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Article ; Online: Super-enhancer acquisition drives oncogene expression in triple negative breast cancer.

Raisner, Ryan / Bainer, Russell / Haverty, Peter M / Benedetti, Kelli L / Gascoigne, Karen E

2020 Volume 15, Issue 6, Page(s) e0235343

Abstract: Triple Negative Breast Cancer (TNBC) is a heterogeneous disease lacking known molecular drivers and effective targeted therapies. Cytotoxic chemotherapy remains the mainstay of treatment for TNBCs, which have significantly poorer survival rates compared ... ...

Abstract	Triple Negative Breast Cancer (TNBC) is a heterogeneous disease lacking known molecular drivers and effective targeted therapies. Cytotoxic chemotherapy remains the mainstay of treatment for TNBCs, which have significantly poorer survival rates compared to other breast cancer subtypes. In addition to changes within the coding genome, aberrant enhancer activity is a well-established contributor to tumorigenesis. Here we use H3K27Ac chromatin immunoprecipitation followed by sequencing (ChIP-Seq) to map the active cis-regulatory landscape in TNBC. We identify distinct disease subtypes associated with specific enhancer activity, and over 2,500 unique superenhancers acquired by tumor cells but absent from normal breast tissue. To identify potential actionable disease drivers, we probed the dependency on genes that associate with tumor-specific enhancers by CRISPR screening. In this way we identify a number of tumor-specific dependencies, including a previously uncharacterized dependency on the TGFβ pseudo-receptor BAMBI.
MeSH term(s)	Cell Line, Tumor ; Chromatin Immunoprecipitation ; Enhancer Elements, Genetic/genetics ; Female ; Gene Editing ; Gene Expression Regulation, Neoplastic ; Histones/chemistry ; Histones/genetics ; Histones/metabolism ; Humans ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Oncogenes/genetics ; RNA, Guide, CRISPR-Cas Systems/metabolism ; Triple Negative Breast Neoplasms/genetics ; Triple Negative Breast Neoplasms/pathology
Chemical Substances	BAMBI protein, human ; Histones ; Membrane Proteins ; RNA, Guide, CRISPR-Cas Systems
Language	English
Publishing date	2020-06-25
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0235343
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Induced dicentric chromosome formation promotes genomic rearrangements and tumorigenesis.

Gascoigne, Karen E / Cheeseman, Iain M

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

2013 Volume 21, Issue 4, Page(s) 407–418

Abstract: Chromosomal rearrangements can radically alter gene products and their function, driving tumor formation or progression. However, the molecular origins and evolution of such rearrangements are varied and poorly understood, with cancer cells often ... ...

Abstract	Chromosomal rearrangements can radically alter gene products and their function, driving tumor formation or progression. However, the molecular origins and evolution of such rearrangements are varied and poorly understood, with cancer cells often containing multiple, complex rearrangements. One mechanism that can lead to genomic rearrangements is the formation of a "dicentric" chromosome containing two functional centromeres. Indeed, such dicentric chromosomes have been observed in cancer cells. Here, we tested the ability of a single dicentric chromosome to contribute to genomic instability and neoplastic conversion in vertebrate cells. We developed a system to transiently and reversibly induce dicentric chromosome formation on a single chromosome with high temporal control. We find that induced dicentric chromosomes are frequently damaged and mis-segregated during mitosis, and that this leads to extensive chromosomal rearrangements including translocations with other chromosomes. Populations of pre-neoplastic cells in which a single dicentric chromosome is induced acquire extensive genomic instability and display hallmarks of cellular transformation including anchorage-independent growth in soft agar. Our results suggest that a single dicentric chromosome could contribute to tumor initiation.
MeSH term(s)	Animals ; Carcinogenesis/genetics ; Cell Line, Tumor ; Centromere/genetics ; Chromosome Aberrations ; Fluorescent Antibody Technique ; Gene Rearrangement ; Genomic Instability ; Genomics/methods ; In Situ Hybridization, Fluorescence ; Mice ; Mitosis/genetics ; Translocation, Genetic
Language	English
Publishing date	2013-06-22
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; 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/s10577-013-9368-6
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Article ; Online: CDK-dependent phosphorylation and nuclear exclusion coordinately control kinetochore assembly state.

Gascoigne, Karen E / Cheeseman, Iain M

The Journal of cell biology

2013 Volume 201, Issue 1, Page(s) 23–32

Abstract: Accurate chromosome segregation requires assembly of the multiprotein kinetochore complex. Prior work has identified more than 100 different kinetochore components in human cells. However, little is known about the regulatory processes that specify their ...

Abstract	Accurate chromosome segregation requires assembly of the multiprotein kinetochore complex. Prior work has identified more than 100 different kinetochore components in human cells. However, little is known about the regulatory processes that specify their assembly upon mitotic entry and disassembly at mitotic exit. In this paper, we used a live-cell imaging-based assay to quantify kinetochore disassembly kinetics and systematically analyze the role of potential regulatory mechanisms in controlling kinetochore assembly state. We find that kinetochore assembly and disassembly was driven primarily by mitotic phosphorylation downstream of cyclin-dependent kinase (CDK). In addition, we demonstrate that nuclear exclusion of the Ndc80 complex helped restrict kinetochore formation to mitosis. Combining constitutive CDK-dependent phosphorylation of CENP-T and forced nuclear localization of the Ndc80 complex partially prevented kinetochore disassembly at mitotic exit and led to chromosome segregation defects in subsequent divisions. In total, we find that the coordinated temporal regulation of outer kinetochore assembly is essential for accurate cell division.
MeSH term(s)	Active Transport, Cell Nucleus/physiology ; Cell Line ; Cell Nucleus/genetics ; Cell Nucleus/metabolism ; Chromosomal Proteins, Non-Histone/genetics ; Chromosomal Proteins, Non-Histone/metabolism ; Chromosome Segregation/physiology ; Cyclin-Dependent Kinases/genetics ; Cyclin-Dependent Kinases/metabolism ; Cytoskeletal Proteins ; Humans ; Kinetochores/metabolism ; Mitosis/physiology ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Phosphorylation/physiology
Chemical Substances	CENPT protein, human ; Chromosomal Proteins, Non-Histone ; Cytoskeletal Proteins ; NDC80 protein, human ; Nuclear Proteins ; Cyclin-Dependent Kinases (EC 2.7.11.22)
Language	English
Publishing date	2013-03-25
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	218154-x
ISSN	1540-8140 ; 0021-9525
ISSN (online)	1540-8140
ISSN	0021-9525
DOI	10.1083/jcb.201301006
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Article ; Online: Super-enhancer acquisition drives oncogene expression in triple negative breast cancer.

Ryan Raisner / Russell Bainer / Peter M Haverty / Kelli L Benedetti / Karen E Gascoigne

PLoS ONE, Vol 15, Iss 6, p e

2020 Volume 0235343

Abstract	Triple Negative Breast Cancer (TNBC) is a heterogeneous disease lacking known molecular drivers and effective targeted therapies. Cytotoxic chemotherapy remains the mainstay of treatment for TNBCs, which have significantly poorer survival rates compared to other breast cancer subtypes. In addition to changes within the coding genome, aberrant enhancer activity is a well-established contributor to tumorigenesis. Here we use H3K27Ac chromatin immunoprecipitation followed by sequencing (ChIP-Seq) to map the active cis-regulatory landscape in TNBC. We identify distinct disease subtypes associated with specific enhancer activity, and over 2,500 unique superenhancers acquired by tumor cells but absent from normal breast tissue. To identify potential actionable disease drivers, we probed the dependency on genes that associate with tumor-specific enhancers by CRISPR screening. In this way we identify a number of tumor-specific dependencies, including a previously uncharacterized dependency on the TGFβ pseudo-receptor BAMBI.
Keywords	Medicine ; R ; Science ; Q
Subject code	610 ; 616
Language	English
Publishing date	2020-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: T time for point centromeres.

Gascoigne, Karen E / Cheeseman, Iain M

Nature cell biology

2012 Volume 14, Issue 6, Page(s) 559–561

Abstract: The diverse nature of eukaryotic centromere structure has led to a prevailing view that the kinetochore-chromatin interface is fundamentally different in distinct species. Two studies now challenge this dogma with the identification of budding yeast ... ...

Abstract	The diverse nature of eukaryotic centromere structure has led to a prevailing view that the kinetochore-chromatin interface is fundamentally different in distinct species. Two studies now challenge this dogma with the identification of budding yeast homologues of the vertebrate centromere DNA-binding proteins CENP-T and CENP-W.
MeSH term(s)	Animals ; Cell Cycle Proteins/metabolism ; Centromere/metabolism ; Chromosomal Proteins, Non-Histone/metabolism ; Cytoskeletal Proteins ; Humans ; Kinetochores/metabolism ; Microtubule-Associated Proteins/metabolism ; Nuclear Proteins/metabolism ; Protein-Serine-Threonine Kinases/metabolism ; Saccharomyces cerevisiae/metabolism ; Saccharomyces cerevisiae Proteins/metabolism
Chemical Substances	CENPT protein, human ; Cell Cycle Proteins ; Chromosomal Proteins, Non-Histone ; Cnn1 protein, S cerevisiae ; Cytoskeletal Proteins ; MTW1 protein, S cerevisiae ; Microtubule-Associated Proteins ; NDC80 protein, human ; Nuclear Proteins ; Saccharomyces cerevisiae Proteins ; Spc105 protein, S cerevisiae ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; MPS1 protein, S cerevisiae (EC 2.7.12.2)
Language	English
Publishing date	2012-05-30
Publishing country	England
Document type	News ; Comment
ZDB-ID	1474722-4
ISSN	1476-4679 ; 1465-7392
ISSN (online)	1476-4679
ISSN	1465-7392
DOI	10.1038/ncb2509
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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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Article ; Online: Distinct organization and regulation of the outer kinetochore KMN network downstream of CENP-C and CENP-T.

Rago, Florencia / Gascoigne, Karen E / Cheeseman, Iain M

Current biology : CB

2015 Volume 25, Issue 5, Page(s) 671–677

Abstract: The kinetochore provides a vital connection between chromosomes and spindle microtubules [1, 2]. Defining the molecular architecture of the core kinetochore components is critical for understanding the mechanisms by which the kinetochore directs ... ...

Abstract	The kinetochore provides a vital connection between chromosomes and spindle microtubules [1, 2]. Defining the molecular architecture of the core kinetochore components is critical for understanding the mechanisms by which the kinetochore directs chromosome segregation. The KNL1/Mis12 complex/Ndc80 complex (KMN) network acts as the primary microtubule-binding interface at kinetochores [3] and provides a platform to recruit regulatory proteins [4]. Recent work found that the inner kinetochore components CENP-C and CENP-T act in parallel to recruit the KMN network to kinetochores [5-8]. However, due to the presence of these dual pathways, it has not been possible to distinguish differences in the nature of kinetochore assembly downstream of CENP-C or CENP-T. Here, we separated these pathways by targeting CENP-C and CENP-T independently to an ectopic chromosomal locus in human cells. Our work reveals that the organization of the KMN network components downstream of CENP-C and CENP-T is distinct. CENP-C recruits the Ndc80 complex through its interactions with KNL1 and the Mis12 complex. In contrast, CENP-T directly interacts with Ndc80, which in turn promotes KNL1/Mis12 complex recruitment through a separate region on CENP-T, resulting in functional relationships for KMN network localization that are inverted relative to the CENP-C pathway. We also find that distinct regulatory paradigms control the assembly of these pathways, with Aurora B kinase promoting KMN network recruitment to CENP-C and cyclin-dependent kinase (CDK) regulating KMN network recruitment to CENP-T. This work reveals unexpected complexity for the architecture and regulation of the core components of the kinetochore-microtubule interface.
MeSH term(s)	Cell Line, Tumor ; Chromosomal Proteins, Non-Histone/genetics ; Chromosomal Proteins, Non-Histone/metabolism ; Chromosome Segregation/physiology ; Cytoskeletal Proteins ; Fluorescent Antibody Technique ; Gene Components ; Humans ; Kinetochores/physiology ; M Phase Cell Cycle Checkpoints/physiology ; Microtubule-Associated Proteins/metabolism ; Multiprotein Complexes/metabolism ; Nuclear Proteins/metabolism ; Phosphorylation
Chemical Substances	CENPT protein, human ; Chromosomal Proteins, Non-Histone ; Cytoskeletal Proteins ; Knl1 protein, human ; MIS12 protein, human ; Microtubule-Associated Proteins ; Multiprotein Complexes ; NDC80 protein, human ; Nuclear Proteins ; centromere protein C
Language	English
Publishing date	2015-02-05
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1071731-6
ISSN	1879-0445 ; 0960-9822
ISSN (online)	1879-0445
ISSN	0960-9822
DOI	10.1016/j.cub.2015.01.059
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Article ; Online: Kinetochore assembly: if you build it, they will come.

Gascoigne, Karen E / Cheeseman, Iain M

Current opinion in cell biology

2010 Volume 23, Issue 1, Page(s) 102–108

Abstract: Accurate chromosome segregation requires the interaction of chromosomes with the microtubules from the mitotic spindle. This interaction is mediated by the macro-molecular kinetochore complex, which assembles only at the centromeric region of each ... ...

Abstract	Accurate chromosome segregation requires the interaction of chromosomes with the microtubules from the mitotic spindle. This interaction is mediated by the macro-molecular kinetochore complex, which assembles only at the centromeric region of each chromosome. However, how this site is specified and how assembly of the kinetochore structure is regulated in coordination with cell cycle progression remains unclear. Recent studies have begun to shed light on the mechanisms underlying assembly of this complex structure.
MeSH term(s)	Animals ; Humans ; Kinetochores/metabolism ; Microfilament Proteins/metabolism ; Protein Processing, Post-Translational
Chemical Substances	Microfilament Proteins
Language	English
Publishing date	2010-08-09
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1026381-0
ISSN	1879-0410 ; 0955-0674
ISSN (online)	1879-0410
ISSN	0955-0674
DOI	10.1016/j.ceb.2010.07.007
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Article ; Online: Multiple-gene targeting and mismatch tolerance can confound analysis of genome-wide pooled CRISPR screens.

Fortin, Jean-Philippe / Tan, Jenille / Gascoigne, Karen E / Haverty, Peter M / Forrest, William F / Costa, Michael R / Martin, Scott E

Genome biology

2019 Volume 20, Issue 1, Page(s) 21

Abstract: Background: Genome-wide loss-of-function screens using the CRISPR/Cas9 system allow the efficient discovery of cancer cell vulnerabilities. While several studies have focused on correcting for DNA cleavage toxicity biases associated with copy number ... ...

Abstract	Background: Genome-wide loss-of-function screens using the CRISPR/Cas9 system allow the efficient discovery of cancer cell vulnerabilities. While several studies have focused on correcting for DNA cleavage toxicity biases associated with copy number alterations, the effects of sgRNAs co-targeting multiple genomic loci in CRISPR screens have not been discussed. Results: In this work, we analyze CRISPR essentiality screen data from 391 cancer cell lines to characterize biases induced by multi-target sgRNAs. We investigate two types of multi-targets: on-targets predicted through perfect sequence complementarity and off-targets predicted through sequence complementarity with up to two nucleotide mismatches. We find that the number of on-targets and off-targets both increase sgRNA activity in a cell line-specific manner and that existing additive models of gene knockout effects fail at capturing genetic interactions that may occur between co-targeted genes. We use synthetic lethality between paralog genes to show that genetic interactions can introduce biases in essentiality scores estimated from multi-target sgRNAs. We further show that single-mismatch tolerant sgRNAs can confound the analysis of gene essentiality and lead to incorrect co-essentiality functional networks. Lastly, we also find that single nucleotide polymorphisms located in protospacer regions can impair on-target activity as a result of mismatch tolerance. Conclusion: We show the impact of multi-target effects on estimating cancer cell dependencies and the impact of off-target effects caused by mismatch tolerance in sgRNA-DNA binding.
MeSH term(s)	Cell Line, Tumor ; Clustered Regularly Interspaced Short Palindromic Repeats ; Gene Targeting ; Genomics/methods ; Humans ; Myosin Light Chains/genetics ; Neoplasms/genetics ; RNA, Guide, CRISPR-Cas Systems ; SOX9 Transcription Factor/genetics ; SOXE Transcription Factors/genetics
Chemical Substances	Myosin Light Chains ; RNA, Guide, CRISPR-Cas Systems ; SOX10 protein, human ; SOX9 Transcription Factor ; SOX9 protein, human ; SOXE Transcription Factors
Language	English
Publishing date	2019-01-25
Publishing country	England
Document type	Journal Article
ZDB-ID	2040529-7
ISSN	1474-760X ; 1474-760X
ISSN (online)	1474-760X
ISSN	1474-760X
DOI	10.1186/s13059-019-1621-7
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Article: How do anti-mitotic drugs kill cancer cells?

Gascoigne, Karen E / Taylor, Stephen S

Journal of cell science

2009 Volume 122, Issue Pt 15, Page(s) 2579–2585

Abstract: In 2007, over 12-million people were diagnosed with cancer. According to the American Cancer Society, at least one third of these individuals are not expected to survive the disease, making cancer the second most prevalent cause of death worldwide. ... ...

Abstract	In 2007, over 12-million people were diagnosed with cancer. According to the American Cancer Society, at least one third of these individuals are not expected to survive the disease, making cancer the second most prevalent cause of death worldwide. Systemic chemotherapy forms the mainstay of cancer treatment, and agents that disrupt mitotic spindle assembly - so called ;anti-mitotics' - are commonly used to treat a wide variety of cancers. Traditional anti-mitotic agents include the microtubule toxins such as taxol, other taxanes and the vinca alkaloids, all of which have proven successful in the clinic. However, patient response remains highly unpredictable, and drug resistance is common. In addition, toxicity is a problem. To address these limitations, a new generation of anti-mitotic drugs is being developed. As the first wave of these new agents enters clinical trails, much hope rests on their outcome. Meanwhile, significant attention is being focused on trying to predict which tumour types are likely to respond. In this Commentary, we outline recent advances in our understanding of how cancer cells respond to anti-mitotic drugs, and discuss the relevance of these studies to their use in the clinic.
MeSH term(s)	Antimitotic Agents/pharmacology ; Cell Death ; Humans ; Mitosis/drug effects ; Neoplasms/pathology
Chemical Substances	Antimitotic Agents
Language	English
Publishing date	2009-08-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2993-2
ISSN	1477-9137 ; 0021-9533
ISSN (online)	1477-9137
ISSN	0021-9533
DOI	10.1242/jcs.039719
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Zs.A 1200: 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: Induced dicentric chromosome formation promotes genomic rearrangements and tumorigenesis

Gascoigne, Karen E / Cheeseman, Iain M

Chromosome research. 2013 July, v. 21, no. 4

2013

Abstract	Chromosomal rearrangements can radically alter gene products and their function, driving tumor formation or progression. However, the molecular origins and evolution of such rearrangements are varied and poorly understood, with cancer cells often containing multiple, complex rearrangements. One mechanism that can lead to genomic rearrangements is the formation of a “dicentric” chromosome containing two functional centromeres. Indeed, such dicentric chromosomes have been observed in cancer cells. Here, we tested the ability of a single dicentric chromosome to contribute to genomic instability and neoplastic conversion in vertebrate cells. We developed a system to transiently and reversibly induce dicentric chromosome formation on a single chromosome with high temporal control. We find that induced dicentric chromosomes are frequently damaged and mis-segregated during mitosis, and that this leads to extensive chromosomal rearrangements including translocations with other chromosomes. Populations of pre-neoplastic cells in which a single dicentric chromosome is induced acquire extensive genomic instability and display hallmarks of cellular transformation including anchorage-independent growth in soft agar. Our results suggest that a single dicentric chromosome could contribute to tumor initiation.
Keywords	agar ; carcinogenesis ; centromeres ; chromosome translocation ; evolution ; genes ; mitosis ; vertebrates
Language	English
Dates of publication	2013-07
Size	p. 407-418.
Publishing place	Springer-Verlag
Document type	Article
ZDB-ID	1161632-5
ISSN	1573-6849 ; 0967-3849
ISSN (online)	1573-6849
ISSN	0967-3849
DOI	10.1007/s10577-013-9368-6
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