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.
May 2025 in “Frontiers in Bioengineering and Biotechnology” In this study, the researchers reported that a novel exosome-based treatment, EX104, effectively reversed hair follicle miniaturization and promoted hair growth in a mouse model of androgenetic alopecia, showing results comparable to minoxidil and surpassing it in stimulating capillary growth and follicular proliferation.
17 citations
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July 2024 in “Frontiers in Oncology” This review discusses recent advances in understanding Merkel cell carcinoma biology, including the development of genetically-engineered mouse models and potential therapeutic targets, but reports no new clinical results.
May 2025 in “OPAL (Open@LaTrobe) (La Trobe University)” This study found that the multifunctional exosome-based delivery platform EX104 reversed hair follicle miniaturization and promoted hair growth in a mouse model of androgenetic alopecia, performing comparably to minoxidil while also enhancing capillary growth and follicular proliferation.
4 citations
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May 2018 in “International Journal of Molecular Sciences” This review discusses genetically-engineered mouse models for studying melanocytes and reports no new experimental findings; it emphasizes their potential to address unanswered questions in melanoma biology.
1 citations
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January 2016 in “Elsevier eBooks” This review examines the origins and mechanisms of tumor initiation in common skin cancers, but does not present new experimental findings; it emphasizes the need for further research on cancer stem cells.
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.
5 citations
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December 2024 in “Bioengineering” In this study, conditioned medium from genetically engineered mesenchymal stem cells significantly improved wound healing, re-epithelialization, hair follicle formation, and angiogenesis in diabetic mice, suggesting a promising new approach for diabetic ulcer care.
September 2023 in “bioRxiv (Cold Spring Harbor Laboratory)” This study describes the use of a genetically engineered mouse model, mTurquoise2-Col4a1, to fluorescently label collagen IV and observe basement membrane dynamics during skin development, revealing its stability and pliability during rapid growth phases.
2 citations
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January 2025 in “Journal of Nanobiotechnology” This study demonstrated that genetically engineered, ATP-responsive nanozymes effectively reduce cardiac fibrosis by targeting activated cardiac fibroblasts, resulting in decreased myofibroblast accumulation and improved cardiac function, suggesting that this approach has significant potential for therapeutic applications.
This study found that IL-1α and IL-7 secreted from keratinocytes in a genetically engineered mouse model can stimulate the expansion of γδT-cells, aiding in the proliferation of epidermal stem cells for wound healing.
June 2006 in “Experimental dermatology” This paper reviews potential animal models for studying hidradenitis suppurativa, specifically suggesting that certain mouse models with genetic mutations might be useful, but it reports no new experimental findings.
February 2026 in “International Journal of Nanomedicine” This study demonstrated that engineered exosomes carrying EGF and FGF restored hair density and follicle integrity in an androgenetic alopecia mouse model by reactivating hair follicle growth factors, offering a novel therapeutic approach without immunogenic reactions or systemic toxicity.
This study found that Mdm2 is critical for limiting p53 activity to maintain normal stem cell function in mouse skin, with impacts on tissue homeostasis and aging.
27 citations
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May 2018 in “Journal of Dermatological Science” This study suggests that M2 macrophages play a key role in promoting wound-induced hair neogenesis in mice by producing growth factors like Igf1 and Fgf2.
April 2016 in “The journal of investigative dermatology/Journal of investigative dermatology” This study found that hair follicles may provide a safe space for tumor cells in mice, suggesting a potential target for cancer prevention during the dormant phase of tumor development.
60 citations
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July 2011 in “Stem Cells and Development” This review discusses recent findings on hair follicle morphogenesis and regeneration, focusing on molecular signals and stem cells, and suggests that understanding these processes may aid in developing new strategies for wound healing.
7 citations
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November 2018 in “British Journal of Dermatology” Alopecia areata is caused by immune system issues, and JAK inhibitors might help treat it.
January 2025 in “Research” This perspective highlights research suggesting that cellular senescence in melanocytes may unexpectedly aid hair regeneration by activating hair follicle stem cells, challenging traditional views of senescence as purely detrimental.
January 2018 in “eScholarship (California Digital Library)” This study suggests that hair follicle stem cells have a unique metabolic profile that may play a critical role in their maintenance and response to cancer-related changes, potentially contributing to the "Warburg Effect.
90 citations
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October 1996 in “Dermatologic Clinics” This study found that red ginseng oil may enhance hair growth and protect skin from UV damage in mouse models by promoting regenerative processes and reducing inflammation.
5 citations
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February 2011 in “Expert Opinion on Drug Discovery” This review discusses techniques and models for assessing hair growth activity but reports no new clinical findings, emphasizing the need for standardization and improved animal models.
29 citations
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November 2011 in “Veterinary pathology” This study reports that eccrine sweat glands in mice predominantly develop on the footpads, offering a reference for skin research involving genetically engineered mice.
276 citations
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December 2017 in “Journal of Dermatological Science” This review discusses the limitations of animal models, particularly mice, in accurately predicting human skin wound healing outcomes and emphasizes understanding species-specific differences in skin characteristics for better translation to clinical settings.
October 2025 in “Burns & Trauma” This review highlights recent advancements in engineered probiotics for wound healing, reporting that genetically engineered strains of Lactobacillus reuteri and Lactococcus cremoris have shown promise in promoting faster wound healing in pre-clinical and clinical settings, particularly for diabetic foot ulcers.
64 citations
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March 2004 in “Journal of Clinical Investigation” This study found that inhibiting the enzyme ornithine decarboxylase (ODC) prevented UVB-induced basal cell carcinomas in a mouse model, suggesting ODC is a potential target for chemoprevention strategies.
1 citations
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November 2025 in “Science Advances” This research identified two genetic variants that influence the white-spotted coat patterns in Holstein-Friesian cattle, involving regulatory changes in the MITF and KIT genes, confirmed through mouse models, along with possible effects on coat patterns in other cattle breeds.
160 citations
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June 2008 in “American Journal Of Pathology” This review discusses the effects of the epidermal growth factor receptor system on skin biology and pathology, relying on animal models to analyze roles in cellular processes, wound healing, and tumorigenesis, but reports no new results.
25 citations
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August 2014 in “Endocrinology” This study created a humanized mouse model of hereditary vitamin D-resistant rickets that lacks alopecia, indicating the mutant receptor's potential to explore the syndrome's characteristics beyond vitamin D binding.