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Article ; Online: Too much to handle - how gaining chromosomes destabilizes the genome.

Passerini, Verena / Storchová, Zuzana

2016 Volume 15, Issue 21, Page(s) 2867–2874

Abstract: Most eukaryotic organisms are diploid, with 2 chromosome sets in their nuclei. Whole chromosomal aneuploidy, a deviation from multiples of the haploid chromosome number, arises from chromosome segregation errors and often has detrimental consequences for ...

Abstract	Most eukaryotic organisms are diploid, with 2 chromosome sets in their nuclei. Whole chromosomal aneuploidy, a deviation from multiples of the haploid chromosome number, arises from chromosome segregation errors and often has detrimental consequences for cells. In humans, numerical aneuploidy severely impairs embryonic development and the rare survivors develop disorders characterized by multiple pathologies. Moreover, as many as 75 % of malignant tumors display aneuploidy. Although the exact contribution of aneuploidy to tumorigenesis remains unclear, previous studies have suggested that aneuploidy may affect the maintenance of genome integrity. We found that human cells with extra chromosomes showed phenotypes suggestive of replication defects, a phenomenon which we went on to characterize as being due to the aneuploidy-driven downregulation of replication factors, in particular of the replicative helicase MCM2-7. Thus, missegregation of even a single chromosome can further promote genomic instability and thereby contribute to tumor development. In this review we will examine the possible causes of downregulation of replicative factors and discuss the consequences of genomic instability in aneuploid cells.
MeSH term(s)	Aneuploidy ; Chromosome Aberrations ; DNA Replication ; Genomic Instability ; Humans ; Models, Biological ; Neoplasms/genetics
Language	English
Publishing date	2016-09-16
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2146183-1
ISSN	1551-4005 ; 1538-4101 ; 1554-8627
ISSN (online)	1551-4005
ISSN	1538-4101 ; 1554-8627
DOI	10.1080/15384101.2016.1231285
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Article ; Online: Loss of CREBBP and KMT2D cooperate to accelerate lymphomagenesis and shape the lymphoma immune microenvironment.

Nature communications

2024 Volume 15, Issue 1, Page(s) 2879

Abstract: Despite regulating overlapping gene enhancers and pathways, CREBBP and KMT2D mutations recurrently co-occur in germinal center (GC) B cell-derived lymphomas, suggesting potential oncogenic cooperation. Herein, we report that combined haploinsufficiency ... ...

Abstract	Despite regulating overlapping gene enhancers and pathways, CREBBP and KMT2D mutations recurrently co-occur in germinal center (GC) B cell-derived lymphomas, suggesting potential oncogenic cooperation. Herein, we report that combined haploinsufficiency of Crebbp and Kmt2d induces a more severe mouse lymphoma phenotype (vs either allele alone) and unexpectedly confers an immune evasive microenvironment manifesting as CD8
MeSH term(s)	Animals ; Mice ; B-Lymphocytes/metabolism ; Chromatin/genetics ; Chromatin/metabolism ; Germinal Center/metabolism ; Lymphoma, Large B-Cell, Diffuse/genetics ; Mutation ; Tumor Microenvironment/genetics
Chemical Substances	Chromatin ; Kmt2d protein, mouse (EC 2.1.1.43) ; Crebbp protein, mouse (EC 2.3.1.48)
Language	English
Publishing date	2024-04-03
Publishing country	England
Document type	Journal Article
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-024-47012-1
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Article ; Online: Multimodal and spatially resolved profiling identifies distinct patterns of T cell infiltration in nodal B cell lymphoma entities.

Roider, Tobias / Baertsch, Marc A / Fitzgerald, Donnacha / Vöhringer, Harald / Brinkmann, Berit J / Czernilofsky, Felix / Knoll, Mareike / Llaó-Cid, Laura / Mathioudaki, Anna / Faßbender, Bianca / Herbon, Maxime / Lautwein, Tobias / Bruch, Peter-Martin / Liebers, Nora / Schürch, Christian M / Passerini, Verena / Seifert, Marc / Brobeil, Alexander / Mechtersheimer, Gunhild /

Müller-Tidow, Carsten / Weigert, Oliver / Seiffert, Martina / Nolan, Garry P / Huber, Wolfgang / Dietrich, Sascha

Nature cell biology

2024 Volume 26, Issue 3, Page(s) 478–489

Abstract: The redirection of T cells has emerged as an attractive therapeutic principle in B cell non-Hodgkin lymphoma (B-NHL). However, a detailed characterization of lymphoma-infiltrating T cells across B-NHL entities is missing. Here we present an in-depth T ... ...

Abstract	The redirection of T cells has emerged as an attractive therapeutic principle in B cell non-Hodgkin lymphoma (B-NHL). However, a detailed characterization of lymphoma-infiltrating T cells across B-NHL entities is missing. Here we present an in-depth T cell reference map of nodal B-NHL, based on cellular indexing of transcriptomes and epitopes, T cell receptor sequencing, flow cytometry and multiplexed immunofluorescence applied to 101 lymph nodes from patients with diffuse large B cell, mantle cell, follicular or marginal zone lymphoma, and from healthy controls. This multimodal resource revealed quantitative and spatial aberrations of the T cell microenvironment across and within B-NHL entities. Quantitative differences in PD1
MeSH term(s)	Humans ; T-Lymphocytes/pathology ; B-Lymphocytes/pathology ; Lymphoma, B-Cell, Marginal Zone/pathology ; Transforming Growth Factor beta ; Tumor Microenvironment
Chemical Substances	Transforming Growth Factor beta
Language	English
Publishing date	2024-02-20
Publishing country	England
Document type	Journal Article
ZDB-ID	1474722-4
ISSN	1476-4679 ; 1465-7392
ISSN (online)	1476-4679
ISSN	1465-7392
DOI	10.1038/s41556-024-01358-2
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Zs.A 5169: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Book ; Online ; Thesis: Aneuploidy triggers a conserved global response and impairs cellular homeostasis

Passerini, Verena [Verfasser] / Jentsch, Stefan [Akademischer Betreuer]

2016

Author's details	Verena Passerini ; Betreuer: Stefan Jentsch
Keywords	Biowissenschaften, Biologie ; Life Science, Biology
Subject code	sg570
Language	English
Publisher	Universitätsbibliothek der Ludwig-Maximilians-Universität
Publishing place	München
Document type	Book ; Online ; Thesis
Database	Digital theses on the web

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Article ; Online: Novel insights into the pathogenesis of follicular lymphoma by molecular profiling of localized and systemic disease forms.

Kalmbach, Sabrina / Grau, Michael / Zapukhlyak, Myroslav / Leich, Ellen / Jurinovic, Vindi / Hoster, Eva / Staiger, Annette M / Kurz, Katrin S / Weigert, Oliver / Gaitzsch, Erik / Passerini, Verena / Engelhard, Marianne / Herfarth, Klaus / Beiske, Klaus / Micci, Francesca / Möller, Peter / Bernd, Heinz-Wolfram / Feller, Alfred C / Klapper, Wolfram /

Stein, Harald / Hansmann, Martin-Leo / Hartmann, Sylvia / Dreyling, Martin / Holte, Harald / Lenz, Georg / Rosenwald, Andreas / Ott, German / Horn, Heike

Leukemia

2023 Volume 37, Issue 10, Page(s) 2058–2065

Abstract: Knowledge on the pathogenesis of FL is mainly based on data derived from advanced/systemic stages of FL (sFL) and only small cohorts of localized FL (lFL) have been characterized intensively so far. Comprehensive analysis with profiling of somatic copy ... ...

Abstract	Knowledge on the pathogenesis of FL is mainly based on data derived from advanced/systemic stages of FL (sFL) and only small cohorts of localized FL (lFL) have been characterized intensively so far. Comprehensive analysis with profiling of somatic copy number alterations (SCNA) and whole exome sequencing (WES) was performed in 147 lFL and 122 sFL. Putative targets were analyzed for gene and protein expression. Overall, lFL and sFL, as well as BCL2 translocation-positive (BCL2+) and -negative (BCL2-) FL showed overlapping features in SCNA and mutational profiles. Significant differences between lFL and sFL, however, were detected for SCNA frequencies, e.g., in 18q-gains (14% lFL vs. 36% sFL; p = 0.0003). Although rare in lFL, gains in 18q21 were associated with inferior progression-free survival (PFS). The mutational landscape of lFL and sFL included typical genetic lesions. However, ARID1A mutations were significantly more often detected in sFL (29%) compared to lFL (6%, p = 0.0001). In BCL2 + FL mutations in KMT2D, BCL2, ABL2, IGLL5 and ARID1A were enriched, while STAT6 mutations more frequently occurred in BCL2- FL. Although the landscape of lFL and sFL showed overlapping features, molecular profiling revealed novel insights and identified gains in 18q21 as prognostic marker in lFL.
MeSH term(s)	Humans ; Lymphoma, Follicular/genetics ; Lymphoma, Follicular/metabolism ; Translocation, Genetic ; Proto-Oncogene Proteins c-bcl-2/genetics ; Proto-Oncogene Proteins c-bcl-2/metabolism ; Mutation ; In Situ Hybridization, Fluorescence
Chemical Substances	Proto-Oncogene Proteins c-bcl-2
Language	English
Publishing date	2023-08-10
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	807030-1
ISSN	1476-5551 ; 0887-6924
ISSN (online)	1476-5551
ISSN	0887-6924
DOI	10.1038/s41375-023-01995-w
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Article ; Online: HSF1 deficiency and impaired HSP90-dependent protein folding are hallmarks of aneuploid human cells.

Donnelly, Neysan / Passerini, Verena / Dürrbaum, Milena / Stingele, Silvia / Storchová, Zuzana

The EMBO journal

2014 Volume 33, Issue 20, Page(s) 2374–2387

Abstract: Aneuploidy is a hallmark of cancer and is associated with malignancy and poor prognosis. Recent studies have revealed that aneuploidy inhibits proliferation, causes distinct alterations in the transcriptome and proteome and disturbs cellular proteostasis. ...

Abstract	Aneuploidy is a hallmark of cancer and is associated with malignancy and poor prognosis. Recent studies have revealed that aneuploidy inhibits proliferation, causes distinct alterations in the transcriptome and proteome and disturbs cellular proteostasis. However, the molecular mechanisms underlying the changes in gene expression and the impairment of proteostasis are not understood. Here, we report that human aneuploid cells are impaired in HSP90-mediated protein folding. We show that aneuploidy impairs induction of the heat shock response suggesting that the activity of the transcription factor heat shock factor 1 (HSF1) is compromised. Indeed, increased levels of HSF1 counteract the effects of aneuploidy on HSP90 expression and protein folding, identifying HSF1 overexpression as the first aneuploidy-tolerating mutation in human cells. Thus, impaired HSF1 activity emerges as a critical factor underlying the phenotypes linked to aneuploidy. Finally, we demonstrate that deficient protein folding capacity directly shapes gene expression in aneuploid cells. Our study provides mechanistic insight into the causes of the disturbed proteostasis in aneuploids and deepens our understanding of the role of HSF1 in cytoprotection and carcinogenesis.
MeSH term(s)	Aneuploidy ; Cell Line ; Cell Survival ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Gene Expression ; Gene Expression Regulation ; HSP90 Heat-Shock Proteins/genetics ; HSP90 Heat-Shock Proteins/metabolism ; Heat Shock Transcription Factors ; Heat-Shock Response/genetics ; Humans ; Mutation ; Phenotype ; Promoter Regions, Genetic/genetics ; Proteasome Endopeptidase Complex ; Protein Folding ; Proteome ; Proteostasis Deficiencies ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Transcriptome
Chemical Substances	DNA-Binding Proteins ; HSF1 protein, human ; HSP90 Heat-Shock Proteins ; Heat Shock Transcription Factors ; Proteome ; Transcription Factors ; Proteasome Endopeptidase Complex (EC 3.4.25.1)
Language	English
Publishing date	2014-09-09
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	586044-1
ISSN	1460-2075 ; 0261-4189
ISSN (online)	1460-2075
ISSN	0261-4189
DOI	10.15252/embj.201488648
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Zs.A 1808: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: PARP14 is a novel target in STAT6 mutant follicular lymphoma.

Mentz, Michael / Keay, William / Strobl, Carolin Dorothea / Antoniolli, Martina / Adolph, Louisa / Heide, Michael / Lechner, Axel / Haebe, Sarah / Osterode, Elisa / Kridel, Robert / Ziegenhain, Christoph / Wange, Lucas Esteban / Hildebrand, Johannes Adrian / Shree, Tanaya / Silkenstedt, Elisabeth / Staiger, Annette M / Ott, German / Horn, Heike / Szczepanowski, Monika /

Richter, Julia / Levy, Ronald / Rosenwald, Andreas / Enard, Wolfgang / Zimber-Strobl, Ursula / von Bergwelt-Baildon, Michael / Hiddemann, Wolfgang / Klapper, Wolfram / Schmidt-Supprian, Marc / Rudelius, Martina / Bararia, Deepak / Passerini, Verena / Weigert, Oliver

Leukemia

2022 Volume 36, Issue 9, Page(s) 2281–2292

Abstract: The variable clinical course of follicular lymphoma (FL) is determined by the molecular heterogeneity of tumor cells and complex interactions within the tumor microenvironment (TME). IL-4 producing follicular helper T cells ( ... ...

Abstract	The variable clinical course of follicular lymphoma (FL) is determined by the molecular heterogeneity of tumor cells and complex interactions within the tumor microenvironment (TME). IL-4 producing follicular helper T cells (T
MeSH term(s)	Humans ; Immunohistochemistry ; Interleukin-4 ; Lymphoma, B-Cell ; Lymphoma, Follicular ; Poly(ADP-ribose) Polymerases ; STAT6 Transcription Factor ; Transcriptional Activation ; Tumor Microenvironment
Chemical Substances	STAT6 Transcription Factor ; STAT6 protein, human ; Interleukin-4 (207137-56-2) ; PARP14 protein, human (EC 2.4.2.30) ; Poly(ADP-ribose) Polymerases (EC 2.4.2.30)
Language	English
Publishing date	2022-07-18
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	807030-1
ISSN	1476-5551 ; 0887-6924
ISSN (online)	1476-5551
ISSN	0887-6924
DOI	10.1038/s41375-022-01641-x
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Article ; Online: Unique features of the transcriptional response to model aneuploidy in human cells.

Dürrbaum, Milena / Kuznetsova, Anastasia Yurievna / Passerini, Verena / Stingele, Silvia / Stoehr, Gabriele / Storchová, Zuzana

BMC genomics

2014 Volume 15, Page(s) 139

Abstract: Background: Aneuploidy, a karyotype deviating from multiples of a haploid chromosome set, affects the physiology of eukaryotes. In humans, aneuploidy is linked to pathological defects such as developmental abnormalities, mental retardation or cancer, ... ...

Abstract	Background: Aneuploidy, a karyotype deviating from multiples of a haploid chromosome set, affects the physiology of eukaryotes. In humans, aneuploidy is linked to pathological defects such as developmental abnormalities, mental retardation or cancer, but the underlying mechanisms remain elusive. There are many different types and origins of aneuploidy, but whether there is a uniform cellular response to aneuploidy in human cells has not been addressed so far. Results: Here we evaluate the transcription profiles of eleven trisomic and tetrasomic cell lines and two cell lines with complex aneuploid karyotypes. We identify a characteristic aneuploidy response pattern defined by upregulation of genes linked to endoplasmic reticulum, Golgi apparatus and lysosomes, and downregulation of DNA replication, transcription as well as ribosomes. Strikingly, complex aneuploidy elicits the same transcriptional changes as trisomy. To uncover the triggers of the response, we compared the profiles with transcription changes in human cells subjected to stress conditions. Interestingly, we found an overlap only with the response to treatment with the autophagy inhibitor bafilomycin A1. Finally, we identified 23 genes whose expression is significantly altered in all aneuploids and which may thus serve as aneuploidy markers. Conclusions: Our analysis shows that despite the variability in chromosome content, aneuploidy triggers uniform transcriptional response in human cells. A common response independent of the type of aneuploidy might be exploited as a novel target for cancer therapy. Moreover, the potential aneuploidy markers identified in our analysis might represent novel biomarkers to assess the malignant potential of a tumor.
MeSH term(s)	Aneuploidy ; Genetic Markers ; HCT116 Cells ; Humans ; Karyotype ; Models, Genetic ; RNA, Messenger/metabolism ; Tetrasomy ; Trisomy
Chemical Substances	Genetic Markers ; RNA, Messenger
Language	English
Publishing date	2014-02-18
Publishing country	England
Document type	Journal Article
ISSN	1471-2164
ISSN (online)	1471-2164
DOI	10.1186/1471-2164-15-139
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Article ; Online: The presence of extra chromosomes leads to genomic instability

Verena Passerini / Efrat Ozeri-Galai / Mirjam S. de Pagter / Neysan Donnelly / Sarah Schmalbrock / Wigard P. Kloosterman / Batsheva Kerem / Zuzana Storchová

Nature Communications, Vol 7, Iss 1, Pp 1-

2016 Volume 12

Abstract: One of the hallmarks of cancer cells is aneuploidy, however the molecular effects are poorly understood. Here the authors show that trisomic and tetrasomic cells display increased genomic instability and reduced levels of the helicase MCM2-7. ...

Abstract	One of the hallmarks of cancer cells is aneuploidy, however the molecular effects are poorly understood. Here the authors show that trisomic and tetrasomic cells display increased genomic instability and reduced levels of the helicase MCM2-7.
Keywords	Science ; Q
Language	English
Publishing date	2016-02-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: The presence of extra chromosomes leads to genomic instability.

Passerini, Verena / Ozeri-Galai, Efrat / de Pagter, Mirjam S / Donnelly, Neysan / Schmalbrock, Sarah / Kloosterman, Wigard P / Kerem, Batsheva / Storchová, Zuzana

Nature communications

2016 Volume 7, Page(s) 10754

Abstract: Aneuploidy is a hallmark of cancer and underlies genetic disorders characterized by severe developmental defects, yet the molecular mechanisms explaining its effects on cellular physiology remain elusive. Here we show, using a series of human cells with ... ...

Abstract	Aneuploidy is a hallmark of cancer and underlies genetic disorders characterized by severe developmental defects, yet the molecular mechanisms explaining its effects on cellular physiology remain elusive. Here we show, using a series of human cells with defined aneuploid karyotypes, that gain of a single chromosome increases genomic instability. Next-generation sequencing and SNP-array analysis reveal accumulation of chromosomal rearrangements in aneuploids, with break point junction patterns suggestive of replication defects. Trisomic and tetrasomic cells also show increased DNA damage and sensitivity to replication stress. Strikingly, we find that aneuploidy-induced genomic instability can be explained by the reduced expression of the replicative helicase MCM2-7. Accordingly, restoring near-wild-type levels of chromatin-bound MCM helicase partly rescues the genomic instability phenotypes. Thus, gain of chromosomes triggers replication stress, thereby promoting genomic instability and possibly contributing to tumorigenesis.
MeSH term(s)	Aneuploidy ; Cell Cycle/genetics ; Cell Line ; Chromosomes, Human, Pair 21/genetics ; Chromosomes, Human, Pair 3/genetics ; Chromosomes, Human, Pair 5/genetics ; Chromosomes, Human, Pair 8/genetics ; Comparative Genomic Hybridization ; DNA/biosynthesis ; Fluorescent Antibody Technique ; Genomic Instability/genetics ; HCT116 Cells ; High-Throughput Nucleotide Sequencing ; Humans ; Metaphase/genetics ; Microscopy, Confocal ; Minichromosome Maintenance Proteins/metabolism ; Neoplasms/genetics ; Oligonucleotide Array Sequence Analysis ; Polymorphism, Single Nucleotide ; Sequence Analysis, DNA ; Tetrasomy/genetics ; Trisomy/genetics
Chemical Substances	DNA (9007-49-2) ; Minichromosome Maintenance Proteins (EC 3.6.4.12)
Language	English
Publishing date	2016-02-15
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2041-1723
ISSN (online)	2041-1723
DOI	10.1038/ncomms10754
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