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Article: Epigenetic mechanisms of induced pluripotency.

Gładych, Marta / Andrzejewska, Anastazja / Oleksiewicz, Urszula / Estécio, Marcos R H

Contemporary oncology (Poznan, Poland)

2015 Volume 19, Issue 1A, Page(s) A30–8

Abstract: Reprogramming of somatic cells to induced pluripotent stem cells (iPSCs) requires profound alterations in the epigenetic landscape. During reprogramming, a change in chromatin structure resets the gene expression and stabilises self-renewal. ... ...

Abstract	Reprogramming of somatic cells to induced pluripotent stem cells (iPSCs) requires profound alterations in the epigenetic landscape. During reprogramming, a change in chromatin structure resets the gene expression and stabilises self-renewal. Reprogramming is a highly inefficient process, in part due to multiple epigenetic barriers. Although many epigenetic factors have already been shown to affect self-renewal and pluripotency in embryonic stem cells (ESCs), only a few of them have been examined in the context of dedifferentiation. In order to improve current protocols of iPSCs generation, it is essential to identify epigenetic drivers and blockages of somatic cell reprogramming.
Language	English
Publishing date	2015-01-29
Publishing country	Poland
Document type	Journal Article ; Review
ISSN	1428-2526
ISSN	1428-2526
DOI	10.5114/wo.2014.47135
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Article: Dissecting DNA hypermethylation in cancer

Estécio, Marcos R.H / Issa, Jean-Pierre J

FEBS letters. 2011 July 7, v. 585, no. 13

2011

Abstract: There is compelling evidence to support the importance of DNA methylation alterations in cancer development. Both losses and gains of DNA methylation are observed, thought to contribute pathophysiologically by inactivating tumor suppressor genes, ... ...

Abstract	There is compelling evidence to support the importance of DNA methylation alterations in cancer development. Both losses and gains of DNA methylation are observed, thought to contribute pathophysiologically by inactivating tumor suppressor genes, inducing chromosomal instability and ectopically activating gene expression. Lesser known are the causes of aberrant DNA methylation. Recent studies have pointed out that intrinsic gene susceptibility to DNA methylation, environmental factors and gene function all have an intertwined participation in this process. Overall, these data support a deterministic rather than a stochastic mechanism for de novo DNA methylation in cancer. In this review article, we discuss the technologies available to study DNA methylation and the endogenous and exogenous factors that influence the onset of de novo methylation in cancer.
Keywords	DNA ; DNA methylation ; environmental factors ; gene expression ; tumor suppressor genes
Language	English
Dates of publication	2011-0707
Size	p. 2078-2086.
Publishing place	Elsevier B.V.
Document type	Article
ZDB-ID	212746-5
ISSN	1873-3468 ; 0014-5793
ISSN (online)	1873-3468
ISSN	0014-5793
DOI	10.1016/j.febslet.2010.12.001
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Article ; Online: Dissecting DNA hypermethylation in cancer.

Estécio, Marcos R H / Issa, Jean-Pierre J

FEBS letters

2010 Volume 585, Issue 13, Page(s) 2078–2086

Abstract	There is compelling evidence to support the importance of DNA methylation alterations in cancer development. Both losses and gains of DNA methylation are observed, thought to contribute pathophysiologically by inactivating tumor suppressor genes, inducing chromosomal instability and ectopically activating gene expression. Lesser known are the causes of aberrant DNA methylation. Recent studies have pointed out that intrinsic gene susceptibility to DNA methylation, environmental factors and gene function all have an intertwined participation in this process. Overall, these data support a deterministic rather than a stochastic mechanism for de novo DNA methylation in cancer. In this review article, we discuss the technologies available to study DNA methylation and the endogenous and exogenous factors that influence the onset of de novo methylation in cancer.
MeSH term(s)	Animals ; DNA Methylation/genetics ; Humans ; Neoplasms/genetics
Language	English
Publishing date	2010-12-10
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	212746-5
ISSN	1873-3468 ; 0014-5793
ISSN (online)	1873-3468
ISSN	0014-5793
DOI	10.1016/j.febslet.2010.12.001
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Article ; Online: Cigarette smoke exposure accelerates AML progression in FLT3-ITD models.

Figueroa, Mary / Ma, Huaxian / Alfayez, Mansour / Morales-Mantilla, Daniel Enrique / Wang, Fei / Lu, Yue / Estecio, Marcos R / King, Katherine Y / Kleinerman, Eugenie / Moghaddam, Seyed Javad / Daver, Naval / Andreeff, Michael / Konopleva, Marina / DiNardo, Courtney / Chandra, Joya

Blood advances

2023 Volume 7, Issue 21, Page(s) 6624–6629

MeSH term(s)	Humans ; Cigarette Smoking/adverse effects ; Leukemia, Myeloid, Acute/etiology ; Mutation ; fms-Like Tyrosine Kinase 3/genetics
Chemical Substances	fms-Like Tyrosine Kinase 3 (EC 2.7.10.1) ; FLT3 protein, human (EC 2.7.10.1)
Language	English
Publishing date	2023-07-24
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2915908-8
ISSN	2473-9537 ; 2473-9529
ISSN (online)	2473-9537
ISSN	2473-9529
DOI	10.1182/bloodadvances.2023010111
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Article ; Online: SINE retrotransposons cause epigenetic reprogramming of adjacent gene promoters.

Estécio, Marcos R H / Gallegos, Juan / Dekmezian, Mhair / Lu, Yue / Liang, Shoudan / Issa, Jean-Pierre J

Molecular cancer research : MCR

2012 Volume 10, Issue 10, Page(s) 1332–1342

Abstract: ... loss of activating histone marks, thus resulting in a repressed state. SINE sequences themselves did ... not immediately acquire DNA methylation but were marked by H3K9me2 and H3K27me3. Moreover ...

Abstract	Almost half of the human genome and as much as 40% of the mouse genome is composed of repetitive DNA sequences. The majority of these repeats are retrotransposons of the SINE and LINE families, and such repeats are generally repressed by epigenetic mechanisms. It has been proposed that these elements can act as methylation centers from which DNA methylation spreads into gene promoters in cancer. Contradictory to a methylation center function, we have found that retrotransposons are enriched near promoter CpG islands that stay methylation-free in cancer. Clearly, it is important to determine which influence, if any, these repetitive elements have on nearby gene promoters. Using an in vitro system, we confirm here that SINE B1 elements can influence the activity of downstream gene promoters, with acquisition of DNA methylation and loss of activating histone marks, thus resulting in a repressed state. SINE sequences themselves did not immediately acquire DNA methylation but were marked by H3K9me2 and H3K27me3. Moreover, our bisulfite sequencing data did not support that gain of DNA methylation in gene promoters occurred by methylation spreading from SINE B1 repeats. Genome-wide analysis of SINE repeats distribution showed that their enrichment is directly correlated with the presence of USF1, USF2, and CTCF binding, proteins with insulator function. In summary, our work supports the concept that SINE repeats interfere negatively with gene expression and that their presence near gene promoters is counter-selected, except when the promoter is protected by an insulator element.
MeSH term(s)	Adaptor Proteins, Signal Transducing/genetics ; Alu Elements/genetics ; Animals ; Antigens, CD ; Cadherins/genetics ; Cellular Reprogramming/genetics ; Chromatin/metabolism ; Cyclin-Dependent Kinase Inhibitor p19/genetics ; DNA Methylation/genetics ; Epigenesis, Genetic ; Gene Silencing ; Genes/genetics ; Humans ; Insulator Elements/genetics ; Long Interspersed Nucleotide Elements/genetics ; Mice ; MutL Protein Homolog 1 ; NIH 3T3 Cells ; Nuclear Proteins/genetics ; Promoter Regions, Genetic ; Protein Binding/genetics ; Short Interspersed Nucleotide Elements/genetics ; Transcription Initiation Site ; Transcription, Genetic ; Tumor Suppressor Protein p14ARF/genetics
Chemical Substances	Adaptor Proteins, Signal Transducing ; Antigens, CD ; CDH1 protein, human ; Cadherins ; Cdkn2d protein, mouse ; Chromatin ; Cyclin-Dependent Kinase Inhibitor p19 ; Mlh1 protein, mouse ; Nuclear Proteins ; Tumor Suppressor Protein p14ARF ; MutL Protein Homolog 1 (EC 3.6.1.3)
Language	English
Publishing date	2012-09-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2098788-2
ISSN	1557-3125 ; 1541-7786
ISSN (online)	1557-3125
ISSN	1541-7786
DOI	10.1158/1541-7786.MCR-12-0351
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Article ; Online: Single-cell multimodal glioma analyses identify epigenetic regulators of cellular plasticity and environmental stress response.

Nature genetics

2021 Volume 53, Issue 10, Page(s) 1456–1468

Abstract: Glioma intratumoral heterogeneity enables adaptation to challenging microenvironments and contributes to therapeutic resistance. We integrated 914 single-cell DNA methylomes, 55,284 single-cell transcriptomes and bulk multi-omic profiles across 11 adult ... ...

Abstract	Glioma intratumoral heterogeneity enables adaptation to challenging microenvironments and contributes to therapeutic resistance. We integrated 914 single-cell DNA methylomes, 55,284 single-cell transcriptomes and bulk multi-omic profiles across 11 adult IDH mutant or IDH wild-type gliomas to delineate sources of intratumoral heterogeneity. We showed that local DNA methylation disorder is associated with cell-cell DNA methylation differences, is elevated in more aggressive tumors, links with transcriptional disruption and is altered during the environmental stress response. Glioma cells under in vitro hypoxic and irradiation stress increased local DNA methylation disorder and shifted cell states. We identified a positive association between genetic and epigenetic instability that was supported in bulk longitudinally collected DNA methylation data. Increased DNA methylation disorder associated with accelerated disease progression and recurrently selected DNA methylation changes were enriched for environmental stress response pathways. Our work identified an epigenetically facilitated adaptive stress response process and highlights the importance of epigenetic heterogeneity in shaping therapeutic outcomes.
MeSH term(s)	Brain Neoplasms/genetics ; Cell Plasticity/genetics ; Clonal Evolution ; DNA Copy Number Variations/genetics ; DNA Methylation/genetics ; Epigenesis, Genetic ; Gene Expression Regulation, Neoplastic ; Genetic Heterogeneity ; Genome, Human ; Glioma/genetics ; Humans ; Mutation/genetics ; Phylogeny ; Promoter Regions, Genetic/genetics ; Single-Cell Analysis ; Stress, Physiological/genetics ; Tumor Microenvironment/genetics
Language	English
Publishing date	2021-09-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1108734-1
ISSN	1546-1718 ; 1061-4036
ISSN (online)	1546-1718
ISSN	1061-4036
DOI	10.1038/s41588-021-00926-8
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Article ; Online: Differentially methylated genes and androgen receptor re-expression in small cell prostate carcinomas.

Kleb, Brittany / Estécio, Marcos R H / Zhang, Jiexin / Tzelepi, Vassiliki / Chung, Woonbok / Jelinek, Jaroslav / Navone, Nora M / Tahir, Salahaldin / Marquez, Victor E / Issa, Jean-Pierre / Maity, Sankar / Aparicio, Ana

Epigenetics

2016 Volume 11, Issue 3, Page(s) 184–193

Abstract: Small cell prostate carcinoma (SCPC) morphology is rare at initial diagnosis but often emerges during prostate cancer progression and portends a dismal prognosis. It does not express androgen receptor (AR) or respond to hormonal therapies. Clinically ... ...

Abstract	Small cell prostate carcinoma (SCPC) morphology is rare at initial diagnosis but often emerges during prostate cancer progression and portends a dismal prognosis. It does not express androgen receptor (AR) or respond to hormonal therapies. Clinically applicable markers for its early detection and treatment with effective chemotherapy are needed. Our studies in patient tumor-derived xenografts (PDX) revealed that AR-negative SCPC (AR(-)SCPC) expresses neural development genes instead of the prostate luminal epithelial genes characteristic of AR-positive castration-resistant adenocarcinomas (AR(+)ADENO). We hypothesized that the differences in cellular lineage programs are reflected in distinct epigenetic profiles. To address this hypothesis, we compared the DNA methylation profiles of AR(-) and AR(+) PDX using methylated CpG island amplification and microarray (MCAM) analysis and identified a set of differentially methylated promoters, validated in PDX and corresponding donor patient samples. We used the Illumina 450K platform to examine additional regions of the genome and the correlation between the DNA methylation profiles of the PDX and their corresponding patient tumors. Struck by the low frequency of AR promoter methylation in the AR(-)SCPC, we investigated this region's specific histone modification patterns by chromatin immunoprecipitation. We found that the AR promoter was enriched in silencing histone modifications (H3K27me3 and H3K9me2) and that EZH2 inhibition with 3-deazaneplanocin A (DZNep) resulted in AR expression and growth inhibition in AR(-)SCPC cell lines. We conclude that the epigenome of AR(-) is distinct from that of AR(+) castration-resistant prostate carcinomas, and that the AR(-) phenotype can be reversed with epigenetic drugs.
MeSH term(s)	Adenosine/administration & dosage ; Adenosine/analogs & derivatives ; Animals ; Carcinoma, Small Cell/genetics ; Carcinoma, Small Cell/pathology ; Cell Line, Tumor ; Cell Lineage/genetics ; CpG Islands/genetics ; DNA Methylation/genetics ; Enhancer of Zeste Homolog 2 Protein/antagonists & inhibitors ; Enhancer of Zeste Homolog 2 Protein/genetics ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Male ; Mice ; Promoter Regions, Genetic ; Prostatic Neoplasms, Castration-Resistant/genetics ; Prostatic Neoplasms, Castration-Resistant/pathology ; Receptors, Androgen/biosynthesis ; Receptors, Androgen/genetics ; Xenograft Model Antitumor Assays
Chemical Substances	Receptors, Androgen ; 3-deazaneplanocin (544SH4020S) ; EZH2 protein, human (EC 2.1.1.43) ; Enhancer of Zeste Homolog 2 Protein (EC 2.1.1.43) ; Adenosine (K72T3FS567)
Language	English
Publishing date	2016-03-03
Publishing country	United States
Document type	Journal Article
ISSN	1559-2308
ISSN (online)	1559-2308
DOI	10.1080/15592294.2016.1146851
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Article ; Online: Transcriptomic Signatures of Hypomethylating Agent Failure in Myelodysplastic Syndromes and Chronic Myelomonocytic Leukemia.

Darbaniyan, Faezeh / Zheng, Hong / Kanagal-Shamanna, Rashmi / Lockyer, Pamela / Montalban-Bravo, Guillermo / Estecio, Marcos / Lu, Yue / Soltysiak, Kelly A / Chien, Kelly S / Yang, Hui / Sasaki, Koji / Class, Caleb / Ganan-Gomez, Irene / Do, Kim-Anh / Garcia-Manero, Guillermo / Wei, Yue

Experimental hematology

2022 Volume 115, Page(s) 44–53

Abstract: Hypomethylating agents (HMAs) are the standard of care for myelodysplastic syndromes (MDS) and chronic myelomonocytic leukemia (CMML). HMA treatment failure is a major clinical problem and its mechanisms are poorly characterized. We performed RNA ... ...

Abstract	Hypomethylating agents (HMAs) are the standard of care for myelodysplastic syndromes (MDS) and chronic myelomonocytic leukemia (CMML). HMA treatment failure is a major clinical problem and its mechanisms are poorly characterized. We performed RNA sequencing in CD34
MeSH term(s)	Humans ; Mice ; Animals ; Leukemia, Myelomonocytic, Chronic/drug therapy ; Leukemia, Myelomonocytic, Chronic/genetics ; Transcriptome ; Myelodysplastic Syndromes/drug therapy ; Myelodysplastic Syndromes/genetics ; Myelodysplastic Syndromes/metabolism ; Azacitidine/pharmacology ; Azacitidine/therapeutic use ; Leukemia, Myelomonocytic, Juvenile/drug therapy
Chemical Substances	Azacitidine (M801H13NRU)
Language	English
Publishing date	2022-09-21
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	185107-x
ISSN	1873-2399 ; 0531-5573 ; 0301-472X
ISSN (online)	1873-2399
ISSN	0531-5573 ; 0301-472X
DOI	10.1016/j.exphem.2022.09.002
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Article ; Online: Myotonic dystrophy type 1 (DM1) clinical subtypes and CTCF site methylation status flanking the CTG expansion are mutant allele length-dependent.

Morales, Fernando / Corrales, Eyleen / Zhang, Baili / Vásquez, Melissa / Santamaría-Ulloa, Carolina / Quesada, Hazel / Sirito, Mario / Estecio, Marcos R / Monckton, Darren G / Krahe, Ralf

Human molecular genetics

2021 Volume 31, Issue 2, Page(s) 262–274

Abstract: Myotonic dystrophy type 1 (DM1) is a complex disease with a wide spectrum of symptoms. The exact relationship between mutant CTG repeat expansion size and clinical outcome remains unclear. DM1 congenital patients (CDM) inherit the largest expanded ... ...

Abstract	Myotonic dystrophy type 1 (DM1) is a complex disease with a wide spectrum of symptoms. The exact relationship between mutant CTG repeat expansion size and clinical outcome remains unclear. DM1 congenital patients (CDM) inherit the largest expanded alleles, which are associated with abnormal and increased DNA methylation flanking the CTG repeat. However, DNA methylation at the DMPK locus remains understudied. Its relationship to DM1 clinical subtypes, expansion size and age-at-onset is not yet completely understood. Using pyrosequencing-based methylation analysis on 225 blood DNA samples from Costa Rican DM1 patients, we determined that the size of the estimated progenitor allele length (ePAL) is not only a good discriminator between CDM and non-CDM cases (with an estimated threshold at 653 CTG repeats), but also for all DM1 clinical subtypes. Secondly, increased methylation at both CTCF sites upstream and downstream of the expansion was almost exclusively present in CDM cases. Thirdly, levels of abnormal methylation were associated with clinical subtype, age and ePAL, with strong correlations between these variables. Fourthly, both ePAL and the intergenerational expansion size were significantly associated with methylation status. Finally, methylation status was associated with ePAL and maternal inheritance, with almost exclusively maternal transmission of CDM. In conclusion, increased DNA methylation at the CTCF sites flanking the DM1 expansion could be linked to ePAL, and both increased methylation and the ePAL could be considered biomarkers for the CDM phenotype.
MeSH term(s)	Alleles ; CCCTC-Binding Factor ; DNA Methylation/genetics ; Humans ; Myotonic Dystrophy/genetics ; Myotonin-Protein Kinase/genetics ; Trinucleotide Repeat Expansion/genetics
Chemical Substances	CCCTC-Binding Factor ; CTCF protein, human ; Myotonin-Protein Kinase (EC 2.7.11.1)
Language	English
Publishing date	2021-08-25
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1108742-0
ISSN	1460-2083 ; 0964-6906
ISSN (online)	1460-2083
ISSN	0964-6906
DOI	10.1093/hmg/ddab243
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Article: Methylated CpG Island Amplification and Microarray (MCAM) for High-Throughput Analysis of DNA Methylation.

Estécio, Marcos R H / Yan, Pearlly S / Huang, Tim H-M / Issa, Jean-Pierre J

CSH protocols

2008 Volume 2008, Page(s) pdb.prot4974

Abstract: INTRODUCTIONThis protocol describes the use of methylated CpG island amplification (MCA) in combination with a microarray platform to analyze genome-wide DNA methylation in a high-throughput fashion. In this approach, termed MCAM, methylated CpG islands ... ...

Abstract	INTRODUCTIONThis protocol describes the use of methylated CpG island amplification (MCA) in combination with a microarray platform to analyze genome-wide DNA methylation in a high-throughput fashion. In this approach, termed MCAM, methylated CpG islands are selectively targeted using oligonucleotide adaptors after two rounds of digestion with a combination of methylation-sensitive and methylation-insensitive nucleases. They are then amplified using PCR. The resulting amplicons, representing the methylated fraction of the genome, are labeled with fluorochromes. Subsequently, a comparative hybridization of reference and test samples (typically normal and tumor DNA specimens) is done on a microarray platform.
Language	English
Publishing date	2008-03-01
Publishing country	United States
Document type	Journal Article
DOI	10.1101/pdb.prot4974
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