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Article ; Online: Characterizing chromosomal instability-driven cancer evolution and cell fitness at a glance.

Tijhuis, Andréa E / Foijer, Floris

2024 Volume 137, Issue 1

Abstract: Chromosomal instability (CIN), an increased rate of chromosome segregation errors during mitosis, is a hallmark of cancer cells. CIN leads to karyotype differences between cells and thus large-scale heterogeneity among individual cancer cells; therefore, ...

Abstract	Chromosomal instability (CIN), an increased rate of chromosome segregation errors during mitosis, is a hallmark of cancer cells. CIN leads to karyotype differences between cells and thus large-scale heterogeneity among individual cancer cells; therefore, it plays an important role in cancer evolution. Studying CIN and its consequences is technically challenging, but various technologies have been developed to track karyotype dynamics during tumorigenesis, trace clonal lineages and link genomic changes to cancer phenotypes at single-cell resolution. These methods provide valuable insight not only into the role of CIN in cancer progression, but also into cancer cell fitness. In this Cell Science at a Glance article and the accompanying poster, we discuss the relationship between CIN, cancer cell fitness and evolution, and highlight techniques that can be used to study the relationship between these factors. To that end, we explore methods of assessing cancer cell fitness, particularly for chromosomally unstable cancer.
MeSH term(s)	Humans ; Neoplasms/genetics ; Carcinogenesis ; Chromosomal Instability/genetics ; Cell Transformation, Neoplastic ; Cell Nucleus Division
Language	English
Publishing date	2024-01-15
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2993-2
ISSN	1477-9137 ; 0021-9533
ISSN (online)	1477-9137
ISSN	0021-9533
DOI	10.1242/jcs.260199
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Article ; Online: Taking the STING out of CIN.

van den Brink, Anouk / Foijer, Floris

Trends in cancer

2023 Volume 9, Issue 12, Page(s) 992–994

Abstract: Chromosomal instability (CIN), a hallmark of cancer, promotes cell-intrinsic inflammatory signaling. Although inflammation is generally considered tumor-suppressive, this relationship is more complex in cancers with CIN. We discuss new findings by Li et ... ...

Abstract	Chromosomal instability (CIN), a hallmark of cancer, promotes cell-intrinsic inflammatory signaling. Although inflammation is generally considered tumor-suppressive, this relationship is more complex in cancers with CIN. We discuss new findings by Li et al. that can explain how cancer cells with CIN tolerate, adopt, and rewire the CIN-induced inflammatory response to fuel tumorigenesis.
MeSH term(s)	Humans ; Neoplasms/genetics ; Chromosomal Instability ; Cell Transformation, Neoplastic
Language	English
Publishing date	2023-10-06
Publishing country	United States
Document type	Journal Article
ZDB-ID	2852626-0
ISSN	2405-8025 ; 2405-8033 ; 2405-8033
ISSN (online)	2405-8025 ; 2405-8033
ISSN	2405-8033
DOI	10.1016/j.trecan.2023.09.010
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Article ; Online: Chromosomal Instability-Driven Cancer Progression: Interplay with the Tumour Microenvironment and Therapeutic Strategies.

Zheng, Siqi / Guerrero-Haughton, Erika / Foijer, Floris

Cells

2023 Volume 12, Issue 23

Abstract: Chromosomal instability (CIN) is a prevalent characteristic of solid tumours and haematological malignancies. CIN results in an increased frequency of chromosome mis-segregation events, thus yielding numerical and structural copy number alterations, a ... ...

Abstract	Chromosomal instability (CIN) is a prevalent characteristic of solid tumours and haematological malignancies. CIN results in an increased frequency of chromosome mis-segregation events, thus yielding numerical and structural copy number alterations, a state also known as aneuploidy. CIN is associated with increased chances of tumour recurrence, metastasis, and acquisition of resistance to therapeutic interventions, and this is a dismal prognosis. In this review, we delve into the interplay between CIN and cancer, with a focus on its impact on the tumour microenvironment-a driving force behind metastasis. We discuss the potential therapeutic avenues that have resulted from these insights and underscore their crucial role in shaping innovative strategies for cancer treatment.
MeSH term(s)	Humans ; Tumor Microenvironment/genetics ; Neoplasm Recurrence, Local ; Chromosomal Instability/genetics ; Aneuploidy ; Hematologic Neoplasms
Language	English
Publishing date	2023-11-26
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells12232712
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Article ; Online: Amyotrophic Lateral Sclerosis, FUS and Protein Synthesis Defects.

Assoni, Amanda Faria / Foijer, Floris / Zatz, Mayana

Stem cell reviews and reports

2022 Volume 19, Issue 3, Page(s) 625–638

Abstract: Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease that mainly affects the motor system. It is a very heterogeneous disorder, so far more than 40 genes have been described as responsible for ALS. The cause of motor neuron degeneration is ... ...

Abstract	Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease that mainly affects the motor system. It is a very heterogeneous disorder, so far more than 40 genes have been described as responsible for ALS. The cause of motor neuron degeneration is not yet fully understood, but there is consensus in the literature that it is the result of a complex interplay of several pathogenic processes, which include alterations in nucleocytoplasmic transport, defects in transcription and splicing, altered formation and/or disassembly of stress granules and impaired proteostasis. These defects result in protein aggregation, impaired DNA repair, mitochondrial dysfunction and oxidative stress, neuroinflammation, impaired axonal transport, impaired vesicular transport, excitotoxicity, as well as impaired calcium influx. We argue here that all the above functions ultimately lead to defects in protein synthesis. Fused in Sarcoma (FUS) is one of the genes associated with ALS. It causes ALS type 6 when mutated and is found mislocalized to the cytoplasm in the motor neurons of sporadic ALS patients (without FUS mutations). In addition, FUS plays a role in all cellular functions that are impaired in degenerating motor neurons. Moreover, ALS patients with FUS mutations present the first symptoms significantly earlier than in other forms of the disease. Therefore, the aim of this review is to further discuss ALS6, detail the cellular functions of FUS, and suggest that the localization of FUS, as well as protein synthesis rates, could be hallmarks of the ALS phenotype and thus good therapeutic targets.
MeSH term(s)	Humans ; Amyotrophic Lateral Sclerosis/pathology ; Neurodegenerative Diseases ; Motor Neurons/pathology ; Mutation ; Cytoplasm/genetics ; Cytoplasm/metabolism ; Cytoplasm/pathology ; RNA-Binding Protein FUS/genetics ; RNA-Binding Protein FUS/metabolism
Chemical Substances	RNA-Binding Protein FUS ; FUS protein, human
Language	English
Publishing date	2022-12-14
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2495577-2
ISSN	2629-3277 ; 1558-6804 ; 1550-8943
ISSN (online)	2629-3277 ; 1558-6804
ISSN	1550-8943
DOI	10.1007/s12015-022-10489-8
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Article ; Online: Chromosomal instability and inflammation: a catch-22 for cancer cells.

van den Brink, Anouk / Suárez Peredo Rodríguez, Maria F / Foijer, Floris

Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology

2023 Volume 31, Issue 3, Page(s) 19

Abstract: Chromosomal instability (CIN), an increased rate of chromosomal segregation abnormalities, drives intratumor heterogeneity and affects most human cancers. In addition to chromosome copy number alterations, CIN results in chromosome(s) (fragments) being ... ...

Abstract	Chromosomal instability (CIN), an increased rate of chromosomal segregation abnormalities, drives intratumor heterogeneity and affects most human cancers. In addition to chromosome copy number alterations, CIN results in chromosome(s) (fragments) being mislocalized into the cytoplasm in the form of micronuclei. Micronuclei can be detected by cGAS, a double-strand nucleic acid sensor, which will lead to the production of the second messenger 2'3'-cGAMP, activation of an inflammatory response, and downstream immune cell activation. However, the molecular network underlying the CIN-induced inflammatory response is still poorly understood. Furthermore, there is emerging evidence that cancers that display CIN circumvent this CIN-induced inflammatory response, and thus immune surveillance. The STAT1, STAT3, and NF-κB signaling cascades appear to play an important role in the CIN-induced inflammatory response. In this review, we discuss how these pathways are involved in signaling CIN in cells and how they are intertwined. A better understanding of how CIN is being signaled in cells and how cancer cells circumvent this is of the utmost importance for better and more selective cancer treatment.
MeSH term(s)	Humans ; Aneuploidy ; Chromosomal Instability ; Neoplasms/genetics ; Chromosome Aberrations ; Inflammation/genetics
Language	English
Publishing date	2023-08-10
Publishing country	Netherlands
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	1161632-5
ISSN	1573-6849 ; 0967-3849
ISSN (online)	1573-6849
ISSN	0967-3849
DOI	10.1007/s10577-023-09730-y
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Article ; Online: Understanding How Genetic Mutations Collaborate with Genomic Instability in Cancer.

Jilderda, Laura J / Zhou, Lin / Foijer, Floris

Cells

2021 Volume 10, Issue 2

Abstract: Chromosomal instability is the process of mis-segregation for ongoing chromosomes, which leads to cells with an abnormal number of chromosomes, also known as an aneuploid state. Induced aneuploidy is detrimental during development and in primary cells ... ...

Abstract	Chromosomal instability is the process of mis-segregation for ongoing chromosomes, which leads to cells with an abnormal number of chromosomes, also known as an aneuploid state. Induced aneuploidy is detrimental during development and in primary cells but aneuploidy is also a hallmark of cancer cells. It is therefore believed that premalignant cells need to overcome aneuploidy-imposed stresses to become tumorigenic. Over the past decade, some aneuploidy-tolerating pathways have been identified through small-scale screens, which suggest that aneuploidy tolerance pathways can potentially be therapeutically exploited. However, to better understand the processes that lead to aneuploidy tolerance in cancer cells, large-scale and unbiased genetic screens are needed, both in euploid and aneuploid cancer models. In this review, we describe some of the currently known aneuploidy-tolerating hits, how large-scale genome-wide screens can broaden our knowledge on aneuploidy specific cancer driver genes, and how we can exploit the outcomes of these screens to improve future cancer therapy.
MeSH term(s)	Aneuploidy ; Animals ; Genetic Testing ; Genomic Instability/genetics ; Humans ; Models, Genetic ; Mutation/genetics ; Neoplasms
Language	English
Publishing date	2021-02-06
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells10020342
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Article ; Online: Understanding How Genetic Mutations Collaborate with Genomic Instability in Cancer

Laura J. Jilderda / Lin Zhou / Floris Foijer

Cells, Vol 10, Iss 342, p

2021 Volume 342

Abstract	Chromosomal instability is the process of mis-segregation for ongoing chromosomes, which leads to cells with an abnormal number of chromosomes, also known as an aneuploid state. Induced aneuploidy is detrimental during development and in primary cells but aneuploidy is also a hallmark of cancer cells. It is therefore believed that premalignant cells need to overcome aneuploidy-imposed stresses to become tumorigenic. Over the past decade, some aneuploidy-tolerating pathways have been identified through small-scale screens, which suggest that aneuploidy tolerance pathways can potentially be therapeutically exploited. However, to better understand the processes that lead to aneuploidy tolerance in cancer cells, large-scale and unbiased genetic screens are needed, both in euploid and aneuploid cancer models. In this review, we describe some of the currently known aneuploidy-tolerating hits, how large-scale genome-wide screens can broaden our knowledge on aneuploidy specific cancer driver genes, and how we can exploit the outcomes of these screens to improve future cancer therapy.
Keywords	aneuploidy ; chromosomal instability ; genome wide screens ; cancer ; Biology (General) ; QH301-705.5
Language	English
Publishing date	2021-02-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article ; Online: Exploiting aneuploidy-imposed stresses and coping mechanisms to battle cancer.

Zhou, Lin / Jilderda, Laura J / Foijer, Floris

Open biology

2020 Volume 10, Issue 9, Page(s) 200148

Abstract: Aneuploidy, an irregular number of chromosomes in cells, is a hallmark feature of cancer. Aneuploidy results from chromosomal instability (CIN) and occurs in almost 90% of all tumours. While many cancers display an ongoing CIN phenotype, cells can also ... ...

Abstract	Aneuploidy, an irregular number of chromosomes in cells, is a hallmark feature of cancer. Aneuploidy results from chromosomal instability (CIN) and occurs in almost 90% of all tumours. While many cancers display an ongoing CIN phenotype, cells can also be aneuploid without displaying CIN. CIN drives tumour evolution as ongoing chromosomal missegregation will yield a progeny of cells with variable aneuploid karyotypes. The resulting aneuploidy is initially toxic to cells because it leads to proteotoxic and metabolic stress, cell cycle arrest, cell death, immune cell activation and further genomic instability. In order to overcome these aneuploidy-imposed stresses and adopt a malignant fate, aneuploid cancer cells must develop aneuploidy-tolerating mechanisms to cope with CIN. Aneuploidy-coping mechanisms can thus be considered as promising therapeutic targets. However, before such therapies can make it into the clinic, we first need to better understand the molecular mechanisms that are activated upon aneuploidization and the coping mechanisms that are selected for in aneuploid cancer cells. In this review, we discuss the key biological responses to aneuploidization, some of the recently uncovered aneuploidy-coping mechanisms and some strategies to exploit these in cancer therapy.
MeSH term(s)	Adaptation, Physiological ; Aneuploidy ; Biomarkers ; Cellular Senescence ; Chromosomal Instability ; Disease Management ; Disease Susceptibility ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Molecular Targeted Therapy ; Neoplasms/genetics ; Neoplasms/metabolism ; Neoplasms/pathology ; Neoplasms/therapy ; Signal Transduction/drug effects ; Stress, Physiological
Chemical Substances	Biomarkers
Language	English
Publishing date	2020-09-02
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2630944-0
ISSN	2046-2441 ; 2046-2441
ISSN (online)	2046-2441
ISSN	2046-2441
DOI	10.1098/rsob.200148
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Extra centrosomes delay DNA damage-driven tumorigenesis.

Braun, Vincent Z / Karbon, Gerlinde / Schuler, Fabian / Schapfl, Marina A / Weiss, Johannes G / Petermann, Paul Y / Spierings, Diana C J / Tijhuis, Andrea E / Foijer, Floris / Labi, Verena / Villunger, Andreas

Science advances

2024 Volume 10, Issue 13, Page(s) eadk0564

Abstract: Deregulated centrosome numbers are frequently found in human cancer and can promote malignancies in model organisms. Current research aims to clarify if extra centrosomes are cause or consequence of malignant transformation, and if their biogenesis can ... ...

Abstract	Deregulated centrosome numbers are frequently found in human cancer and can promote malignancies in model organisms. Current research aims to clarify if extra centrosomes are cause or consequence of malignant transformation, and if their biogenesis can be targeted for therapy. Here, we show that oncogene-driven blood cancer is inert to genetic manipulation of centrosome numbers, whereas the formation of DNA damage-induced malignancies is delayed. We provide first evidence that this unexpected phenomenon is connected to extra centrosomes eliciting a pro-death signal engaging the apoptotic machinery. Apoptosis induction requires the PIDDosome multi-protein complex, as it can be abrogated by loss of any of its three components,
MeSH term(s)	Humans ; Centrosome ; Apoptosis/genetics ; Neoplasms/metabolism ; Cell Transformation, Neoplastic/genetics ; Cell Transformation, Neoplastic/metabolism ; DNA Damage
Language	English
Publishing date	2024-03-29
Publishing country	United States
Document type	Journal Article
ZDB-ID	2810933-8
ISSN	2375-2548 ; 2375-2548
ISSN (online)	2375-2548
ISSN	2375-2548
DOI	10.1126/sciadv.adk0564
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Article ; Online: A kinesin-based approach for inducing chromosome-specific mis-segregation in human cells.

Truong, My Anh / Cané-Gasull, Paula / de Vries, Sippe G / Nijenhuis, Wilco / Wardenaar, René / Kapitein, Lukas C / Foijer, Floris / Lens, Susanne Ma

The EMBO journal

2023 Volume 42, Issue 10, Page(s) e111559

Abstract: Various cancer types exhibit characteristic and recurrent aneuploidy patterns. The origins of these cancer type-specific karyotypes are still unknown, partly because introducing or eliminating specific chromosomes in human cells still poses a challenge. ... ...

Abstract	Various cancer types exhibit characteristic and recurrent aneuploidy patterns. The origins of these cancer type-specific karyotypes are still unknown, partly because introducing or eliminating specific chromosomes in human cells still poses a challenge. Here, we describe a novel strategy to induce mis-segregation of specific chromosomes in different human cell types. We employed Tet repressor or nuclease-dead Cas9 to link a microtubule minus-end-directed kinesin (Kinesin14VIb) from Physcomitrella patens to integrated Tet operon repeats and chromosome-specific endogenous repeats, respectively. By live- and fixed-cell imaging, we observed poleward movement of the targeted loci during (pro)metaphase. Kinesin14VIb-mediated pulling forces on the targeted chromosome were counteracted by forces from kinetochore-attached microtubules. This tug-of-war resulted in chromosome-specific segregation errors during anaphase and revealed that spindle forces can heavily stretch chromosomal arms. By single-cell whole-genome sequencing, we established that kinesin-induced targeted mis-segregations predominantly result in chromosomal arm aneuploidies after a single cell division. Our kinesin-based strategy opens the possibility to investigate the immediate cellular responses to specific aneuploidies in different cell types; an important step toward understanding how tissue-specific aneuploidy patterns evolve.
MeSH term(s)	Humans ; Kinesins/genetics ; Kinesins/metabolism ; Spindle Apparatus/genetics ; Spindle Apparatus/metabolism ; Kinetochores/metabolism ; Microtubules/metabolism ; Chromosome Segregation ; Anaphase ; Aneuploidy
Chemical Substances	Kinesins (EC 3.6.4.4)
Language	English
Publishing date	2023-04-11
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.2022111559
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