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Article ; Online: A Murine Kitl Allele Regulates Skin Mast Cell Density across 58 Collaborative Mouse Cross Strains.

Walker, Graeme J / Galbraith, Jack A / Baz, Betoul / Ferguson, Blake / Handoko, Herlina Y / Khosrotehrani, Kiarash

The Journal of investigative dermatology

2022 Volume 142, Issue 8, Page(s) 2275–2280.e4

MeSH term(s)	Alleles ; Animals ; Cell Count ; Mast Cells ; Mice ; Skin
Language	English
Publishing date	2022-01-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80136-7
ISSN	1523-1747 ; 0022-202X
ISSN (online)	1523-1747
ISSN	0022-202X
DOI	10.1016/j.jid.2021.12.032
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Article ; Online: Further assessment of exome-wide UVR footprints in melanoma and their possible relevance.

Mukhopadhyay, Pamela / Roberts, James A / Walker, Graeme J

Molecular carcinogenesis

2017 Volume 56, Issue 6, Page(s) 1673–1679

Abstract: C>T substitutions at dipyrimidine sites dominate the melanoma genome. We recently analyzed the exomes of spontaneous and neonatal UVR-induced murine melanomas, noting a dramatic change in the genomic footprint at C>T substitutions in the latter. Here we ... ...

Abstract	C>T substitutions at dipyrimidine sites dominate the melanoma genome. We recently analyzed the exomes of spontaneous and neonatal UVR-induced murine melanomas, noting a dramatic change in the genomic footprint at C>T substitutions in the latter. Here we re-analyzed published exome-wide footprints in human melanomas stratified in terms of likely previous sun exposure. Acral and mucosal melanomas were heterogeneous in terms of base substitution types, but most C>Ts occurred in the context of 3'G, probably resulting from spontaneous deamination of the cytosine. C>Ts in sun-exposed melanomas were statistically different from acral/mucosal lesions only in preferring an adjacent 5'T and 3'C. Pyrimidine dimer adducts can form between any pyrimidine (TT, TC, CT, CC). Hence in melanoma C>Ts are overwhelmingly induced at TC or CC photoproducts, or, there are peculiarities in DNA repair that favor the mutation of cytosines with these two pyrimidines adjacent. If melanoma UVR footprints at C>Ts reflect a specific dimer type (eg, 6-4 photoproduct or cyclobutane pyrimidine dimer), these could be removed post UVR, for instance using photolyases, to potentially reduce melanoma risk. If specific modes of DNA repair and/or replication cause these footprints, methodically downregulating selected DNA polymerases in UVR-induced animal models of melanoma, combined with exome sequencing, could begin to assess this. Finally, a preponderance of TpCpC as opposed to NpCpG at C>Ts exome-wide is likely to be a good indicator of whether a melanoma has incurred even a small amount of sun damage. This information will assist epidemiological studies in predicting individual levels of sun exposure.
MeSH term(s)	Animals ; Exome/radiation effects ; Humans ; Melanoma/genetics ; Mutation/radiation effects ; Neoplasms, Radiation-Induced/genetics ; Pyrimidine Dimers/genetics ; Ultraviolet Rays
Chemical Substances	Pyrimidine Dimers
Language	English
Publishing date	2017
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1004029-8
ISSN	1098-2744 ; 0899-1987
ISSN (online)	1098-2744
ISSN	0899-1987
DOI	10.1002/mc.22623
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Zs.A 2664: Show issues

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Article ; Online: Clinicopathological characterization of mouse models of melanoma.

Ferguson, Blake / Soyer, H Peter / Walker, Graeme J

Methods in molecular biology (Clifton, N.J.)

2015 Volume 1267, Page(s) 251–261

Abstract: Mouse models of melanoma have proven invaluable in the delineation of key molecular events involved in disease progression in humans and provide potential preclinical models for therapeutic testing (Damsky and Bosenberg, Pigment Cell Melanoma Res 25(4): ... ...

Abstract	Mouse models of melanoma have proven invaluable in the delineation of key molecular events involved in disease progression in humans and provide potential preclinical models for therapeutic testing (Damsky and Bosenberg, Pigment Cell Melanoma Res 25(4):404-405, 2012; Walker et al., Pigment Cell Melanoma Res 24(6):1158-1176, 2011). Here we concentrate on the clinicopathological analysis of melanocytic tumors.
MeSH term(s)	Animals ; Dermoscopy ; Disease Models, Animal ; Eosine Yellowish-(YS)/metabolism ; Hematoxylin/metabolism ; Immunohistochemistry ; Melanocytes/pathology ; Melanocytes/radiation effects ; Melanoma/diagnosis ; Melanoma/etiology ; Melanoma/metabolism ; Melanoma/pathology ; Membrane Glycoproteins/metabolism ; Mice ; Oxidoreductases/metabolism ; Paraffin Embedding ; SOXE Transcription Factors/metabolism ; Skin Neoplasms/diagnosis ; Skin Neoplasms/etiology ; Skin Neoplasms/metabolism ; Skin Neoplasms/pathology ; Staining and Labeling ; Tissue Fixation ; Ultraviolet Rays/adverse effects
Chemical Substances	Membrane Glycoproteins ; SOXE Transcription Factors ; Sox10 protein, mouse ; Oxidoreductases (EC 1.-) ; Tyrp1 protein, mouse (EC 1.14.18.-) ; Eosine Yellowish-(YS) (TDQ283MPCW) ; Hematoxylin (YKM8PY2Z55)
Language	English
Publishing date	2015
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-4939-2297-0_11
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Article ; Online: Mouse models for actinic keratosis and squamous cell carcinoma.

Handoko, Herlina Y / Ferguson, Blake / Walker, Graeme J

Current problems in dermatology

2015 Volume 46, Page(s) 42–48

Abstract: This manuscript focuses on the use of mice to study the genetics and biology of cutaneous squamous cell carcinoma (SCC). Mice develop actinic keratosis-like lesions and SCC resembling those seen in humans. As an animal model, the mouse provides great ... ...

Abstract	This manuscript focuses on the use of mice to study the genetics and biology of cutaneous squamous cell carcinoma (SCC). Mice develop actinic keratosis-like lesions and SCC resembling those seen in humans. As an animal model, the mouse provides great experimental flexibility and has been useful in investigating aspects of the genetics and biology of SCC that are difficult to study in humans. We discuss the pros and cons of the various murine models available. How well mouse pathology in general mimics human disease remains an open question due to the vast differences in animal strain backgrounds and the fact that only one strain is typically tested in any particular experiment. Nonetheless, the murine epidermis is thinner than the human epidermis, and this must be kept in mind when making inferences from mechanistic data obtained with mice. We outline new strategies for non-biased screens to discover genes driving SCC progression. Such work has revealed a very complex interactive molecular network, and as with other complex diseases, the picture is being pieced together using systems biology strategies to which mouse tumour models are amenable. Such approaches do not focus on single genes or proteins but try to integrate the complex interactions of many types of genetic and biological information.
MeSH term(s)	Animals ; Carcinoma, Squamous Cell/chemically induced ; Carcinoma, Squamous Cell/genetics ; Disease Models, Animal ; Keratosis, Actinic/chemically induced ; Keratosis, Actinic/genetics ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Neoplasms, Experimental/chemically induced ; Neoplasms, Experimental/genetics ; Skin Neoplasms/chemically induced ; Skin Neoplasms/genetics
Language	English
Publishing date	2015
Publishing country	Switzerland
Document type	Journal Article
ISSN	1662-2944 ; 0070-2064 ; 1421-5721
ISSN (online)	1662-2944
ISSN	0070-2064 ; 1421-5721
DOI	10.1159/000366534
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Article ; Online: Murine dorsal hair type is genetically determined by polymorphisms in candidate genes that influence BMP and WNT signalling.

Villani, Rehan M / Johnson, Ayaka / Galbraith, Jack A / Baz, Betoul / Handoko, Herlina Y / Walker, Graeme J / Khosrotehrani, Kiarash

Experimental dermatology

2020 Volume 29, Issue 5, Page(s) 450–461

Abstract: Mouse dorsal coat hair types, guard, awl, auchene and zigzag, develop in three consecutive waves. To date, it is unclear if these hair types are determined genetically through expression of specific factors or can change based on their mesenchymal ... ...

Abstract	Mouse dorsal coat hair types, guard, awl, auchene and zigzag, develop in three consecutive waves. To date, it is unclear if these hair types are determined genetically through expression of specific factors or can change based on their mesenchymal environment. We undertook a novel approach to this question by studying individual hair type in 67 Collaborative Cross (CC) mouse lines and found significant variation in the proportion of each type between strains. Variation in the proportion of zigzag, awl and auchene, but not guard hair, was largely due to germline genetic variation. We utilised this variation to map a quantitative trait locus (QTL) on chromosome 12 that appears to influence a decision point switch controlling the propensity for either second (awl and auchene) or third wave (zigzag) hairs to develop. This locus contains two strong candidates, Sostdc1 and Twist1, each of which carry several ENCODE regulatory variants, specific to the causal allele, that can influence gene expression, are expressed in the developing hair follicle, and have been previously reported to be involved in regulating human and murine hair behaviour, but not hair subtype determination. Both of these genes are likely to play a part in hair type determination via regulation of BMP and/or WNT signalling.
MeSH term(s)	Adaptor Proteins, Signal Transducing/genetics ; Animals ; Bone Morphogenetic Proteins/metabolism ; Chromosome Mapping ; Crosses, Genetic ; Dermis/metabolism ; Genetic Linkage ; Genome-Wide Association Study ; Hair/physiology ; Mice ; Phenotype ; Polymorphism, Genetic ; Quantitative Trait Loci ; Signal Transduction ; Species Specificity ; Twist-Related Protein 1/genetics ; Wnt Proteins/metabolism
Chemical Substances	Adaptor Proteins, Signal Transducing ; Bone Morphogenetic Proteins ; Sostdc1 protein, mouse ; Twist-Related Protein 1 ; Wnt Proteins ; Twist1 protein, mouse (136253-27-5)
Language	English
Publishing date	2020-03-20
Publishing country	Denmark
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1130936-2
ISSN	1600-0625 ; 0906-6705
ISSN (online)	1600-0625
ISSN	0906-6705
DOI	10.1111/exd.14090
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Zs.A 3508: Show issues

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Article ; Online: Keratinocyte Cytokine Networks Associated with Human Melanocytic Nevus Development.

Chitsazan, Arash / Mukhopadhyay, Pamela / Ferguson, Blake / Handoko, Herlina Y / Walker, Graeme J

The Journal of investigative dermatology

2018 Volume 139, Issue 1, Page(s) 177–185

Abstract: Melanocytes can group together in nevi, commonly thought to form because of intrinsic somatic mutations involving MAPK pathway activation. However, the role of the microenvironment, in particular keratinocytes, in nevogenesis is rarely studied. ... ...

Abstract	Melanocytes can group together in nevi, commonly thought to form because of intrinsic somatic mutations involving MAPK pathway activation. However, the role of the microenvironment, in particular keratinocytes, in nevogenesis is rarely studied. Melanocytes proliferate during the hair follicle growth phase and in some basal cell carcinomas, allowing us to construct keratinocyte gene expression clusters correlated with melanocyte activation. We asked whether such correlations are evident in the more subtle context of regulation of melanocyte behavior in normal skin. We considered genes which, when mutated in keratinocytes in mice, lead to nevogenesis. Across the human GTEx normal skin database, their expression was correlated with that of keratinocyte cytokines KITLG, HGF, FGF2, EDN1, and melanocyte markers. These cytokines have pleiotropic effects on melanocyte-specific and pigmentation genes and also influence mast cell gene expression. We show five classes of keratinocyte genes that, via germline genetic variation, influence melanocyte activity. These include genes involved in SHH signaling, structural keratins, ribosomal biogenesis, and stem cell governance. In agreement with the finding of KITLG linked to nevogenesis in human genome-wide association studies, we provide evidence that specific keratinocyte cytokines are components of networks that may drive or exacerbate nevus development.
MeSH term(s)	Animals ; Cytokines/biosynthesis ; Cytokines/genetics ; Gene Expression Regulation, Neoplastic ; Genome-Wide Association Study ; Humans ; Keratinocytes/metabolism ; Keratinocytes/pathology ; Mice ; Mice, Knockout ; Nevus, Pigmented/genetics ; Nevus, Pigmented/metabolism ; Nevus, Pigmented/pathology ; RNA, Neoplasm/genetics ; Skin Neoplasms/genetics ; Skin Neoplasms/metabolism ; Skin Neoplasms/pathology
Chemical Substances	Cytokines ; RNA, Neoplasm
Language	English
Publishing date	2018-09-25
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80136-7
ISSN	1523-1747 ; 0022-202X
ISSN (online)	1523-1747
ISSN	0022-202X
DOI	10.1016/j.jid.2018.06.180
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Article ; Online: hSSB2 (NABP1) is required for the recruitment of RPA during the cellular response to DNA UV damage.

Boucher, Didier / Kariawasam, Ruvini / Burgess, Joshua / Gimenez, Adrian / Ocampo, Tristan E / Ferguson, Blake / Naqi, Ali / Walker, Graeme J / Bolderson, Emma / Gamsjaeger, Roland / O'Byrne, Kenneth J / Cubeddu, Liza / Khanna, Kum Kum / Richard, Derek J

Scientific reports

2021 Volume 11, Issue 1, Page(s) 20256

Abstract: Maintenance of genomic stability is critical to prevent diseases such as cancer. As such, eukaryotic cells have multiple pathways to efficiently detect, signal and repair DNA damage. One common form of exogenous DNA damage comes from ultraviolet B (UVB) ... ...

Abstract	Maintenance of genomic stability is critical to prevent diseases such as cancer. As such, eukaryotic cells have multiple pathways to efficiently detect, signal and repair DNA damage. One common form of exogenous DNA damage comes from ultraviolet B (UVB) radiation. UVB generates cyclobutane pyrimidine dimers (CPD) that must be rapidly detected and repaired to maintain the genetic code. The nucleotide excision repair (NER) pathway is the main repair system for this type of DNA damage. Here, we determined the role of the human Single-Stranded DNA Binding protein 2, hSSB2, in the response to UVB exposure. We demonstrate that hSSB2 levels increase in vitro and in vivo after UVB irradiation and that hSSB2 rapidly binds to chromatin. Depletion of hSSB2 results in significantly decreased Replication Protein A (RPA32) phosphorylation and impaired RPA32 localisation to the site of UV-induced DNA damage. Delayed recruitment of NER protein Xeroderma Pigmentosum group C (XPC) was also observed, leading to increased cellular sensitivity to UVB. Finally, hSSB2 was shown to have affinity for single-strand DNA containing a single CPD and for duplex DNA with a two-base mismatch mimicking a CPD moiety. Altogether our data demonstrate that hSSB2 is involved in the cellular response to UV exposure.
MeSH term(s)	Animals ; Cell Line ; Chromatin/metabolism ; DNA Damage ; DNA Repair ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Gene Expression Regulation/radiation effects ; HeLa Cells ; Humans ; Phosphorylation/radiation effects ; Replication Protein A/metabolism ; Ultraviolet Rays/adverse effects ; Up-Regulation
Chemical Substances	Chromatin ; DNA-Binding Proteins ; Replication Protein A ; SSBP2 protein, human ; RPA2 protein, human (EC 2.7.7.7)
Language	English
Publishing date	2021-10-12
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-021-99355-0
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Article ; Online: Different genetic mechanisms mediate spontaneous versus UVR-induced malignant melanoma.

Ferguson, Blake / Handoko, Herlina Y / Mukhopadhyay, Pamela / Chitsazan, Arash / Balmer, Lois / Morahan, Grant / Walker, Graeme J

eLife

2019 Volume 8

Abstract: Genetic variation conferring resistance and susceptibility to carcinogen-induced tumorigenesis is frequently studied in mice. We have now turned this idea to melanoma using the collaborative cross (CC), a resource of mouse strains designed to discover ... ...

Abstract	Genetic variation conferring resistance and susceptibility to carcinogen-induced tumorigenesis is frequently studied in mice. We have now turned this idea to melanoma using the collaborative cross (CC), a resource of mouse strains designed to discover genes for complex diseases. We studied melanoma-prone transgenic progeny across seventy CC genetic backgrounds. We mapped a strong quantitative trait locus for rapid onset spontaneous melanoma onset to
MeSH term(s)	Animals ; Animals, Newborn ; Animals, Outbred Strains ; Cell Proliferation ; Chromosome Mapping ; Chromosomes, Mammalian/genetics ; Disease Models, Animal ; Gene Expression Regulation, Neoplastic ; Gene Regulatory Networks ; Genetic Loci ; Humans ; Melanocytes/metabolism ; Melanocytes/pathology ; Melanoma/genetics ; Melanoma/pathology ; Mice, Transgenic ; Monomeric GTP-Binding Proteins/genetics ; Proto-Oncogene Proteins B-raf/genetics ; Quantitative Trait Loci/genetics ; Reproducibility of Results ; Skin/metabolism ; Skin/pathology ; Skin Neoplasms/genetics ; Skin Neoplasms/pathology ; Ultraviolet Rays ; Melanoma, Cutaneous Malignant
Chemical Substances	Braf protein, mouse (EC 2.7.11.1) ; Proto-Oncogene Proteins B-raf (EC 2.7.11.1) ; Monomeric GTP-Binding Proteins (EC 3.6.5.2) ; Nras protein, mouse (EC 3.6.5.2)
Language	English
Publishing date	2019-01-25
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2687154-3
ISSN	2050-084X ; 2050-084X
ISSN (online)	2050-084X
ISSN	2050-084X
DOI	10.7554/eLife.42424
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Article ; Online: Unexpected High Levels of BRN2/POU3F2 Expression in Human Dermal Melanocytic Nevi.

Chitsazan, Arash / Lambie, Duncan / Ferguson, Blake / Handoko, Herlina Y / Gabrielli, Brian / Walker, Graeme J / Boyle, Glen M

The Journal of investigative dermatology

2019 Volume 140, Issue 6, Page(s) 1299–1302.e4

MeSH term(s)	Cohort Studies ; Dermis/cytology ; Dermis/pathology ; Disease Progression ; Disease-Free Survival ; Epidermis/pathology ; Gene Expression Regulation, Neoplastic ; Homeodomain Proteins/analysis ; Homeodomain Proteins/metabolism ; Humans ; Immunohistochemistry ; Keratinocytes/metabolism ; Melanocytes/metabolism ; Melanoma/genetics ; Melanoma/mortality ; Melanoma/pathology ; Nevus, Pigmented/genetics ; Nevus, Pigmented/pathology ; POU Domain Factors/analysis ; POU Domain Factors/metabolism ; SOXE Transcription Factors/metabolism ; Skin Neoplasms/genetics ; Skin Neoplasms/mortality ; Skin Neoplasms/pathology ; Survival Analysis
Chemical Substances	Homeodomain Proteins ; POU Domain Factors ; SOX10 protein, human ; SOXE Transcription Factors ; transcription factor Brn-2
Language	English
Publishing date	2019-12-24
Publishing country	United States
Document type	Letter ; Research Support, Non-U.S. Gov't
ZDB-ID	80136-7
ISSN	1523-1747 ; 0022-202X
ISSN (online)	1523-1747
ISSN	0022-202X
DOI	10.1016/j.jid.2019.12.007
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Article ; Online: Modeling epidermal melanoma in mice: moving into new realms but with unexpected complexities.

Handoko, Herlina Y / Box, Neil F / Walker, Graeme J

The Journal of investigative dermatology

2012 Volume 132, Issue 9, Page(s) 2299–2302

MeSH term(s)	Animals ; Cell Transformation, Neoplastic/genetics ; Cell Transformation, Neoplastic/metabolism ; Cell Transformation, Neoplastic/pathology ; Disease Models, Animal ; Epidermis/metabolism ; Epidermis/pathology ; Humans ; Melanoma/genetics ; Melanoma/metabolism ; Melanoma/pathology ; Mice ; Skin Neoplasms/genetics ; Skin Neoplasms/metabolism ; Skin Neoplasms/pathology
Language	English
Publishing date	2012-09
Publishing country	United States
Document type	Letter ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80136-7
ISSN	1523-1747 ; 0022-202X
ISSN (online)	1523-1747
ISSN	0022-202X
DOI	10.1038/jid.2012.200
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