141 citations
,
August 2018 in “Nature Reviews Microbiology” This review discusses the molecular mechanisms by which oncogenic viruses contribute to cancer development through manipulation of host cellular functions and highlights the need for further research into virus-associated cancers, reporting no new results.
17 citations
,
September 2019 in “Journal of Cell Biology” This study found that despite carrying an activating Hras mutation, hair follicle stem cells integrate into normal skin without causing tumors, unlike similar mutations in the epidermis, suggesting unique tumor-suppressing mechanisms in hair follicles.
12 citations
,
March 2011 in “Journal of pathology” In this study, activation of oncogenic K-ras in a mouse model caused the oral mucosa to rapidly progress from squamous hyperplasia to carcinoma within 14 days, demonstrating its acute sensitivity.
2 citations
,
November 2022 in “bioRxiv (Cold Spring Harbor Laboratory)” This study found that metabolic adaptations in skin epithelial stem cells, specifically redox ratio recovery and glycolytic flux modulation, define competitive outcomes between wild-type and mutant cells in different oncogenic environments.
December 2017 in “British Journal of Dermatology” Targeted therapy for skin cancer is complex due to the role of the hedgehog pathway in both cancer and hair growth.
September 2022 in “bioRxiv (Cold Spring Harbor Laboratory)” In this study, researchers using live mice observed that oncogenic Kras mutation disrupts hair follicle architecture by sustaining ERK signal activation, which affects stem cell behavior and tissue integrity.
July 2022 in “Journal of Investigative Dermatology” This study found that the KrasG12D mutation alters ERK signal dynamics in hair follicle stem cells, leading to tissue deformation, and suggests a collective effect of mutant cells is necessary for disruption.
150 citations
,
June 1999 in “Oncogene” 
67 citations
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November 2019 in “Nature Communications” This study demonstrated that a c-Kit-CreER-driven mouse model confirms melanocyte stem cells as a genuine source of melanoma, paralleling human melanoma in heterogeneity and gene signatures.
32 citations
,
February 2017 in “Oncotarget” This workshop review discusses the dual role of cellular senescence in cancer, highlighting both its anticancer effects and pro-tumorigenic potential, while reporting no new research results.
109 citations
,
December 2003 in “American Journal of Pathology” This study observed that the ontogenetic transition from scarless repair in early fetal rat wounds to scar-forming repair in late gestation is associated with differential TGF-β ligand and receptor expression patterns.
19 citations
,
April 2024 in “Nature Cell Biology” 
23 citations
,
May 2013 in “Virology” This study found that HPV16 oncogene expression in multipotent epithelial stem cells led to abnormal mobilization, altering their quiescence without affecting other stem cell markers, suggesting a distinct stem cell compartment.
10 citations
,
October 2000 in “PubMed” This study found that transgenic mice expressing HPV E6/E7 in the outer root sheath experience continuous hair follicle cycling due to delayed catagen entrance and insensitivity to telogen resting signals.
7 citations
,
October 2011 in “BMC Cancer” This study found no evidence that HDGF expression transforms melanocytes into tumors in a mouse model, although it may play a role in cell differentiation and tumor progression.
47 citations
,
January 1998 in “Molecular Carcinogenesis” This study observed that targeted expression of the neu oncogene in transgenic mice led to significant epidermal hyperplasia and a carcinoma-like appearance, suggesting a crucial role for erbB2 signaling in epidermal proliferation and carcinogenesis.
This study found that the survival and proliferation of mouse melanocytes expressing the GNAQQ209L oncogene were impaired by interactions with the epidermal microenvironment, suggesting a possible mechanism for the rarity of these mutations in epidermal melanomas.
This study found that GNAQQ209L expression in mouse melanocytes led to reduced survival in the interfollicular epidermis due to paracrine signaling, while GNAQQ209L boosted survival in a different microenvironment.
In this study, researchers discovered that the HrasG12V oncogenic mutation in murine skin epithelial cells initially promotes progenitor cell renewal but later leads to a balanced differentiation, stabilizing clone growth.
In this study, researchers observed that oncogenic HrasG12V in single murine epidermal cells leads to an initial increase in progenitor cell renewal, but ultimately results in balanced cell fate choices that limit clone growth.
19 citations
,
June 2008 in “Journal of Investigative Dermatology” This study found that transgenic mice with expression of HPV16 E6/E7 oncogenes showed improved ear tissue regeneration, including hair follicles and cartilage, without tumor formation.
9 citations
,
May 2019 in “Experimental Cell Research” This study found that Hedgehog signaling likely contributes to cervical carcinogenesis, and while itraconazole reduced growth in mice, it did so through pathways other than inhibiting Hedgehog signaling.
May 1961 in “Tumori Journal” This study found that vitamin A treatment in rats reduced hyperplastic-dysplastic changes and sebaceous gland hypertrophy associated with 3,4-benzpyrene-induced tumors.
114 citations
,
July 2003 in “PubMed” This study found that KSR1 is necessary for v-Ha-ras-mediated skin tumor formation but not for MT-driven mammary cancer, indicating its potential as a therapeutic target in Ras/MAPK signaling-related tumors.
This study found that in mice, the epidermal microenvironment reverses the oncogenic effects of GNAQQ209L in melanocytes, inhibiting their survival and proliferation through paracrine signals.
1 citations
,
July 2017 in “Cancer Research” This study found that overexpression of NSD3 in the mammary gland of transgenic mice led to mammary hyperplasia, dysplasia, and invasive ductal carcinoma, mirroring patterns seen in human breast cancer.
5 citations
,
January 2021 in “iScience” Using a combination of specific cell cycle regulators is better for safely keeping hair root cells alive indefinitely compared to cancer-related methods.
110 citations
,
August 2004 in “British Journal of Dermatology” In this study, researchers identified the ventral matrix as the primary source of nail plate formation, while the dorsal portion is generated by the apical matrix.
July 2026 in “International Journal of Stem Cells” This review highlights that genetically engineered mouse models are valuable for studying melanoma development and progression by mimicking human skin biology, revealing key signaling pathways and molecular mechanisms that contribute to melanoma heterogeneity and offering insights into potential therapeutic targets.
213 citations
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December 1994 in “Medical Entomology and Zoology” This article reviews various aspects of skin cancer, including animal models, molecular mechanisms, immunity roles, and potential chemoprevention strategies, but reports no new experimental results.