibodies generally do not penetrate cellular membranes to target intracellular molecules, many of which underlie incurable diseases. Here we show that covalently conjugating phosphorothioated DNA oligonucleotides to antibodies enabled their efficient cellular internalization. Antibody cell penetration was partially mediated by membrane potential alteration. Moreover, without an antigen to bind, intracellular levels of the modified antibodies underwent cellular clearance, which involved efflux and lysosomal degradation, enabling detection of intended intracellular molecules as tested in fibroblasts, tumor cells, and T cells. This target-dependent cellular retention of modified antibodies extended to in vivo studies. Both local and systemic administrations of low doses of modified antibodies effectively inhibited intracellular targets, such as transcription factors Myc, interferon regulatory factor 4, and tyrosine-protein kinase SRC, and expression of their downstream genes in tumors, resulting in tumor cell apoptosis and tumor growth inhibition. This simple modification enables the use of antibodies to detect and modulate intracellular molecules in both cultured living cells and in whole animals, forming the foundation for a new paradigm for antibody-based research, diagnostics, and therapeutics.
MeSH term(s)	Animals ; Antibodies, Monoclonal/administration & dosage ; Antibodies, Monoclonal/chemistry ; Cell Line, Tumor ; Cell Membrane Permeability/drug effects ; Drug Delivery Systems/methods ; Humans ; Immunoconjugates/administration & dosage ; Immunoconjugates/chemistry ; Immunoconjugates/pharmacology ; Melanoma/drug therapy ; Melanoma/pathology ; Mice ; Oligodeoxyribonucleotides/chemistry ; Oligodeoxyribonucleotides/pharmacology ; Xenograft Model Antitumor Assays
Chemical Substances	Antibodies, Monoclonal ; Immunoconjugates ; Oligodeoxyribonucleotides
Language	English
Publishing date	2019-07-25
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.127474
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Potent antitumor effects of cell-penetrating peptides targeting STAT3 axis

Maryam Aftabizadeh / Yi-Jia Li / Qianqian Zhao / Chunyan Zhang / Nigus Ambaye / Jieun Song / Toshikage Nagao / Christoph Lahtz / Marwan Fakih / David K. Ann / Hua Yu / Andreas Herrmann

JCI Insight, Vol 6, Iss

2021 Volume 2

Abstract	To date, there are no inhibitors that directly and specifically target activated STAT3 and c-Myc in the clinic. Although peptide-based inhibitors can selectively block activated targets, their clinical usage is limited because of low cell penetration and/or serum stability. Here, we generated cell-penetrating acetylated (acet.) STAT3, c-Myc, and Gp130 targeting peptides by attaching phosphorothioated (PS) polymer backbone to peptides. The cell-penetrating peptides efficiently penetrated cells and inhibited activation of the intended targets and their downstream genes. Locally or systemically treating tumor-bearing mice with PS-acet.-STAT3 peptide at low concentrations effectively blocked STAT3 in vivo, resulting in significant antitumor effects in 2 human xenograft models. Moreover, PS-acet.-STAT3 peptide penetrated and activated splenic CD8+ T cells in vitro. Treating immune-competent mice bearing mouse melanoma with PS-acet.-STAT3 peptide inhibited STAT3 in tumor-infiltrating T cells, downregulating tumor-infiltrating CD4+ T regulatory cells while activating CD8+ T effector cells. Similarly, systemic injections of the cell-penetrating c-Myc and Gp130 peptides prevented pancreatic tumor growth and induced antitumor immune responses. Taken together, we have developed therapeutic peptides that effectively and specifically block challenging cancer targets, resulting in antitumor effects through both direct tumor cell killing and indirectly through antitumor immune responses.
Keywords	Oncology ; Therapeutics ; Medicine ; R
Language	English
Publishing date	2021-01-01T00:00:00Z
Publisher	American Society for Clinical investigation
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Integrin α6 signaling induces STAT3-TET3-mediated hydroxymethylation of genes critical for maintenance of glioma stem cells.

Herrmann, Andreas / Lahtz, Christoph / Song, Jieun / Aftabizadeh, Maryam / Cherryholmes, Gregory A / Xin, Hong / Adamus, Tomasz / Lee, Heehyoung / Grunert, David / Armstrong, Brian / Chu, Peiguo / Brown, Christine / Lim, Michael / Forman, Stephen / Yu, Hua

Oncogene

2019 Volume 39, Issue 10, Page(s) 2156–2169

Abstract: Both the extracellular matrix (ECM) and DNA epigenetic regulation are critical for maintaining stem cell phenotype and cancer progression. Whether and how ECM regulates epigenetic alterations to influence cancer stem cells (CSCs) remain to be explored. ... ...

Abstract	Both the extracellular matrix (ECM) and DNA epigenetic regulation are critical for maintaining stem cell phenotype and cancer progression. Whether and how ECM regulates epigenetic alterations to influence cancer stem cells (CSCs) remain to be explored. Here we report that ECM through laminin-integrin α6 upregulates ten-eleven translocation enzyme 3 (TET3) dioxygenase. TET3 in turn mediates DNA cytosine 5'-hydroxymethylation (5hmC) and upregulates genes critical for maintenance of glioma stem cells (GSCs). Activating integrin α6-FAK pathway increases STAT3 activity, TET3 expression and 5hmC levels in GSCs. Moreover, targeting STAT3 disrupts integrin α6-FAK signaling and inhibits TET3
MeSH term(s)	5-Methylcytosine ; Animals ; Cell Line ; DNA Methylation ; Dioxygenases/genetics ; Dioxygenases/metabolism ; Epigenesis, Genetic ; Female ; Gene Expression Regulation, Neoplastic ; Glioma/enzymology ; Glioma/genetics ; Glioma/metabolism ; Humans ; Integrin alpha6/metabolism ; Male ; Mice, Nude ; Neoplastic Stem Cells/enzymology ; Neoplastic Stem Cells/metabolism ; STAT3 Transcription Factor/metabolism ; Signal Transduction
Chemical Substances	Integrin alpha6 ; STAT3 Transcription Factor ; STAT3 protein, human ; 5-Methylcytosine (6R795CQT4H) ; TET3 protein, human (EC 1.-) ; Dioxygenases (EC 1.13.11.-)
Language	English
Publishing date	2019-12-09
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	639046-8
ISSN	1476-5594 ; 0950-9232
ISSN (online)	1476-5594
ISSN	0950-9232
DOI	10.1038/s41388-019-1134-6
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: UVB irradiation does not directly induce detectable changes of DNA methylation in human keratinocytes.

Lahtz, Christoph / Kim, Sang-In / Bates, Steven E / Li, Arthur X / Wu, Xiwei / Pfeifer, Gerd P

F1000Research

2013 Volume 2, Page(s) 45

Abstract: Unprotected exposure to UVB radiation from the sun and the resulting DNA damage are thought to be responsible for physiological changes in the skin and for a variety of skin cancers, including basal cell and squamous cell carcinoma and malignant melanoma. ...

Abstract	Unprotected exposure to UVB radiation from the sun and the resulting DNA damage are thought to be responsible for physiological changes in the skin and for a variety of skin cancers, including basal cell and squamous cell carcinoma and malignant melanoma. Although the mutagenic effects of UVB have been well documented and studied mechanistically, there is only limited information as to whether UV light may also be responsible for inducing epigenetic changes in the genome of exposed cells. DNA methylation is a stable epigenetic modification involved in gene control. To study the effects of UVB radiation on DNA methylation, we repeatedly exposed normal human keratinocytes to a UVB light source. After a recovery period, we analyzed global DNA methylation patterns in the irradiated and control cells using the methylated-CpG island recovery assay (MIRA) method in combination with high-resolution microarrays. Bioinformatics analysis revealed only a limited number of possible differences between UVB-exposed and control cells. However, these minor apparent changes could not be independently confirmed by bisulfite sequencing-based approaches. This study reveals that UVB irradiation of keratinocytes has no recognizable global effect on DNA methylation patterns and suggests that changes in DNA methylation, as observed in skin cancers, are not immediate consequences of human exposure to solar UVB irradiation.
Language	English
Publishing date	2013-02-13
Publishing country	England
Document type	Journal Article
ZDB-ID	2699932-8
ISSN	2046-1402
ISSN	2046-1402
DOI	10.12688/f1000research.2-45.v1
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Methylation of PTEN as a prognostic factor in malignant melanoma of the skin.

Lahtz, Christoph / Stranzenbach, René / Fiedler, Eckhard / Helmbold, Peter / Dammann, Reinhard H

The Journal of investigative dermatology

2010 Volume 130, Issue 2, Page(s) 620–622

MeSH term(s)	DNA Methylation ; Disease Progression ; Disease-Free Survival ; Epigenesis, Genetic ; Gene Expression Regulation, Neoplastic ; Humans ; Melanoma/diagnosis ; Melanoma/genetics ; Melanoma/metabolism ; Mutation ; PTEN Phosphohydrolase/genetics ; Point Mutation ; Prognosis ; Promoter Regions, Genetic ; Proportional Hazards Models ; Skin Neoplasms/diagnosis ; Skin Neoplasms/genetics ; Skin Neoplasms/metabolism
Chemical Substances	PTEN Phosphohydrolase (EC 3.1.3.67) ; PTEN protein, human (EC 3.1.3.67)
Language	English
Publishing date	2010-02
Publishing country	United States
Document type	Letter ; Research Support, Non-U.S. Gov't
ZDB-ID	80136-7
ISSN	1523-1747 ; 0022-202X
ISSN (online)	1523-1747
ISSN	0022-202X
DOI	10.1038/jid.2009.226
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: A Targeted Vaccine against COVID-19: S1-Fc Vaccine Targeting the Antigen-Presenting Cell Compartment Elicits Protection against SARS-CoV-2 Infection

bioRxiv

Abstract: Vaccination efficacy is enhanced by targeting the antigen-presenting cell compartment. Here, we show that S1-Fc antigen delivery targeting the FcγR+ antigen-presenting cell compartment elicits anti-SARS-CoV-2 S1-antigen specific IgG production in vivo ... ...

Abstract	Vaccination efficacy is enhanced by targeting the antigen-presenting cell compartment. Here, we show that S1-Fc antigen delivery targeting the FcγR+ antigen-presenting cell compartment elicits anti-SARS-CoV-2 S1-antigen specific IgG production in vivo exerting biologically functional and protective activity against live virus infection, assessed in a stringent experimental virus challenge assay in vitro. The S1-domain of the SARS-CoV-2 spike protein was genetically fused to a human immunoglobulin Fc moiety, which contributes to mediate S1-Fc cellular internalization by FcγR+ antigen-presenting cells. Immediately upon administration intramuscularly, our novel vaccine candidate recombinant rS1-Fc homes to lymph nodes in vivo where FcγR+ antigen-presenting cells reside. Seroconversion is achieved as early as day 7, mounting considerably increased levels of anti-S1 IgGs in vivo. Interestingly, immunization at elevated doses with non-expiring S1-Fc encoding dsDNA favors the education of a desired antigen-specific adaptive T cell response. However, low-dose immunization, safeguarding patient safety, using recombinant rS1-Fc, elicits a considerably elevated protection amplitude against live SARS-CoV-2 infection. Our promising findings on rS1-Fc protein immunization prompted us to further develop an affordable and safe product for delivery to our communities in need for COVID-19 vaccinations.
Keywords	covid19
Publisher	BioRxiv; WHO
Document type	Article ; Online
DOI	10.1101/2020.06.29.178616
Database	COVID19

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