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Book ; Conference proceedings: Proceedings from an International Symposium on Interferon-Alpha Therapy in Malignant Diseases

Aguet, Michel

held in Athens, 1 - 4 November 1990

(British journal of haematology ; 79, Suppl. 1)

1991

Title variant	Interferon-alpha therapy in malignant diseases
Event/congress	International Symposium on Interferon Alpha Therapy in Malignant Diseases (1990, Athen)
Author's details	ed. by M. Aguet
Series title	British journal of haematology ; 79, Suppl. 1
Collection
Keywords	Neoplasms / drug therapy / congresses ; Interferon-Alpha / therapeutic use / congresses
Language	English
Size	IV, 104 S. : Ill., graph. Darst.
Publisher	Blackwell Scientific
Publishing place	Oxford u.a.
Publishing country	Great Britain
Document type	Book ; Conference proceedings
HBZ-ID	HT003926926
Database	Catalogue ZB MED Medicine, Health

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Uh III Zs 182 -79,Suppl.1-	verfügbar in Königswinter	Königswinter

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Article ; Online: Cancer Metastasis: A Reappraisal of Its Underlying Mechanisms and Their Relevance to Treatment.

Riggi, Nicolo / Aguet, Michel / Stamenkovic, Ivan

Annual review of pathology

2017 Volume 13, Page(s) 117–140

Abstract: Metastases are responsible for the vast majority of cancer-related deaths, but, despite intense efforts to understand their underlying mechanisms with the goal of uncovering effective therapeutic targets, treatment of metastatic cancer has progressed ... ...

Abstract	Metastases are responsible for the vast majority of cancer-related deaths, but, despite intense efforts to understand their underlying mechanisms with the goal of uncovering effective therapeutic targets, treatment of metastatic cancer has progressed minimally. In this review, we examine the biological programs currently proposed to be key drivers of metastasis. On the basis of evidence from a growing body of research, we discuss to what extent the cellular and molecular mechanisms that are suggested to underlie cancer cell dissemination are specific to the metastatic process, as opposed to representing natural primary tumor progression. Our review highlights the contrast between the abundance of insight gained into the events that constitute the metastatic cascade and the paucity of therapeutic options.
MeSH term(s)	Humans ; Neoplasm Invasiveness/pathology ; Neoplasm Metastasis/pathology ; Neoplasms/pathology ; Neoplastic Stem Cells/pathology
Language	English
Publishing date	2017-10-25
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2227429-7
ISSN	1553-4014 ; 1553-4006
ISSN (online)	1553-4014
ISSN	1553-4006
DOI	10.1146/annurev-pathol-020117-044127
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Article ; Online: Epithelial Wnt secretion drives the progression of inflammation-induced colon carcinoma in murine model.

Degirmenci, Bahar / Dincer, Cansu / Demirel, Habibe Cansu / Berkova, Linda / Moor, Andreas E / Kahraman, Abdullah / Hausmann, George / Aguet, Michel / Tuncbag, Nurcan / Valenta, Tomas / Basler, Konrad

iScience

2021 Volume 24, Issue 12, Page(s) 103369

Abstract: Colon cancer is initiated by stem cells that escape the strict control. This process is often driven through aberrant activation of Wnt signaling by mutations in components acting downstream of the receptor complex that unfetter tumor cells from the need ...

Abstract	Colon cancer is initiated by stem cells that escape the strict control. This process is often driven through aberrant activation of Wnt signaling by mutations in components acting downstream of the receptor complex that unfetter tumor cells from the need for Wnts. Here we describe a class of colon cancer that does not depend on mutated core components of the Wnt pathway. Genetically blocking Wnt secretion from epithelial cells of such tumors results in apoptosis, reduced expression of colon cancer markers, followed by enhanced tumor differentiation. In contrast to the normal colonic epithelium, such tumor cells autosecrete Wnts to maintain their uncontrolled proliferative behavior. In humans, we determined certain cases of colon cancers in which the Wnt pathway is hyperactive, but not through mutations in its core components. Our findings illuminate the path in therapy to find further subtypes of Wnt-dependent colon cancer that might be responsive to Wnt secretion inhibitors.
Language	English
Publishing date	2021-10-28
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2021.103369
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Article ; Online: TBX3 acts as tissue-specific component of the Wnt/β-catenin transcriptional complex.

Zimmerli, Dario / Borrelli, Costanza / Jauregi-Miguel, Amaia / Söderholm, Simon / Brütsch, Salome / Doumpas, Nikolaos / Reichmuth, Jan / Murphy-Seiler, Fabienne / Aguet, MIchel / Basler, Konrad / Moor, Andreas E / Cantù, Claudio

eLife

2020 Volume 9

Abstract: BCL9 and PYGO are β-catenin cofactors that enhance the transcription of Wnt target genes. They have been proposed as therapeutic targets to diminish Wnt signaling output in intestinal malignancies. Here we find that, in colorectal cancer cells and in ... ...

Abstract	BCL9 and PYGO are β-catenin cofactors that enhance the transcription of Wnt target genes. They have been proposed as therapeutic targets to diminish Wnt signaling output in intestinal malignancies. Here we find that, in colorectal cancer cells and in developing mouse forelimbs, BCL9 proteins sustain the action of β-catenin in a largely PYGO-independent manner. Our genetic analyses implied that BCL9 necessitates other interaction partners in mediating its transcriptional output. We identified the transcription factor TBX3 as a candidate tissue-specific member of the β-catenin transcriptional complex. In developing forelimbs, both TBX3 and BCL9 occupy a large number of Wnt-responsive regulatory elements, genome-wide. Moreover, mutations in
MeSH term(s)	Animals ; Female ; HCT116 Cells ; Humans ; Male ; Mice ; Organ Specificity ; T-Box Domain Proteins/genetics ; T-Box Domain Proteins/metabolism ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Tumor Cells, Cultured ; Wnt Signaling Pathway ; Zebrafish
Chemical Substances	BCL9 protein, mouse ; T-Box Domain Proteins ; TBX3 protein, human ; Tbx3 protein, mouse ; Transcription Factors
Language	English
Publishing date	2020-08-18
Publishing country	England
Document type	Journal Article
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.58123
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Article ; Online: Pax6-dependent, but β-catenin-independent, function of Bcl9 proteins in mouse lens development.

Cantù, Claudio / Zimmerli, Dario / Hausmann, George / Valenta, Tomas / Moor, Andreas / Aguet, Michel / Basler, Konrad

Genes & development

2014 Volume 28, Issue 17, Page(s) 1879–1884

Abstract: Bcl9 and Bcl9l (Bcl9/9l) encode Wnt signaling components that mediate the interaction between β-catenin and Pygopus (Pygo) via two evolutionarily conserved domains, HD1 and HD2, respectively. We generated mouse strains lacking these domains to probe the ... ...

Abstract	Bcl9 and Bcl9l (Bcl9/9l) encode Wnt signaling components that mediate the interaction between β-catenin and Pygopus (Pygo) via two evolutionarily conserved domains, HD1 and HD2, respectively. We generated mouse strains lacking these domains to probe the β-catenin-dependent and β-catenin-independent roles of Bcl9/9l and Pygo during mouse development. While lens development is critically dependent on the presence of the HD1 domain, it is not affected by the lack of the HD2 domain, indicating that Bcl9/9l act in this context in a β-catenin-independent manner. Furthermore, we uncover a new regulatory circuit in which Pax6, the master regulator of eye development, directly activates Bcl9/9l transcription.
MeSH term(s)	Animals ; Cells, Cultured ; Eye Proteins/genetics ; Eye Proteins/metabolism ; Gene Expression Regulation, Developmental ; Gene Knock-In Techniques ; Homeodomain Proteins/genetics ; Homeodomain Proteins/metabolism ; Intracellular Signaling Peptides and Proteins/metabolism ; Lens, Crystalline/embryology ; Mice ; Mice, Inbred C57BL ; Neoplasm Proteins/genetics ; Neoplasm Proteins/metabolism ; PAX6 Transcription Factor ; Paired Box Transcription Factors/genetics ; Paired Box Transcription Factors/metabolism ; Protein Structure, Tertiary/genetics ; Repressor Proteins/genetics ; Repressor Proteins/metabolism ; Signal Transduction ; Transcription Factors/metabolism ; Wnt Proteins/metabolism ; beta Catenin/genetics ; beta Catenin/metabolism
Chemical Substances	BCL9 protein, human ; BCL9L protein, mouse ; Eye Proteins ; Homeodomain Proteins ; Intracellular Signaling Peptides and Proteins ; Neoplasm Proteins ; PAX6 Transcription Factor ; PAX6 protein, human ; Paired Box Transcription Factors ; Pax6 protein, mouse ; Repressor Proteins ; Transcription Factors ; Wnt Proteins ; beta Catenin ; pygopus 2 protein, mouse
Language	English
Publishing date	2014-09-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	806684-x
ISSN	1549-5477 ; 0890-9369
ISSN (online)	1549-5477
ISSN	0890-9369
DOI	10.1101/gad.246140.114
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Article ; Online: Epithelial Wnt secretion drives the progression of inflammation-induced colon carcinoma in murine model

Degirmenci, Bahar / Dincer, Cansu / Demirel, Habibe Cansu / Berkova, Linda / Moor, Andreas E. / Kahraman, Abdullah / Hausmann, George / Aguet, Michel / Tuncbag, Nurcan / Valenta, Tomas / Basler, Konrad

iScience, 24 (12)

2021

Abstract	Colon cancer is initiated by stem cells that escape the strict control. This process is often driven through aberrant activation of Wnt signaling by mutations in components acting downstream of the receptor complex that unfetter tumor cells from the need for Wnts. Here we describe a class of colon cancer that does not depend on mutated core components of the Wnt pathway. Genetically blocking Wnt secretion from epithelial cells of such tumors results in apoptosis, reduced expression of colon cancer markers, followed by enhanced tumor differentiation. In contrast to the normal colonic epithelium, such tumor cells autosecrete Wnts to maintain their uncontrolled proliferative behavior. In humans, we determined certain cases of colon cancers in which the Wnt pathway is hyperactive, but not through mutations in its core components. Our findings illuminate the path in therapy to find further subtypes of Wnt-dependent colon cancer that might be responsive to Wnt secretion inhibitors. ISSN:2589-0042
Keywords	Molecular physiology ; Immunology ; Cell biology ; Cancer ; Omics
Subject code	570
Language	English
Publishing date	2021-12-17
Publisher	Elsevier
Publishing country	ch
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: The Pygo2-H3K4me2/3 interaction is dispensable for mouse development and Wnt signaling-dependent transcription.

Cantù, Claudio / Valenta, Tomas / Hausmann, George / Vilain, Nathalie / Aguet, Michel / Basler, Konrad

Development (Cambridge, England)

2013 Volume 140, Issue 11, Page(s) 2377–2386

Abstract: Pygopus has been discovered as a fundamental Wnt signaling component in Drosophila. The mouse genome encodes two Pygopus homologs, Pygo1 and Pygo2. They serve as context-dependent β-catenin coactivators, with Pygo2 playing the more important role. All ... ...

Abstract	Pygopus has been discovered as a fundamental Wnt signaling component in Drosophila. The mouse genome encodes two Pygopus homologs, Pygo1 and Pygo2. They serve as context-dependent β-catenin coactivators, with Pygo2 playing the more important role. All Pygo proteins share a highly conserved plant homology domain (PHD) that allows them to bind di- and trimethylated lysine 4 of histone H3 (H3K4me2/3). Despite the structural conservation of this domain, the relevance of histone binding for the role of Pygo2 as a Wnt signaling component and as a reader of chromatin modifications remains speculative. Here we generate a knock-in mouse line, homozygous for a Pygo2 mutant defective in chromatin binding. We show that even in the absence of the potentially redundant Pygo1, Pygo2 does not require the H3K4me2/3 binding activity to sustain its function during mouse development. Indeed, during tissue homeostasis, Wnt/β-catenin-dependent transcription is largely unaffected. However, the Pygo2-chromatin interaction is relevant in testes, where, importantly, Pygo2 binds in vivo to the chromatin in a PHD-dependent manner. Its presence on regulatory regions does not affect the transcription of nearby genes; rather, it is important for the recruitment of the histone acetyltransferase Gcn5 to chromatin, consistent with a testis-specific and Wnt-unrelated role for Pygo2 as a chromatin remodeler.
MeSH term(s)	Animals ; Chromatin Assembly and Disassembly ; Drosophila Proteins/genetics ; Drosophila Proteins/metabolism ; Drosophila melanogaster/genetics ; Drosophila melanogaster/physiology ; Female ; Fertility ; Gene Expression Regulation, Developmental ; Gene Knock-In Techniques ; Genotype ; Histones/metabolism ; Intracellular Signaling Peptides and Proteins/genetics ; Intracellular Signaling Peptides and Proteins/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Protein Interaction Domains and Motifs ; Testis/metabolism ; Wnt Signaling Pathway ; p300-CBP Transcription Factors/metabolism
Chemical Substances	Drosophila Proteins ; Histones ; Intracellular Signaling Peptides and Proteins ; pygo protein, Drosophila ; pygopus 2 protein, mouse ; p300-CBP Transcription Factors (EC 2.3.1.48) ; p300-CBP-associated factor (EC 2.3.1.48)
Language	English
Publishing date	2013-05-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	90607-4
ISSN	1477-9129 ; 0950-1991
ISSN (online)	1477-9129
ISSN	0950-1991
DOI	10.1242/dev.093591
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Ub I Zs.183: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Mutations in

Cantù, Claudio / Felker, Anastasia / Zimmerli, Dario / Prummel, Karin D / Cabello, Elena M / Chiavacci, Elena / Méndez-Acevedo, Kevin M / Kirchgeorg, Lucia / Burger, Sibylle / Ripoll, Jorge / Valenta, Tomas / Hausmann, George / Vilain, Nathalie / Aguet, Michel / Burger, Alexa / Panáková, Daniela / Basler, Konrad / Mosimann, Christian

Genes & development

2018 Volume 32, Issue 21-22, Page(s) 1443–1458

Abstract: Bcl9 and Pygopus (Pygo) are obligate Wnt/β-catenin cofactors ... ...

Abstract	Bcl9 and Pygopus (Pygo) are obligate Wnt/β-catenin cofactors in
MeSH term(s)	Adaptor Proteins, Signal Transducing ; Animals ; Heart/embryology ; Heart Defects, Congenital/genetics ; Intracellular Signaling Peptides and Proteins/genetics ; Mice ; Mutation ; Myocardium/metabolism ; Transcription Factors/genetics ; Wnt Signaling Pathway ; Zebrafish/embryology ; Zebrafish/genetics ; Zebrafish Proteins/genetics ; beta Catenin/metabolism
Chemical Substances	Adaptor Proteins, Signal Transducing ; BCL9 protein, mouse ; BCL9L protein, mouse ; Intracellular Signaling Peptides and Proteins ; Pygo1 protein, mouse ; Transcription Factors ; Zebrafish Proteins ; beta Catenin ; pygopus 2 protein, mouse
Language	English
Publishing date	2018-10-26
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	806684-x
ISSN	1549-5477 ; 0890-9369
ISSN (online)	1549-5477
ISSN	0890-9369
DOI	10.1101/gad.315531.118
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Article ; Online: Wnt Ligands Secreted by Subepithelial Mesenchymal Cells Are Essential for the Survival of Intestinal Stem Cells and Gut Homeostasis.

Valenta, Tomas / Degirmenci, Bahar / Moor, Andreas E / Herr, Patrick / Zimmerli, Dario / Moor, Matthias B / Hausmann, George / Cantù, Claudio / Aguet, Michel / Basler, Konrad

Cell reports

2016 Volume 15, Issue 5, Page(s) 911–918

Abstract: Targeting of Wnt signaling represents a promising anti-cancer therapy. However, the consequences of systemically attenuating the Wnt pathway in an adult organism are unknown. Here, we globally prevent Wnt secretion by genetically ablating Wntless. We ... ...

Abstract	Targeting of Wnt signaling represents a promising anti-cancer therapy. However, the consequences of systemically attenuating the Wnt pathway in an adult organism are unknown. Here, we globally prevent Wnt secretion by genetically ablating Wntless. We find that preventing Wnt signaling in the entire body causes mortality due to impaired intestinal homeostasis. This is caused by the loss of intestinal stem cells. Reconstitution of Wnt/β-catenin signaling via delivery of external Wnt ligands prolongs the survival of intestinal stem cells and reveals the essential role of extra-epithelial Wnt ligands for the renewal of the intestinal epithelium. Wnt2b is a key extra-epithelial Wnt ligand capable of promoting Wnt/β-catenin signaling and intestinal homeostasis. Wnt2b is secreted by subepithelial mesenchymal cells that co-express either Gli1 or Acta2. Subepithelial mesenchymal cells expressing high levels of Wnt2b are predominantly Gli1 positive.
MeSH term(s)	Animals ; Cell Self Renewal ; Cell Survival ; Epithelial Cells/secretion ; Homeostasis ; Intestinal Mucosa/cytology ; Ligands ; Mesenchymal Stromal Cells/secretion ; Mice ; Wnt Proteins/metabolism ; beta Catenin/metabolism
Chemical Substances	Ligands ; Wnt Proteins ; beta Catenin
Language	English
Publishing date	2016--03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2016.03.088
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Article ; Online: The fusion protein SS18-SSX1 employs core Wnt pathway transcription factors to induce a partial Wnt signature in synovial sarcoma.

Cironi, Luisa / Petricevic, Tanja / Fernandes Vieira, Victor / Provero, Paolo / Fusco, Carlo / Cornaz, Sandrine / Fregni, Giulia / Letovanec, Igor / Aguet, Michel / Stamenkovic, Ivan

Scientific reports

2016 Volume 6, Page(s) 22113

Abstract: Expression of the SS18/SYT-SSX fusion protein is believed to underlie the pathogenesis of synovial sarcoma (SS). Recent evidence suggests that deregulation of the Wnt pathway may play an important role in SS but the mechanisms whereby SS18-SSX might ... ...

Abstract	Expression of the SS18/SYT-SSX fusion protein is believed to underlie the pathogenesis of synovial sarcoma (SS). Recent evidence suggests that deregulation of the Wnt pathway may play an important role in SS but the mechanisms whereby SS18-SSX might affect Wnt signaling remain to be elucidated. Here, we show that SS18/SSX tightly regulates the elevated expression of the key Wnt target AXIN2 in primary SS. SS18-SSX is shown to interact with TCF/LEF, TLE and HDAC but not β-catenin in vivo and to induce Wnt target gene expression by forming a complex containing promoter-bound TCF/LEF and HDAC but lacking β-catenin. Our observations provide a tumor-specific mechanistic basis for Wnt target gene induction in SS that can occur in the absence of Wnt ligand stimulation.
MeSH term(s)	Animals ; Axin Protein/genetics ; Axin Protein/metabolism ; Blotting, Western ; Cell Line ; Cell Line, Tumor ; Gene Expression Profiling/methods ; Histone Deacetylases/genetics ; Histone Deacetylases/metabolism ; Humans ; Mice ; Microscopy, Confocal ; Oncogene Proteins, Fusion/genetics ; Oncogene Proteins, Fusion/metabolism ; RNA Interference ; Repressor Proteins/genetics ; Repressor Proteins/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Sarcoma, Synovial/genetics ; Sarcoma, Synovial/metabolism ; Sarcoma, Synovial/pathology ; TCF Transcription Factors/genetics ; TCF Transcription Factors/metabolism ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Wnt Signaling Pathway/genetics ; beta Catenin/genetics ; beta Catenin/metabolism
Chemical Substances	AXIN2 protein, human ; Axin Protein ; Oncogene Proteins, Fusion ; Repressor Proteins ; SS18-SSX1 fusion protein ; TCF Transcription Factors ; TLE1 protein, human ; Transcription Factors ; beta Catenin ; Histone Deacetylases (EC 3.5.1.98)
Language	English
Publishing date	2016-02-24
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/srep22113
Database	MEDical Literature Analysis and Retrieval System OnLINE

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