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Article ; Online: How epigenomics broke the mold: an interview with Peter W Laird.

Laird, Peter W

2022 Volume 14, Issue 6, Page(s) 303–308

Abstract: In this interview, Professor Peter W Laird speaks with Storm Johnson, Commissioning Editor ... ...

Abstract	In this interview, Professor Peter W Laird speaks with Storm Johnson, Commissioning Editor for
MeSH term(s)	DNA Methylation ; Epigenesis, Genetic ; Epigenome ; Epigenomics ; Humans ; Male ; Neoplasms/genetics ; United States
Language	English
Publishing date	2022-03-24
Publishing country	England
Document type	Interview
ZDB-ID	2537199-X
ISSN	1750-192X ; 1750-1911
ISSN (online)	1750-192X
ISSN	1750-1911
DOI	10.2217/epi-2022-0066
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Article: Ultrasensitive amplification-free quantification of a methyl CpG-rich cancer biomarker by single-molecule kinetic fingerprinting.

Dai, Liuhan / Johnson-Buck, Alexander / Laird, Peter W / Tewari, Muneesh / Walter, Nils G

bioRxiv : the preprint server for biology

2024

Abstract: The most well-studied epigenetic marker in humans is the 5-methyl modification of cytosine in DNA, which has great potential as a disease biomarker in liquid biopsies of cell-free DNA. Currently, quantification of DNA methylation relies heavily on ... ...

Abstract	The most well-studied epigenetic marker in humans is the 5-methyl modification of cytosine in DNA, which has great potential as a disease biomarker in liquid biopsies of cell-free DNA. Currently, quantification of DNA methylation relies heavily on bisulfite conversion followed by PCR amplification and NGS or microarray analysis. PCR is subject to potential bias in differential amplification of bisulfite-converted methylated
Language	English
Publishing date	2024-04-10
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.04.06.587997
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Article ; Online: Cell division drives DNA methylation loss in late-replicating domains in primary human cells.

Endicott, Jamie L / Nolte, Paula A / Shen, Hui / Laird, Peter W

Nature communications

2022 Volume 13, Issue 1, Page(s) 6659

Abstract: DNA methylation undergoes dramatic age-related changes, first described more than four decades ago. Loss of DNA methylation within partially methylated domains (PMDs), late-replicating regions of the genome attached to the nuclear lamina, advances with ... ...

Abstract	DNA methylation undergoes dramatic age-related changes, first described more than four decades ago. Loss of DNA methylation within partially methylated domains (PMDs), late-replicating regions of the genome attached to the nuclear lamina, advances with age in normal tissues, and is further exacerbated in cancer. We present here experimental evidence that this DNA hypomethylation is directly driven by proliferation-associated DNA replication. Within PMDs, loss of DNA methylation at low-density CpGs in A:T-rich immediate context (PMD solo-WCGWs) tracks cumulative population doublings in primary cell culture. Cell cycle deceleration results in a proportional decrease in the rate of DNA hypomethylation. Blocking DNA replication via Mitomycin C treatment halts methylation loss. Loss of methylation continues unabated after TERT immortalization until finally reaching a severely hypomethylated equilibrium. Ambient oxygen culture conditions increases the rate of methylation loss compared to low-oxygen conditions, suggesting that some methylation loss may occur during unscheduled, oxidative damage repair-associated DNA synthesis. Finally, we present and validate a model to estimate the relative cumulative replicative histories of human cells, which we call "RepliTali" (Replication Times Accumulated in Lifetime).
MeSH term(s)	Humans ; DNA Methylation/genetics ; Cell Division/genetics ; Genome ; DNA/genetics ; Oxygen
Chemical Substances	DNA (9007-49-2) ; Oxygen (S88TT14065)
Language	English
Publishing date	2022-11-08
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-022-34268-8
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Article ; Online: DAB2IP Is a Bifunctional Tumor Suppressor That Regulates Wild-Type RAS and Inflammatory Cascades in KRAS Mutant Colon Cancer.

Miller, Abigail L / Perurena, Naiara / Gardner, Alycia / Hinoue, Toshinori / Loi, Patrick / Laird, Peter W / Cichowski, Karen

Cancer research

2023 Volume 83, Issue 11, Page(s) 1800–1814

Abstract: The DAB2IP tumor suppressor encodes a RAS GTPase-activating protein. Accordingly, DAB2IP has been shown to be mutated or suppressed in tumor types that typically lack RAS mutations. However, here we report that DAB2IP is mutated or selectively silenced ... ...

Abstract	The DAB2IP tumor suppressor encodes a RAS GTPase-activating protein. Accordingly, DAB2IP has been shown to be mutated or suppressed in tumor types that typically lack RAS mutations. However, here we report that DAB2IP is mutated or selectively silenced in the vast majority of KRAS and BRAF mutant colorectal cancers. In this setting, DAB2IP loss promoted tumor development by activating wild-type H- and N-RAS proteins, which was surprisingly required to achieve robust activation of RAS effector pathways in KRAS-mutant tumors. DAB2IP loss also triggered production of inflammatory mediators and the recruitment of protumorigenic macrophages in vivo. Importantly, tumor growth was suppressed by depleting macrophages or inhibiting cytokine/inflammatory mediator expression with a JAK/TBK1 inhibitor. In human tumors, DAB2IP was lost at early stages of tumor development, and its depletion was associated with an enrichment of macrophage and inflammatory signatures. Together, these findings demonstrate that DAB2IP restrains the activation of the RAS pathway and inflammatory cascades in the colon and that its loss represents a common and unappreciated mechanism for amplifying these two critical oncogenic signals in colorectal cancer. Significance: DAB2IP is lost in early-stage tumors, which amplifies RAS signaling, triggers inflammatory mediators, and recruits macrophages in KRAS-mutant colon cancers.
MeSH term(s)	Humans ; Proto-Oncogene Proteins p21(ras)/genetics ; Proto-Oncogene Proteins p21(ras)/metabolism ; Genes, Tumor Suppressor ; Colonic Neoplasms/genetics ; Signal Transduction ; ras GTPase-Activating Proteins/genetics ; ras GTPase-Activating Proteins/metabolism ; Cell Line, Tumor
Chemical Substances	Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2) ; ras GTPase-Activating Proteins ; KRAS protein, human ; DAB2IP protein, human
Language	English
Publishing date	2023-03-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-22-0370
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Article ; Online: BISCUIT: an efficient, standards-compliant tool suite for simultaneous genetic and epigenetic inference in bulk and single-cell studies.

Zhou, Wanding / Johnson, Benjamin K / Morrison, Jacob / Beddows, Ian / Eapen, James / Katsman, Efrat / Semwal, Ayush / Habib, Walid Abi / Heo, Lyong / Laird, Peter W / Berman, Benjamin P / Triche, Timothy J / Shen, Hui

Nucleic acids research

2024 Volume 52, Issue 6, Page(s) e32

Abstract: Data from both bulk and single-cell whole-genome DNA methylation experiments are under-utilized in many ways. This is attributable to inefficient mapping of methylation sequencing reads, routinely discarded genetic information, and neglected read-level ... ...

Abstract	Data from both bulk and single-cell whole-genome DNA methylation experiments are under-utilized in many ways. This is attributable to inefficient mapping of methylation sequencing reads, routinely discarded genetic information, and neglected read-level epigenetic and genetic linkage information. We introduce the BISulfite-seq Command line User Interface Toolkit (BISCUIT) and its companion R/Bioconductor package, biscuiteer, for simultaneous extraction of genetic and epigenetic information from bulk and single-cell DNA methylation sequencing. BISCUIT's performance, flexibility and standards-compliant output allow large, complex experimental designs to be characterized on clinical timescales. BISCUIT is particularly suited for processing data from single-cell DNA methylation assays, with its excellent scalability, efficiency, and ability to greatly enhance mappability, a key challenge for single-cell studies. We also introduce the epiBED format for single-molecule analysis of coupled epigenetic and genetic information, facilitating the study of cellular and tissue heterogeneity from DNA methylation sequencing.
MeSH term(s)	DNA Methylation ; Epigenesis, Genetic ; Epigenomics ; High-Throughput Nucleotide Sequencing ; Sequence Analysis, DNA ; Sulfites ; Software
Chemical Substances	Sulfites
Language	English
Publishing date	2024-02-22
Publishing country	England
Document type	Journal Article
ZDB-ID	186809-3
ISSN	1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
ISSN (online)	1362-4962 ; 1362-4954
ISSN	0301-5610 ; 0305-1048
DOI	10.1093/nar/gkae097
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Article ; Online: All Things in Moderation: Prevention of Intestinal Adenomas by DNA Hypomethylation.

Lee, Kwang-Ho / Laird, Peter W

Cancer prevention research (Philadelphia, Pa.)

2016 Volume 9, Issue 7, Page(s) 509–511

Abstract: DNA hypomethylation can prevent intestinal tumorigenesis, presumably by reducing epigenetic silencing of tumor-suppressor genes. A study in this issue by Sheaffer and colleagues challenges this notion by showing that severe DNA hypomethylation by tissue- ... ...

Abstract	DNA hypomethylation can prevent intestinal tumorigenesis, presumably by reducing epigenetic silencing of tumor-suppressor genes. A study in this issue by Sheaffer and colleagues challenges this notion by showing that severe DNA hypomethylation by tissue-specific Dnmt1 knockout can actually promote intestinal adenoma formation. Cancer Prev Res; 9(7); 509-11. ©2016 AACRSee related article by Sheaffer, et al., p. 534.
MeSH term(s)	Adenoma/genetics ; DNA ; DNA Methylation ; Genomic Instability ; Humans ; Intestinal Neoplasms/genetics
Chemical Substances	DNA (9007-49-2)
Language	English
Publishing date	2016-05-17
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	2434717-6
ISSN	1940-6215 ; 1940-6207
ISSN (online)	1940-6215
ISSN	1940-6207
DOI	10.1158/1940-6207.CAPR-16-0097
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Article ; Online: Principles and challenges of genomewide DNA methylation analysis.

Laird, Peter W

Nature reviews. Genetics

2010 Volume 11, Issue 3, Page(s) 191–203

Abstract: Methylation of cytosine bases in DNA provides a layer of epigenetic control in many eukaryotes that has important implications for normal biology and disease. Therefore, profiling DNA methylation across the genome is vital to understanding the influence ... ...

Abstract	Methylation of cytosine bases in DNA provides a layer of epigenetic control in many eukaryotes that has important implications for normal biology and disease. Therefore, profiling DNA methylation across the genome is vital to understanding the influence of epigenetics. There has been a revolution in DNA methylation analysis technology over the past decade: analyses that previously were restricted to specific loci can now be performed on a genome-scale and entire methylomes can be characterized at single-base-pair resolution. However, there is such a diversity of DNA methylation profiling techniques that it can be challenging to select one. This Review discusses the different approaches and their relative merits and introduces considerations for data analysis.
MeSH term(s)	Animals ; Chromatin Immunoprecipitation ; Computational Biology ; CpG Islands ; DNA Methylation/genetics ; DNA Restriction Enzymes ; Epigenesis, Genetic ; Gene Expression Profiling ; Genetic Techniques/statistics & numerical data ; Genomics ; Humans ; Nucleic Acid Amplification Techniques ; Reproducibility of Results ; Sequence Analysis, DNA ; Sulfites
Chemical Substances	Sulfites ; DNA Restriction Enzymes (EC 3.1.21.-) ; sodium bisulfite (TZX5469Z6I)
Language	English
Publishing date	2010-02-02
Publishing country	England
Document type	Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2035157-4
ISSN	1471-0064 ; 1471-0056
ISSN (online)	1471-0064
ISSN	1471-0056
DOI	10.1038/nrg2732
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Article ; Online: The USC Epigenome Center.

Laird, Peter W

Epigenomics

2009 Volume 1, Issue 1, Page(s) 29–31

Abstract: The University of Southern California (USC, CA, USA) has a long tradition of excellence in epigenetics. With the recent explosive growth and technological maturation of the field of epigenetics, it became clear that a dedicated high-throughput epigenomic ...

Abstract	The University of Southern California (USC, CA, USA) has a long tradition of excellence in epigenetics. With the recent explosive growth and technological maturation of the field of epigenetics, it became clear that a dedicated high-throughput epigenomic data production facility would be needed to remain at the forefront of epigenetic research. To address this need, USC launched the USC Epigenome Center as the first large-scale center in academics dedicated to epigenomic research. The Center is providing high-throughput data production for large-scale genomic and epigenomic studies, and developing novel analysis tools for epigenomic research. This unique facility promises to be a valuable resource for multidisciplinary research, education and training in genomics, epigenomics, bioinformatics, and translational medicine.
MeSH term(s)	Academies and Institutes ; California ; Computational Biology ; DNA Methylation ; Epigenesis, Genetic ; Histones/metabolism ; Humans ; United States ; Universities
Chemical Substances	Histones
Language	English
Publishing date	2009-10
Publishing country	England
Document type	Journal Article
ISSN	1750-192X
ISSN (online)	1750-192X
DOI	10.2217/epi.09.12
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Article ; Online: Comprehensive Evaluation of The Infinium Human MethylationEPIC v2 BeadChip.

Kaur, Diljeet / Lee, Sol Moe / Goldberg, David / Spix, Nathan J / Hinoue, Toshinori / Li, Hong-Tao / Dwaraka, Varun B / Smith, Ryan / Shen, Hui / Liang, Gangning / Renke, Nicole / Laird, Peter W / Zhou, Wanding

Epigenetics communications

2023 Volume 3, Issue 1

Abstract: Infinium Methylation BeadChips are widely used to profile DNA cytosine modifications in large cohort studies for reasons of cost-effectiveness, accurate quantification, and user-friendly data analysis in characterizing these canonical epigenetic marks. ... ...

Abstract	Infinium Methylation BeadChips are widely used to profile DNA cytosine modifications in large cohort studies for reasons of cost-effectiveness, accurate quantification, and user-friendly data analysis in characterizing these canonical epigenetic marks. In this work, we conducted a comprehensive evaluation of the updated Infinium MethylationEPIC v2 BeadChip (EPICv2). Our evaluation revealed that EPICv2 offers significant improvements over its predecessors, including expanded enhancer coverage, applicability to diverse ancestry groups, support for low-input DNA down to one nanogram, coverage of existing epigenetic clocks, cell type deconvolution panels, and human trait associations, while maintaining accuracy and reproducibility. Using EPICv2, we were able to identify epigenome and sequence signatures in cell line models of
Language	English
Publishing date	2023-09-27
Publishing country	England
Document type	Journal Article
ISSN	2730-7034
ISSN (online)	2730-7034
DOI	10.1186/s43682-023-00021-5
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Article ; Online: SeSAMe: reducing artifactual detection of DNA methylation by Infinium BeadChips in genomic deletions.

Zhou, Wanding / Triche, Timothy J / Laird, Peter W / Shen, Hui

Nucleic acids research

2018 Volume 46, Issue 20, Page(s) e123

Abstract: We report a new class of artifacts in DNA methylation measurements from Illumina HumanMethylation450 and MethylationEPIC arrays. These artifacts reflect failed hybridization to target DNA, often due to germline or somatic deletions and manifest as ... ...

Abstract	We report a new class of artifacts in DNA methylation measurements from Illumina HumanMethylation450 and MethylationEPIC arrays. These artifacts reflect failed hybridization to target DNA, often due to germline or somatic deletions and manifest as incorrectly reported intermediate methylation. The artifacts often survive existing preprocessing pipelines, masquerade as epigenetic alterations and can confound discoveries in epigenome-wide association studies and studies of methylation-quantitative trait loci. We implement a solution, P-value with out-of-band (OOB) array hybridization (pOOBAH), in the R package SeSAMe. Our method effectively masks deleted and hyperpolymorphic regions, reducing or eliminating spurious reports of epigenetic silencing at oft-deleted tumor suppressor genes such as CDKN2A and RB1 in cases with somatic deletions. Furthermore, our method substantially decreases technical variation whilst retaining biological variation, both within and across HM450 and EPIC platform measurements. SeSAMe provides a light-weight, modular DNA methylation data analysis suite, with a performant implementation suitable for efficient analysis of thousands of samples.
MeSH term(s)	Artifacts ; Benchmarking ; DNA Methylation ; DNA Probes ; DNA, Neoplasm/genetics ; Datasets as Topic ; Gene Dosage ; Genome ; Germ-Line Mutation ; High-Throughput Screening Assays/instrumentation ; Humans ; Neoplasms/genetics ; Oligonucleotide Array Sequence Analysis ; Polymorphism, Genetic ; Quantitative Trait Loci ; Reproducibility of Results ; Sequence Deletion ; Software
Chemical Substances	DNA Probes ; DNA, Neoplasm
Language	English
Publishing date	2018-08-07
Publishing country	England
Document type	Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	186809-3
ISSN	1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
ISSN (online)	1362-4962 ; 1362-4954
ISSN	0301-5610 ; 0305-1048
DOI	10.1093/nar/gky691
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