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In this case report, researchers diagnosed a 12-year-old girl with a nevus sebaceus of Jadassohn, characterized by a yellowish-pink plaque on the scalp and a genetic variant, following previous misdiagnosis as alopecia areata.

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.

This study found that injury-induced proliferation of wild-type cells can suppress oncogenic growth in Ras-mosaic skin.

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.

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.

This study found that mutant cells in hair follicles can be tolerated or eliminated by surrounding normal tissue, suggesting the potential for wild-type cells to counteract oncogenic mutations.

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.

This study found that NKIRAS2 expression affects skin tumor suppression and HRAS-driven transformation in mice, indicating its role in carcinogenesis depends on expression level and cellular context.

This study found that mouse hair follicle stem cells in a quiescent state exhibit greater chromatin dynamics and de-differentiation potential, suggesting higher cell fate plasticity compared to their proliferative or differentiated counterparts.

This review discusses the origins of skin and esophageal cancers and reports no clinical results; it emphasizes the role of cyclooxygenase-2 in tumorigenesis and differentiation.

In this study, basal cell carcinoma developed in Ptch-deficient mice only after chemical treatment, not skin wounding, suggesting a second unknown event is necessary for tumor formation.

This review discusses the dual role of cellular senescence in ageing and tissue repair and suggests potential therapeutic applications, with no new experimental results reported.

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.

In this study, re-activating SOX9 in adult epidermal stem cells led to a fate switch towards hair follicle stem cell identity, with altered chromatin dynamics and oncogenic activation, contributing insights into developmental processes and cancer pathways.

This study found that mutations in the TULP3 gene are associated with progressive degeneration of the liver, kidney, and heart in adults, highlighting the importance of early detection and management.

This research found that activating a KrasG12D mutation in mice led to skin thickening, papillomas, and hair growth issues, suggesting that even rare KRAS mutations can mimic human RAS/MAPK syndrome symptoms.

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.

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.

In this study, researchers observed that twins with a novel de novo nonsense variant in HRAS exhibited distinctive features, including neuropsychiatric symptoms, potentially indicating a wider clinical spectrum for conditions known as RASopathies.

This study found that benign tumors with a high risk of malignant progression primarily arise from hair follicle cells when a mutant ras gene is expressed in a specific population of epidermal cells in mice.

This study found that H-Ras activation in aged mouse skin leads to increased dysplasia and progression to in situ squamous cell carcinoma, highlighting an age-linked connection between immune changes, senescence, and cancer risk.

In this study, a somatic KRAS mutation was identified in a Korean infant with nevus sebaceus and associated extracutaneous manifestations, suggesting a diagnosis of nevus sebaceus syndrome.

This dissertation reports that Lrig1 and Lgr6 mark distinct stem cell populations in mouse hair follicles, playing roles in tissue regeneration and tumor development, with Lgr6 regulating Wnt signaling and restraining epidermal lineage commitment.

This study found that chemically induced skin tumors in mice predominantly originated from Lgr6 + and/or Lrig1 + stem cells of the upper hair follicle rather than from other stem cell populations.

This study found that inhibiting AP-1 activity in mice modified tumor development, leading to transdifferentiation between squamous and sebaceous tumors, with molecular analysis suggesting AP-1's role in maintaining tumor cell identity.

This study found that inhibiting AP-1 transcription factors in mice causes squamous tumors to transform into sebaceous tumors and regulates tumor cell lineage.

This study found that inhibiting AP-1 activity in mice can induce lineage transdifferentiation between squamous and sebaceous tumors, suggesting AP-1's role in maintaining tumor cell identity.

In this study, researchers used an integrated in silico approach to demonstrate that Polygonum multiflorum combats androgenetic alopecia via anthraquinone emodin, which targets PI3K catalytic subunits differently from traditional antiandrogenic treatments, showing potential as a novel therapeutic strategy.

This study found that loss of the DNA methyltransferase Dnmt3a, but not Dnmt3b, increased carcinogen-induced squamous tumors in murine epidermis, with combined deletion leading to more aggressive and metastatic carcinomas.