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Article ; Online: A precision environmental health approach to prevention of human disease.

Baccarelli, Andrea / Dolinoy, Dana C / Walker, Cheryl Lyn

2023 Volume 14, Issue 1, Page(s) 2449

Abstract: Human health is determined by the interaction of our environment with the genome, epigenome, and microbiome, which shape the transcriptomic, proteomic, and metabolomic landscape of cells and tissues. Precision environmental health is an emerging field ... ...

Abstract	Human health is determined by the interaction of our environment with the genome, epigenome, and microbiome, which shape the transcriptomic, proteomic, and metabolomic landscape of cells and tissues. Precision environmental health is an emerging field leveraging environmental and system-level ('omic) data to understand underlying environmental causes of disease, identify biomarkers of exposure and response, and develop new prevention and intervention strategies. In this article we provide real-life illustrations of the utility of precision environmental health approaches, identify current challenges in the field, and outline new opportunities to promote health through a precision environmental health framework.
MeSH term(s)	Humans ; Proteomics ; Health Promotion ; Environmental Health ; Microbiota ; Biomarkers
Chemical Substances	Biomarkers
Language	English
Publishing date	2023-04-28
Publishing country	England
Document type	Journal Article ; Review ; 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/s41467-023-37626-2
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Article ; Online: Minireview: Epigenomic Plasticity and Vulnerability to EDC Exposures.

Walker, Cheryl Lyn

Molecular endocrinology (Baltimore, Md.)

2016 Volume 30, Issue 8, Page(s) 848–855

Abstract: The epigenome undergoes significant remodeling during tissue and organ development, which coincides with a period of exquisite sensitivity to environmental exposures. In the case of endocrine-disrupting compounds (EDCs), exposures can reprogram the ... ...

Abstract	The epigenome undergoes significant remodeling during tissue and organ development, which coincides with a period of exquisite sensitivity to environmental exposures. In the case of endocrine-disrupting compounds (EDCs), exposures can reprogram the epigenome of developing tissues to increase susceptibility to diseases later in life, a process termed "developmental reprogramming." Both DNA methylation and histone modifications have been shown to be vulnerable to disruption by EDC exposures, and several mechanisms have been identified by which EDCs can reprogram the epigenome. These include altered methyl donor availability, loss of imprinting control, changes in dioxygenase activity, altered expression of noncoding RNAs, and activation of cell signaling pathways that can phosphorylate, and alter the activity of, histone methyltransferases. This altered epigenomic programming can persist across the life course, and in some instances generations, to alter gene expression in ways that correlate with increased disease susceptibility. Together, these studies on developmental reprogramming of the epigenome by EDCs are providing new insights into epigenomic plasticity that is vulnerable to disruption by environmental exposures.
Language	English
Publishing date	2016-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	639167-9
ISSN	1944-9917 ; 0888-8809
ISSN (online)	1944-9917
ISSN	0888-8809
DOI	10.1210/me.2016-1086
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Article ; Online: Clear cell renal cell carcinoma ontogeny and mechanisms of lethality.

Jonasch, Eric / Walker, Cheryl Lyn / Rathmell, W Kimryn

Nature reviews. Nephrology

2020 Volume 17, Issue 4, Page(s) 245–261

Abstract: The molecular features that define clear cell renal cell carcinoma (ccRCC) initiation and progression are being increasingly defined. The TRACERx Renal studies and others that have described the interaction between tumour genomics and remodelling of the ... ...

Abstract	The molecular features that define clear cell renal cell carcinoma (ccRCC) initiation and progression are being increasingly defined. The TRACERx Renal studies and others that have described the interaction between tumour genomics and remodelling of the tumour microenvironment provide important new insights into the molecular drivers underlying ccRCC ontogeny and progression. Our understanding of common genomic and chromosomal copy number abnormalities in ccRCC, including chromosome 3p loss, provides a mechanistic framework with which to organize these abnormalities into those that drive tumour initiation events, those that drive tumour progression and those that confer lethality. Truncal mutations in ccRCC, including those in VHL, SET2, PBRM1 and BAP1, may engender genomic instability and promote defects in DNA repair pathways. The molecular features that arise from these defects enable categorization of ccRCC into clinically and therapeutically relevant subtypes. Consideration of the interaction of these subtypes with the tumour microenvironment reveals that specific mutations seem to modulate immune cell populations in ccRCC tumours. These findings present opportunities for disease prevention, early detection, prognostication and treatment.
MeSH term(s)	Biomarkers, Tumor/genetics ; Biomarkers, Tumor/metabolism ; Carcinoma, Renal Cell/genetics ; Carcinoma, Renal Cell/metabolism ; Carcinoma, Renal Cell/mortality ; Carcinoma, Renal Cell/pathology ; Disease Progression ; Gene Expression Regulation, Neoplastic ; Humans ; Kidney Neoplasms/genetics ; Kidney Neoplasms/metabolism ; Kidney Neoplasms/mortality ; Kidney Neoplasms/pathology ; Mutation ; Prognosis ; Tumor Microenvironment/genetics
Chemical Substances	Biomarkers, Tumor
Language	English
Publishing date	2020-11-03
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2490366-8
ISSN	1759-507X ; 1759-5061
ISSN (online)	1759-507X
ISSN	1759-5061
DOI	10.1038/s41581-020-00359-2
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Zs.MG 107: Show issues

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Article ; Online: Epigenomic reprogramming of the developing reproductive tract and disease susceptibility in adulthood.

Walker, Cheryl Lyn

Birth defects research. Part A, Clinical and molecular teratology

2011 Volume 91, Issue 8, Page(s) 666–671

Abstract: During development, epigenetic programs are "installed" on the genome that direct differentiation and normal tissue and organ function in adulthood. Consequently, development is also a period of susceptibility to reprogramming of the epigenome. ... ...

Abstract	During development, epigenetic programs are "installed" on the genome that direct differentiation and normal tissue and organ function in adulthood. Consequently, development is also a period of susceptibility to reprogramming of the epigenome. Developmental reprogramming occurs when an adverse stimulus or insult interrupts the proper "install" of epigenetic programs during development, reprogramming normal physiologic responses in such a way as to promote disease later in life. Some of the best examples of developmental reprogramming involve the reproductive tract, where early life exposures to environmental estrogens can increase susceptibility to benign and malignant tumors in adulthood including leiomyoma (fibroids), endometrial, and prostate cancer. Although specific mechanism(s) by which environmental estrogens reprogram the developing epigenome were unknown, both DNA and histone methylation were considered likely targets for epigenetic reprogramming. We have now identified a mechanism by which developmental exposures to environmental estrogens reprogram the epigenome by inducing inappropriate activation of nongenomic estrogen receptor (ER) signaling. Activation of nongenomic ER signaling via the phosphotidylinositol-3-kinase (PI3K) pathway activates the kinase AKT/PKB in the developing reproductive tract, which phosphorylates the histone lysine methyltransferase (HKMT) EZH2, the key "installer" of epigenetic histone H3 lysine 27 trimethylation (H3K27me3). AKT phosphorylation inactivates EZH2, decreasing levels of H3K27 methylation, a repressive mark that inhibits gene expression, in the developing uterus. As a result of this developmental reprogramming, many estrogen-responsive genes become hypersensitive to estrogen in adulthood, exhibiting elevated expression throughout the estrus cycle, and resulting in a "hyper-estrogenized" phenotype in the adult uterus that promotes development of hormone-dependent tumors.
MeSH term(s)	Adult ; Animals ; Disease Susceptibility ; Epigenesis, Genetic/drug effects ; Estrogens/pharmacology ; Female ; Gene Expression Regulation, Developmental ; Genitalia, Female/pathology ; Genitalia, Male/pathology ; Humans ; Male
Chemical Substances	Estrogens
Language	English
Publishing date	2011-06-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2104792-3
ISSN	1542-0760 ; 1542-0752 ; 1542-9733 ; 1542-975X
ISSN (online)	1542-0760
ISSN	1542-0752 ; 1542-9733 ; 1542-975X
DOI	10.1002/bdra.20827
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Zs.A 749: Show issues

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Article ; Online: The peroxisome as a cell signaling organelle.

Tripathi, Durga Nand / Walker, Cheryl Lyn

Current opinion in cell biology

2016 Volume 39, Page(s) 109–112

Abstract: Peroxisomes participate in lipid metabolism, and are a major source of ROS in the cell. Their importance in cellular energy balance and redox homeostasis is well-established, as is the need to maintain peroxisome homeostasis to prevent pathologies ... ...

Abstract	Peroxisomes participate in lipid metabolism, and are a major source of ROS in the cell. Their importance in cellular energy balance and redox homeostasis is well-established, as is the need to maintain peroxisome homeostasis to prevent pathologies associated with too few, or too many, of these organelles. How cells regulate peroxisome number has remained somewhat elusive. Recently, the tumor suppressors ATM and TSC, which regulate mTORC1 signaling, have been localized to peroxisomes. When activated by peroxisomal ROS, ATM signals to TSC to repress mTORC1 signaling and increase autophagic flux in cells, and also phosphorylates the peroxisomal protein PEX 5 to target peroxisomes for selective autophagy (pexophagy), providing a mechanism for regulation of peroxisomal homeostasis using ROS as a rheostat.
MeSH term(s)	Animals ; Autophagy ; Homeostasis ; Humans ; Organelles/metabolism ; Peroxisomes/metabolism ; Signal Transduction
Language	English
Publishing date	2016-04
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1026381-0
ISSN	1879-0410 ; 0955-0674
ISSN (online)	1879-0410
ISSN	0955-0674
DOI	10.1016/j.ceb.2016.02.017
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Article: A Model Linking Sickle Cell Hemoglobinopathies and SMARCB1 Loss in Renal Medullary Carcinoma.

Msaouel, Pavlos / Tannir, Nizar M / Walker, Cheryl Lyn

Clinical cancer research : an official journal of the American Association for Cancer Research

2018 Volume 24, Issue 9, Page(s) 2044–2049

Abstract: Renal medullary carcinoma (RMC) is a highly aggressive malignancy that predominantly afflicts young adults and adolescents with sickle hemoglobinopathies. It is characterized by complete loss of expression of the chromatin remodeler and tumor ... ...

Abstract	Renal medullary carcinoma (RMC) is a highly aggressive malignancy that predominantly afflicts young adults and adolescents with sickle hemoglobinopathies. It is characterized by complete loss of expression of the chromatin remodeler and tumor suppressor
MeSH term(s)	Anemia, Sickle Cell/complications ; Anemia, Sickle Cell/diagnosis ; Anemia, Sickle Cell/genetics ; Animals ; Biomarkers ; Carcinoma, Medullary/complications ; Carcinoma, Medullary/diagnosis ; Carcinoma, Medullary/genetics ; Carcinoma, Renal Cell/complications ; Carcinoma, Renal Cell/diagnosis ; Carcinoma, Renal Cell/genetics ; Cell Transformation, Neoplastic ; Chromosome Mapping ; Disease Susceptibility ; Gene Deletion ; Humans ; Hypoxia/genetics ; Hypoxia/metabolism ; Osmotic Pressure ; SMARCB1 Protein/genetics
Chemical Substances	Biomarkers ; SMARCB1 Protein ; SMARCB1 protein, human
Language	English
Publishing date	2018-02-12
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-17-3296
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Article: An actin-WHAMM interaction linking SETD2 and autophagy

Seervai, Riyad N.H / Grimm, Sandra L / Jangid, Rahul K / Tripathi, Durga Nand / Coarfa, Cristian / Walker, Cheryl Lyn

Biochemical and biophysical research communications. 2020 Sept. 09,

2020

Abstract: The process of autophagy is dysregulated in many cancers including clear cell renal cell carcinoma (ccRCC). Autophagy involves the coordination of numerous autophagy-related (ATG) genes, as well as processes involving the actin cytoskeleton. The histone ... ...

Abstract	The process of autophagy is dysregulated in many cancers including clear cell renal cell carcinoma (ccRCC). Autophagy involves the coordination of numerous autophagy-related (ATG) genes, as well as processes involving the actin cytoskeleton. The histone methyltransferase SETD2, frequently inactivated in ccRCC, has recently been shown to also methylate cytoskeletal proteins, which in the case of actin lysine 68 trimethylation (ActK68me3) regulates actin polymerization dynamics. Here we show that cells lacking SETD2 exhibit autophagy defects, as well as decreased interaction of the actin nucleation promoting factor WHAMM with its target actin, which is required for initiation of autophagy. Interestingly, the WHAMM actin binding deficit could be rescued with pharmacologic induction of actin polymerization in SETD2-null cells using Jasplakinolide. These data indicate that the decreased interaction between WHAMM and its target actin in SETD2-null cells was secondary to altered actin dynamics rather than loss of the SETD2 ActK68me3 mark itself, and underscores the importance of the functional defect in actin polymerization in SETD2-null cells exhibiting autophagy defects.
Keywords	actin ; autophagy ; histones ; lysine ; methyltransferases ; microfilaments ; polymerization ; renal cell carcinoma ; research
Language	English
Dates of publication	2020-0909
Publishing place	Elsevier Inc.
Document type	Article
Note	NAL-AP-2-clean ; Pre-press version
ZDB-ID	205723-2
ISSN	0006-291X ; 0006-291X
ISSN (online)	0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2020.09.025
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Article ; Online: Developmental reprogramming of cancer susceptibility.

Walker, Cheryl Lyn / Ho, Shuk-mei

Nature reviews. Cancer

2012 Volume 12, Issue 7, Page(s) 479–486

Abstract: Gene-environment interactions have been traditionally understood to promote the acquisition of mutations that drive multistage carcinogenesis, and, in the case of inherited defects in tumour suppressor genes, additional mutations are required for cancer ... ...

Abstract	Gene-environment interactions have been traditionally understood to promote the acquisition of mutations that drive multistage carcinogenesis, and, in the case of inherited defects in tumour suppressor genes, additional mutations are required for cancer development. However, the developmental origins of health and disease (DOHAD) hypothesis provides an alternative model whereby environmental exposures during development increase susceptibility to cancer in adulthood, not by inducing genetic mutations, but by reprogramming the epigenome. We hypothesize that this epigenetic reprogramming functions as a new type of gene-environment interaction by which environmental exposures target the epigenome to increase cancer susceptibility.
MeSH term(s)	Disease Susceptibility/etiology ; Epigenesis, Genetic/physiology ; Female ; Gene Expression Regulation, Neoplastic/physiology ; Gene-Environment Interaction ; Humans ; Pregnancy ; Prenatal Exposure Delayed Effects/genetics ; Prenatal Exposure Delayed Effects/pathology
Language	English
Publishing date	2012-06-14
Publishing country	England
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. ; Review
ZDB-ID	2062767-1
ISSN	1474-1768 ; 1474-175X
ISSN (online)	1474-1768
ISSN	1474-175X
DOI	10.1038/nrc3220
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Zs.A 5563: 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: SETD2 safeguards the genome against isochromosome formation.

Mason, Frank M / Kounlavong, Emily S / Tebeje, Anteneh T / Dahiya, Rashmi / Guess, Tiffany / Khan, Abid / Vlach, Logan / Norris, Stephen R / Lovejoy, Courtney A / Dere, Ruhee / Strahl, Brian D / Ohi, Ryoma / Ly, Peter / Walker, Cheryl Lyn / Rathmell, W Kimryn

Proceedings of the National Academy of Sciences of the United States of America

2023 Volume 120, Issue 39, Page(s) e2303752120

Abstract: Isochromosomes are mirror-imaged chromosomes with simultaneous duplication and deletion of genetic material which may contain two centromeres to create isodicentric chromosomes. Although isochromosomes commonly occur in cancer and developmental disorders ...

Abstract	Isochromosomes are mirror-imaged chromosomes with simultaneous duplication and deletion of genetic material which may contain two centromeres to create isodicentric chromosomes. Although isochromosomes commonly occur in cancer and developmental disorders and promote genome instability, mechanisms that prevent isochromosomes are not well understood. We show here that the tumor suppressor and methyltransferase SETD2 is essential to prevent these errors. Using cellular and cytogenetic approaches, we demonstrate that loss of SETD2 or its epigenetic mark, histone H3 lysine 36 trimethylation (H3K36me3), results in the formation of isochromosomes as well as isodicentric and acentric chromosomes. These defects arise during DNA replication and are likely due to faulty homologous recombination by RAD52. These data provide a mechanism for isochromosome generation and demonstrate that SETD2 and H3K36me3 are essential to prevent the formation of this common mutable chromatin structure known to initiate a cascade of genomic instability in cancer.
MeSH term(s)	Humans ; Centromere ; Chromosome Aberrations ; Cytogenetics ; DNA Replication ; Genomic Instability ; Isochromosomes
Chemical Substances	SETD2 protein, human (EC 2.1.1.43)
Language	English
Publishing date	2023-09-18
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2303752120
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Article ; Online: An actin-WHAMM interaction linking SETD2 and autophagy.

Seervai, Riyad N H / Grimm, Sandra L / Jangid, Rahul K / Tripathi, Durga Nand / Coarfa, Cristian / Walker, Cheryl Lyn

Biochemical and biophysical research communications

2020 Volume 558, Page(s) 202–208

Abstract	The process of autophagy is dysregulated in many cancers including clear cell renal cell carcinoma (ccRCC). Autophagy involves the coordination of numerous autophagy-related (ATG) genes, as well as processes involving the actin cytoskeleton. The histone methyltransferase SETD2, frequently inactivated in ccRCC, has recently been shown to also methylate cytoskeletal proteins, which in the case of actin lysine 68 trimethylation (ActK68me3) regulates actin polymerization dynamics. Here we show that cells lacking SETD2 exhibit autophagy defects, as well as decreased interaction of the actin nucleation promoting factor WHAMM with its target actin, which is required for initiation of autophagy. Interestingly, the WHAMM actin binding deficit could be rescued with pharmacologic induction of actin polymerization in SETD2-null cells using Jasplakinolide. These data indicate that the decreased interaction between WHAMM and its target actin in SETD2-null cells was secondary to altered actin dynamics rather than loss of the SETD2 ActK68me3 mark itself, and underscores the importance of the functional defect in actin polymerization in SETD2-null cells exhibiting autophagy defects.
MeSH term(s)	Actins/metabolism ; Autophagy/genetics ; Autophagy/physiology ; Autophagy-Related Proteins/genetics ; Autophagy-Related Proteins/metabolism ; Carcinoma, Renal Cell/genetics ; Carcinoma, Renal Cell/metabolism ; Carcinoma, Renal Cell/pathology ; Cell Line ; Cell Line, Tumor ; Down-Regulation ; Gene Knockout Techniques ; Histone-Lysine N-Methyltransferase/deficiency ; Histone-Lysine N-Methyltransferase/genetics ; Histone-Lysine N-Methyltransferase/metabolism ; Humans ; Kidney Neoplasms/genetics ; Kidney Neoplasms/metabolism ; Kidney Neoplasms/pathology ; Membrane Proteins/metabolism ; Microtubule-Associated Proteins/metabolism
Chemical Substances	Actins ; Autophagy-Related Proteins ; Membrane Proteins ; Microtubule-Associated Proteins ; WHAMM protein, human ; Histone-Lysine N-Methyltransferase (EC 2.1.1.43) ; SETD2 protein, human (EC 2.1.1.43)
Language	English
Publishing date	2020-10-06
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	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2020.09.025
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