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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 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 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.

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.

Using a combination of specific cell cycle regulators is better for safely keeping hair root cells alive indefinitely compared to cancer-related methods.

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.

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

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 that in mice, the epidermal microenvironment reverses the oncogenic effects of GNAQQ209L in melanocytes, inhibiting their survival and proliferation through paracrine signals.

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 indicates that the protein Bcl-2 has a dual role, protecting hair follicle stem cells from apoptosis during regeneration and promoting tumor formation under oncogenic stress.

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 suggests that cancer risk may be influenced by the balance of pro- and anti-oncogenic mutants in normal tissues rather than by the total number of mutations.

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.

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.

This study found that Hoxc13 mutations in mice cause defects in hair, nail, and tongue structures, with the most noticeable issue being brittle hair leading to alopecia.

This review classifies mutant mice with hair abnormalities into six categories, providing an annotated table that serves as a reference for understanding the molecular controls of hair growth.

This study found that mirex and TPA promote papilloma formation in CD-1 mouse skin through distinct populations of mutant Ha-ras cells, resulting in additive tumor yields.

This study used in silico analysis to identify 4-[2-(4-nitrophenyl)ethylcarbamoyl]benzenesulfonyl as a potential inhibitor of the EGFR mutant associated with NSCLC, highlighting the need for further in vitro and in vivo validation.

This study found that Gsdma3 mutations in mice led to thicker skin and longer hair infundibula, possibly by negatively regulating β-catenin expression in the epidermis.

This study found that the Plcd3(mNab) mutation in mice worsens the alopecia caused by Plcd1 loss, suggesting synergistic effects between Plcd1 and Plcd3 on hair follicle health.

This study found that KrasG12D mutant cells are typically cleared from adult pancreas tissues through mechanisms involving the EphA2 receptor, suggesting its role as a tumor suppressor in pancreatic cancer.

This study found that β-sitosterol, a brain-penetrable phytosterol, reduced melanoma cell growth and brain metastasis formation by interfering with mitochondrial respiration, suggesting its potential as an adjuvant therapy to BRAF inhibitors for patients with melanoma brain metastases.

This review discusses stem cell behavior, highlighting their plasticity in tissue repair and the impact of somatic mutations on clonal expansion in early cancer, but reports no new experimental results.

This study explored the immune environment of the hair follicle's bulge region and suggested that its unique signaling may prevent melanoma formation by lacking necessary proinflammatory signals for full oncogenic transformation, indicating potential strategies for melanoma prevention by replicating this immune-privileged environment.

This study found that a catalytically active version of Vav2 significantly altered gene expression patterns in hair follicle stem cells in mice, with these changes varying over the animals' lifespans.

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 review examines cell senescence pathways in melanocytes, highlighting the involvement of telomere attrition, the p16/RB pathway, and cAMP signaling in the context of melanoma development, but reports no new findings.