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This review discusses the paradoxical effects of valproic acid on hair, noting that it can both cause alopecia and stimulate hair growth, but reports no new experimental findings.

This study found that mutations in the Sgk3 gene cause defective hair follicle development and altered hair cycling in mice, with variable phenotypic outcomes depending on different dysfunction patterns of the SGK3 protein.

This study found that in mice, EGFR activation suppresses mitotic regulators like Rcc2 and Stathmin 1, facilitating the transition to catagen in hair follicles.

This study found that the ID2 gene was highly expressed in bulge-derived keratinocytes when exposed to contact sensitizers and may serve as a marker to distinguish sensitizers from irritants during in vitro testing.

In this study, researchers at Johns Hopkins University found that Keratin 17 plays a signaling role in cell growth during a wound response by aiding mTOR pathway activation, beyond its structural functions.

This study found that BMP-2 activates Dlx3 gene transcription in murine keratinocytes by binding with Smad1/Smad4, suggesting a mechanism for BMP signaling's role in skin and hair follicle regulation.

This study identified a new cytokeratin, mK6irs, specifically expressed in the inner root sheath of mouse hair follicles, distinguishing it as a member of the type II cytokeratin family.

This study found that RhoA influences embryonic stem cell proliferation through the PKN1-cyclin D1 pathway in vitro, suggesting RhoA as a potential target for wound healing therapies.

This study identified two novel genes, pmg-1 and pmg-2, expressed in various skin and gland tissues and potentially involved in the differentiation of epithelial cells in epidermal appendages.

This study found that chromosomal microarray analysis identified copy number variations in 12% of patients with dysmorphic features and congenital anomalies, demonstrating its potential as a diagnostic tool, especially for rare CNVs and immune deficiency linked to the deletion of CTLA4.

This study found that overexpression of PKCα in mouse epidermis increases expression of specific proinflammatory mediators and induces inflammation but does not significantly affect epidermal differentiation, proliferation, or tumor promotion with TPA.

This study found that ALRN-6924, a clinical-stage dual inhibitor, can selectively protect human scalp hair follicles from paclitaxel-induced toxicity and damage by inducing transient cell cycle arrest in healthy cells without affecting cancer cells, potentially reducing chemotherapy-induced alopecia.

This study found that PRC1 plays crucial roles in skin epithelial stem cell regulation, with catalytic and non-catalytic functions impacting epidermal integrity, hair development, and Merkel cell dynamics in murine models.

This study found that selectively inactivating ribonucleotide excision repair in mouse epidermis leads to DNA damage, keratinocyte intraepithelial neoplasia, and squamous cell carcinoma, indicating a potential tumor-promoting mechanism related to compromised genome maintenance.

In this study, researchers found that the loss of SETDB1 in epidermal keratinocytes led to altered chromatin states, increased ERV expression, and activation of immune responses, while inhibiting these effects with certain antiviral drugs reduced skin inflammation and hair loss in a mouse model.

The study found that over-expressing ornithine decarboxylase in the outer root sheath of the hair follicle in mice increases UVB-induced tumor growth and invasive squamous cell carcinoma compared to inter-follicular epidermal keratinocytes.

In this study, researchers used computational modeling and virtual screening to identify two FDA-approved drugs, Tadalafil and Finasteride, that may effectively inhibit key proteins involved in melanoma progression, suggesting potential for new therapeutic strategies against aggressive melanoma.

In this study, researchers found that selectively disabling ribonucleotide excision repair in mouse epidermis caused DNA damage, skin inflammation, and led to skin cancer, suggesting a potential role for this repair mechanism in tumorigenesis.

In this study, researchers found that the transcriptional program regulated by PRC2 is not necessary for maintaining hair follicle stem cell quiescence and hair regeneration in vivo.

In this study, researchers found that overexpressing SOX2 in colorectal cancer cell lines can cause DNA damage and cell death, while repressing it reduces tumor growth and cell aggressiveness.

This study demonstrates that YAP and TAZ are essential for initiating basal and squamous cell carcinomas in mice, and suggests targeting these pathways could be beneficial for treating skin cancers.

This study found that in mice, inactivating beta-catenin in the dermal papilla reduces hair follicle progenitor proliferation and disrupts the hair cycle.

This study identified a nonsense mutation in the Sgkl gene as the cause of defective hair growth in a mutant mouse strain, implicating the SGKL signaling pathway in hair development.

In this study, overexpression of ornithine decarboxylase accelerated basal cell carcinoma in Ptch1+/– mice under UVB exposure, while its inhibition reduced tumor induction, suggesting potential chemoprevention strategies in humans.

In this study using a transgenic mouse model, Id2 overexpression in hair follicle stem cells prolonged quiescence by affecting gene expression, partly independent from BMP signaling.

This review examines the role of P-cadherin in skin and hair biology, emphasizing its importance in human hair growth, cycling, and pigmentation, and reports no new research findings.

This Phase II study found that BAY 43-9006, given at 400 mg orally twice daily, led to stable disease in 30% and tumor reduction in 40% of renal cell carcinoma patients.