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This study identified nine novel KRTAP5 family genes associated with human hair formation, demonstrating preferential expression in hair roots and suggesting their role in hair development.

Ritlecitinib may help treat alopecia areata by protecting hair follicles.

This study found that the DKK3-CKAP4 signaling axis is involved in fibroimmune remodeling in androgenetic alopecia and that targeting this pathway may restore a regenerative hair follicle environment, offering a potential therapeutic strategy to counteract hair follicle miniaturization.

Lack of TrkC receptor delays hair follicle development.

This study suggests that AKR1C3 expression may influence PGD2-related pathways in skin squamous cell carcinoma and potentially be involved in androgenetic alopecia, although further investigation is needed to clarify its role.

This study found that inhibiting mTORC2 in glioblastoma cells reduced DNA repair and increased apoptosis, highlighting its potential role in cancer cell survival and DNA damage response.

This study found that dihydrotestosterone (DHT) regulates the degradation of p27 in MCF-7 breast cancer and OVCAR-3 ovarian cancer cells, involving SKP2 as a key factor.

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.

In this study, researchers developed a novel genetic tool using Wif1-CreER knock-in mice for precise labeling and manipulation of dermal papilla cells, which could enhance understanding of hair biology and aid in developing targeted therapies for hair-related disorders.

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 observed that cytokeratin 19 expression in cutaneous carcinomas correlates with the grade of squamous cell carcinomas, with more expression in higher-grade SCCs.

In this study, researchers developed two novel mouse models to investigate how CD271 deletion in keratinocytes affects skin homeostasis, finding that it leads to changes resembling dysplastic skin conditions with immune cell recruitment and inflammatory cytokine release.

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

This study found that selective inactivation of ribonucleotide excision repair in mouse epidermis led to spontaneous DNA damage, skin inflammation, and the development of squamous cell carcinoma, suggesting potential implications for cancer development in humans.

This study found that novel RNA aptamers specifically inhibited FGF5-induced cell proliferation, suggesting their potential as candidates for treating FGF5-related diseases or hair disorders.

This study found that keratin 15 lacks the ability to sequester YAP1 in keratinocytes effectively, unlike keratin 14, and suggests that a higher K15:K14 ratio may promote a progenitor state and inhibit differentiation in epidermal keratinocytes.

This study identifies two previously unreported pathogenic RIPK4 gene variants, suggesting a functional link with cell adhesion molecules in ectodermal dysplasias.

This study found that elevated epidermal ODC activity in transgenic mice promotes skin tumor development by recruiting bulge stem cells, rather than through reactive oxygen species generation by polyamine catabolic oxidases.

This review discusses how increased gene copy number for telomerase components may contribute to telomerase up-regulation in cancer cells, although the exact mechanisms are not fully understood.

This study concluded that the Wnt signaling pathway does not significantly influence human keratoacanthoma development, but the overexpression of Sox9 suggests alternate signaling involvement.

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.

This study found that trichoblastomas and nodular basal cell carcinomas have similar cytokeratin expression patterns, indicating differentiation towards the outer root sheath epithelium.

In this study, researchers reported that the activation of EDA2R by p53 leads to p53-dependent cell death in cancer cells and is involved in chemotherapy-induced hair loss.

PRSS35 enzyme may help start skin tumors and could be a target for cancer treatment.

In this study, two novel clusters of keratin-associated protein genes on human chromosome 11 were analyzed, suggesting their products are crucial for hair formation due to preferential expression in hair roots.

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.

In this study, targeting the expression of a keratin KRT5/KRT8 chimeric cDNA in keratin-deficient mice partially restored structural defects in epidermal cells, but did not fully normalize skin health.

This study found that the protein CCN2 in dermal papilla cells is a physiologically relevant suppressor of hair follicle formation by destabilizing β-catenin, which may help maintain stem cell quiescence.

This study suggests that targeting the activation of transit-amplifying cell-derived progenitor cells may help prevent hair loss from chemotherapy and radiotherapy by promoting hair follicle regeneration.