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Article ; Online: ecDNAs personify cancer gangsters.

Keshavarzian, Tina / Lupien, Mathieu

2022 Volume 82, Issue 3, Page(s) 500–502

Abstract: Alterations to gene regulatory plexuses typify oncogenesis, and two recent studies from Hung, Yost, Xie et al. (Hung et al., 2021) and Yi et al. (2021) collectively reveal the competitive advantage of extrachromosomal DNAs (ecDNAs) to set their own rules ...

Abstract	Alterations to gene regulatory plexuses typify oncogenesis, and two recent studies from Hung, Yost, Xie et al. (Hung et al., 2021) and Yi et al. (2021) collectively reveal the competitive advantage of extrachromosomal DNAs (ecDNAs) to set their own rules to control transcription by clustering into ecDNA hubs through intermolecular interactions that forge hub-specific regulatory plexuses driving high-oncogene expression.
MeSH term(s)	Carcinogenesis/genetics ; Humans ; Neoplasms/genetics ; Oncogenes
Language	English
Publishing date	2022-02-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	1415236-8
ISSN	1097-4164 ; 1097-2765
ISSN (online)	1097-4164
ISSN	1097-2765
DOI	10.1016/j.molcel.2022.01.003
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Article ; Online: Cancer-associated chromatin variants uncover the oncogenic role of transposable elements.

Grillo, Giacomo / Lupien, Mathieu

Current opinion in genetics & development

2022 Volume 74, Page(s) 101911

Abstract: The vast array of cell states found across human tissue arises from chromatin variants, which correspond to segments of the genome, known as DNA elements, adopting a different chromatin state over cell state transitions. Oncogenesis stems from ... ...

Abstract	The vast array of cell states found across human tissue arises from chromatin variants, which correspond to segments of the genome, known as DNA elements, adopting a different chromatin state over cell state transitions. Oncogenesis stems from alterations to the chromatin states over DNA elements that result in cancer-associated chromatin variants. Here, we review how cancer-associated chromatin variants call attention to repetitive DNA elements, and guide the functional characterization of transposable elements to decode their role in oncogenesis. We further discuss prevailing opportunities in the study of repetitive DNA elements to move towards the 'complete cancer genome' goal for precision medicine in oncology.
MeSH term(s)	Carcinogenesis/genetics ; Chromatin/genetics ; DNA Methylation ; DNA Transposable Elements/genetics ; Humans ; Neoplasms/genetics
Chemical Substances	Chromatin ; DNA Transposable Elements
Language	English
Publishing date	2022-04-26
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	1077312-5
ISSN	1879-0380 ; 0959-437X
ISSN (online)	1879-0380
ISSN	0959-437X
DOI	10.1016/j.gde.2022.101911
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Article ; Online: Chromatin Variants Reveal the Genetic Determinants of Oncogenesis in Breast Cancer.

Bahl, Shalini / Carroll, Jason S / Lupien, Mathieu

Cold Spring Harbor perspectives in medicine

2022 Volume 12, Issue 10

Abstract: Breast cancer presents as multiple distinct disease entities. Each tumor harbors diverse cell populations defining a phenotypic heterogeneity that impinges on our ability to treat patients. To date, efforts mainly focused on genetic variants to find ... ...

Abstract	Breast cancer presents as multiple distinct disease entities. Each tumor harbors diverse cell populations defining a phenotypic heterogeneity that impinges on our ability to treat patients. To date, efforts mainly focused on genetic variants to find drivers of inter- and intratumor phenotypic heterogeneity. However, these efforts have failed to fully capture the genetic basis of breast cancer. Through recent technological and analytical approaches, the genetic basis of phenotypes can now be decoded by characterizing chromatin variants. These variants correspond to polymorphisms in chromatin states at DNA sequences that serve a distinct role across cell populations. Here, we review the function and causes of chromatin variants as they relate to breast cancer inter- and intratumor heterogeneity and how they can guide the development of treatment alternatives to fulfill the goal of precision cancer medicine.
MeSH term(s)	Carcinogenesis ; Cell Transformation, Neoplastic ; Chromatin/genetics ; Genetic Heterogeneity ; Humans ; Neoplasms ; Precision Medicine
Chemical Substances	Chromatin
Language	English
Publishing date	2022-10-03
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ISSN	2157-1422
ISSN (online)	2157-1422
DOI	10.1101/cshperspect.a041322
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: ecDNAs personify cancer gangsters

Keshavarzian, Tina / Lupien, Mathieu

Molecular cell. 2022 Feb. 03, v. 82, no. 3

2022

Abstract	Alterations to gene regulatory plexuses typify oncogenesis, and two recent studies from Hung, Yost, Xie et al. (Hung et al., 2021) and Yi et al. (2021) collectively reveal the competitive advantage of extrachromosomal DNAs (ecDNAs) to set their own rules to control transcription by clustering into ecDNA hubs through intermolecular interactions that forge hub-specific regulatory plexuses driving high-oncogene expression.
Keywords	DNA ; carcinogenesis ; cells ; chemical interactions ; neoplasms ; plexus ; regulator genes
Language	English
Dates of publication	2022-0203
Size	p. 500-502.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	1415236-8
ISSN	1097-4164 ; 1097-2765
ISSN (online)	1097-4164
ISSN	1097-2765
DOI	10.1016/j.molcel.2022.01.003
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Human papillomavirus integration transforms chromatin to drive oncogenesis.

Karimzadeh, Mehran / Arlidge, Christopher / Rostami, Ariana / Lupien, Mathieu / Bratman, Scott V / Hoffman, Michael M

Genome biology

2023 Volume 24, Issue 1, Page(s) 142

Abstract: Background: Human papillomavirus (HPV) drives almost all cervical cancers and up to 70% of head and neck cancers. Frequent integration into the host genome occurs predominantly in tumorigenic types of HPV. We hypothesize that changes in chromatin state ... ...

Abstract	Background: Human papillomavirus (HPV) drives almost all cervical cancers and up to 70% of head and neck cancers. Frequent integration into the host genome occurs predominantly in tumorigenic types of HPV. We hypothesize that changes in chromatin state at the location of integration can result in changes in gene expression that contribute to the tumorigenicity of HPV. Results: We find that viral integration events often occur along with changes in chromatin state and expression of genes near the integration site. We investigate whether introduction of new transcription factor binding sites due to HPV integration could invoke these changes. Some regions within the HPV genome, particularly the position of a conserved CTCF binding site, show enriched chromatin accessibility signal. ChIP-seq reveals that the conserved CTCF binding site within the HPV genome binds CTCF in 4 HPV Conclusions: Our results suggest that introduction of a new CTCF binding site due to HPV integration reorganizes chromatin state and upregulates genes essential for tumor viability in some HPV
MeSH term(s)	Humans ; Chromatin ; Human Papillomavirus Viruses ; Papillomavirus Infections ; Head and Neck Neoplasms ; Carcinogenesis
Chemical Substances	Chromatin
Language	English
Publishing date	2023-06-27
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2040529-7
ISSN	1474-760X ; 1474-760X
ISSN (online)	1474-760X
ISSN	1474-760X
DOI	10.1186/s13059-023-02926-9
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Article ; Online: Human papillomavirus integration transforms chromatin to drive oncogenesis

Mehran Karimzadeh / Christopher Arlidge / Ariana Rostami / Mathieu Lupien / Scott V. Bratman / Michael M. Hoffman

Genome Biology, Vol 24, Iss 1, Pp 1-

2023 Volume 27

Abstract: Abstract Background Human papillomavirus (HPV) drives almost all cervical cancers and up to 70% of head and neck cancers. Frequent integration into the host genome occurs predominantly in tumorigenic types of HPV. We hypothesize that changes in chromatin ...

Abstract	Abstract Background Human papillomavirus (HPV) drives almost all cervical cancers and up to 70% of head and neck cancers. Frequent integration into the host genome occurs predominantly in tumorigenic types of HPV. We hypothesize that changes in chromatin state at the location of integration can result in changes in gene expression that contribute to the tumorigenicity of HPV. Results We find that viral integration events often occur along with changes in chromatin state and expression of genes near the integration site. We investigate whether introduction of new transcription factor binding sites due to HPV integration could invoke these changes. Some regions within the HPV genome, particularly the position of a conserved CTCF binding site, show enriched chromatin accessibility signal. ChIP-seq reveals that the conserved CTCF binding site within the HPV genome binds CTCF in 4 HPV+ cancer cell lines. Significant changes in CTCF binding pattern and increases in chromatin accessibility occur exclusively within 100 kbp of HPV integration sites. The chromatin changes co-occur with out-sized changes in transcription and alternative splicing of local genes. Analysis of The Cancer Genome Atlas (TCGA) HPV+ tumors indicates that HPV integration upregulates genes which have significantly higher essentiality scores compared to randomly selected upregulated genes from the same tumors. Conclusions Our results suggest that introduction of a new CTCF binding site due to HPV integration reorganizes chromatin state and upregulates genes essential for tumor viability in some HPV+ tumors. These findings emphasize a newly recognized role of HPV integration in oncogenesis.
Keywords	Biology (General) ; QH301-705.5 ; Genetics ; QH426-470
Subject code	337 ; 570
Language	English
Publishing date	2023-06-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: SMuRF: a novel tool to identify regulatory elements enriched for somatic point mutations.

Guilhamon, Paul / Lupien, Mathieu

BMC bioinformatics

2018 Volume 19, Issue 1, Page(s) 454

Abstract: Background: Single Nucleotide Variants (SNVs), including somatic point mutations and Single Nucleotide Polymorphisms (SNPs), in noncoding cis-regulatory elements (CREs) can affect gene regulation and lead to disease development. Several approaches have ... ...

Abstract	Background: Single Nucleotide Variants (SNVs), including somatic point mutations and Single Nucleotide Polymorphisms (SNPs), in noncoding cis-regulatory elements (CREs) can affect gene regulation and lead to disease development. Several approaches have been developed to identify highly mutated regions, but these do not take into account the specific genomic context, and thus likelihood of mutation, of CREs. Results: Here, we present SMuRF (Significantly Mutated Region Finder), a user-friendly command-line tool to identify these significantly mutated regions from user-defined genomic intervals and SNVs. We demonstrate this using publicly available datasets in which SMuRF identifies 72 significantly mutated CREs in liver cancer, including known mutated gene promoters as well as previously unreported regions. Conclusions: SMuRF is a helpful tool to allow the simple identification of significantly mutated regulatory elements. It is open-source and freely available on GitHub ( https://github.com/LupienLab/SMURF ).
MeSH term(s)	Genomics ; Humans ; Liver Neoplasms/genetics ; Point Mutation ; Regulatory Sequences, Nucleic Acid ; Software
Language	English
Publishing date	2018-11-26
Publishing country	England
Document type	Journal Article
ZDB-ID	2041484-5
ISSN	1471-2105 ; 1471-2105
ISSN (online)	1471-2105
ISSN	1471-2105
DOI	10.1186/s12859-018-2501-y
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Large organized chromatin lysine domains help distinguish primitive from differentiated cell populations.

Madani Tonekaboni, Seyed Ali / Haibe-Kains, Benjamin / Lupien, Mathieu

Nature communications

2021 Volume 12, Issue 1, Page(s) 499

Abstract: The human genome is partitioned into a collection of genomic features, inclusive of genes, transposable elements, lamina interacting regions, early replicating control elements and cis-regulatory elements, such as promoters, enhancers, and anchors of ... ...

Abstract	The human genome is partitioned into a collection of genomic features, inclusive of genes, transposable elements, lamina interacting regions, early replicating control elements and cis-regulatory elements, such as promoters, enhancers, and anchors of chromatin interactions. Uneven distribution of these features within chromosomes gives rise to clusters, such as topologically associating domains (TADs), lamina-associated domains, clusters of cis-regulatory elements or large organized chromatin lysine (K) domains (LOCKs). Here we show that LOCKs from diverse histone modifications discriminate primitive from differentiated cell types. Active LOCKs (H3K4me1, H3K4me3 and H3K27ac) cover a higher fraction of the genome in primitive compared to differentiated cell types while repressive LOCKs (H3K9me3, H3K27me3 and H3K36me3) do not. Active LOCKs in differentiated cells lie proximal to highly expressed genes while active LOCKs in primitive cells tend to be bivalent. Genes proximal to bivalent LOCKs are minimally expressed in primitive cells. Furthermore, bivalent LOCKs populate TAD boundaries and are preferentially bound by regulators of chromatin interactions, including CTCF, RAD21 and ZNF143. Together, our results argue that LOCKs discriminate primitive from differentiated cell populations.
MeSH term(s)	Animals ; Binding Sites/genetics ; Cell Differentiation/genetics ; Chromatin/genetics ; DNA Transposable Elements/genetics ; Enhancer Elements, Genetic/genetics ; Genome, Human/genetics ; Histone Code/genetics ; Histones/genetics ; Humans ; Lysine/genetics ; Promoter Regions, Genetic/genetics
Chemical Substances	Chromatin ; DNA Transposable Elements ; Histones ; histone H3 trimethyl Lys4 ; Lysine (K3Z4F929H6)
Language	English
Publishing date	2021-01-21
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-020-20830-9
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Article ; Online: Detection of metabolic adaptation in a triple-negative breast cancer animal model with [

Kohan, Andres A / Lupien, Mathieu / Cescon, David / Deblois, Geneviève / Ventura, Manuela / Metser, Ur / Veit-Haibach, Patrick

European journal of nuclear medicine and molecular imaging

2023 Volume 51, Issue 5, Page(s) 1261–1267

Abstract: Purpose: Test the feasibility of an image-based method to identify taxane resistance in mouse bearing triple-negative breast cancer (TNBC) tumor xenografts.: Methods: Xenograft tumor-bearing mice from paclitaxel-sensitive and paclitaxel-resistant ... ...

Abstract	Purpose: Test the feasibility of an image-based method to identify taxane resistance in mouse bearing triple-negative breast cancer (TNBC) tumor xenografts. Methods: Xenograft tumor-bearing mice from paclitaxel-sensitive and paclitaxel-resistant TNBC cells (MDA-MD-346) were generated by orthotopic injection into female NOD-SCID mice. When tumors reached 100-150 mm Results: From fifteen mice scanned, five had taxane-sensitive cell line tumors of which two underwent taxol-based treatment. From the remaining 10 mice with taxane-resistant cell line tumors, four underwent taxol-based treatment. Only 13 mice had the tumor sample analyzed histologically. When normalized to the blood pool, both cell lines showed differences in metabolic uptake before and after treatment. Conclusions: Treated and untreated taxane-sensitive and taxane-resistant cell lines have different metabolic properties that could be leveraged before the start of chemotherapy.
MeSH term(s)	Humans ; Female ; Animals ; Mice ; Positron Emission Tomography Computed Tomography/methods ; Triple Negative Breast Neoplasms/diagnostic imaging ; Triple Negative Breast Neoplasms/drug therapy ; Cell Line, Tumor ; Mice, SCID ; Mice, Inbred NOD ; Positron-Emission Tomography/methods ; Paclitaxel/pharmacology ; Paclitaxel/therapeutic use ; Models, Animal ; Drug Resistance ; Xenograft Model Antitumor Assays
Chemical Substances	Paclitaxel (P88XT4IS4D)
Language	English
Publishing date	2023-12-14
Publishing country	Germany
Document type	Journal Article
ZDB-ID	8236-3
ISSN	1619-7089 ; 0340-6997 ; 1619-7070
ISSN (online)	1619-7089
ISSN	0340-6997 ; 1619-7070
DOI	10.1007/s00259-023-06546-0
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Article ; Online: Large organized chromatin lysine domains help distinguish primitive from differentiated cell populations

Seyed Ali Madani Tonekaboni / Benjamin Haibe-Kains / Mathieu Lupien

Nature Communications, Vol 12, Iss 1, Pp 1-

2021 Volume 9

Abstract: Large organized chromatin lysine (K) domains (LOCKs) are a genomic feature derived from the cluster of modified nucleosomes. Here the authors provide evidence that LOCKs discriminate primitive from differentiated cell populations and that they relate to ... ...

Abstract	Large organized chromatin lysine (K) domains (LOCKs) are a genomic feature derived from the cluster of modified nucleosomes. Here the authors provide evidence that LOCKs discriminate primitive from differentiated cell populations and that they relate to transcription regulating events.
Keywords	Science ; Q
Language	English
Publishing date	2021-01-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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