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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.

This study suggests that hair loss disorders like Marie Unna hereditary hypotrichosis may result from mutations that disrupt post-transcriptional regulation of HR protein expression by PCPB2 interacting with Hr mRNA.

In this study, researchers found that TSPyV T antigens can disrupt normal cell differentiation and proliferation in hair follicles and interfollicular epidermis, possibly contributing to trichodysplasia spinulosa pathology.

In this study, researchers found that the cell surface protein Lrig1 plays a crucial role in regulating the suppressive function of regulatory T cells, suggesting it as a potential target for treating autoimmune diseases, as evidenced by experiments in mouse models.

In this study, isotretinoin treatment significantly increased p53 expression in the skin of acne vulgaris patients, correlating with reduced acne severity and suggesting mechanisms for sebum suppression and side effects.

This study found that deleting the Twist1 gene in skin keratinocytes significantly reduced UVB-induced skin cancer and hyperproliferation in mice and suggested Twist1 as a target for skin cancer prevention.

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

This study identified a new gene, mrp4, in mice, which suggests it may have a unique role in the growth and development of hair follicles in the ears and tails.

In this study, researchers established that increased expression of the human GLI-1 gene in mouse skin leads to the development of tumors that closely resemble human basal cell carcinomas, without requiring additional mutations in the p53 or Ha ras genes.

This study found that doxorubicin-induced oxidative stress downregulates FLIPs and phosphorylates EF2, sensitizing prostate cancer cells to TRAIL; antioxidants may reduce doxorubicin's effectiveness, warranting further investigation.

This study found that the protein p63 requires morphogenetic signals to regulate gene expression effectively during skin cell differentiation, highlighting its complex role in therapeutic reprogramming for conditions like epidermolysis bullosa.

This study provides direct evidence that the Wnt-β-catenin pathway promotes TERT expression in stem and cancer cells, linking tumorigenesis with pluripotency.

This study discovered that a network controlled by the gene p63 is crucial for keratinocyte differentiation and is linked to MYC through cell adhesion-related pathways.

This study found that lineage-restricted loss of p63 in murine thymic epithelial cells resulted in severe thymic hypoplasia and absence of hair follicles, indicating p63's critical role in thymic and hair follicle development.

This study found that PRMT5 inhibitors showed potent anti-tumor activity in models of adenoid cystic carcinoma and that combining these inhibitors with lenvatinib may have additional growth-inhibitory effects.

This study explains that while trichothiodystrophy and xeroderma pigmentosum share genetic defects, TTD patients primarily exhibit issues in transcription initiation, not the increased skin cancer risk seen in XP.

In this study, a synthetic antagonist of the p75 neurotrophin receptor was found to significantly inhibit hair follicle regression in murine skin cultures, suggesting a potential role in treating hair disorders characterized by premature catagen entry.

This study suggests that the DNMT3B -579 G>T polymorphism may be a genetic risk factor for colorectal cancer in the Azerbaijani population.

This study identified intramembrane proteolysis as a key feature of Astrotactin2 maturation, providing insights into its role in planar cell polarity hair patterning.

This review highlights the potential of PROTACs to transform cancer treatment by selectively degrading oncogenic proteins, overcoming drug resistance, and reducing toxicity; it also discusses challenges in optimizing these therapies for personalized applications.

PTHrP is important for bone formation and may be targeted for osteoporosis treatment and longevity therapies.

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 commentary discusses the crucial role of the alternative splicing factor Esrp1 in maintaining skin barrier function and its association with skin diseases like atopic dermatitis and psoriasis, but reports no new clinical results.

This study found that 2-methoxyestradiol induces apoptosis in human prostate cancer cells by activating p53 through a pathway dependent on p38/JNK-mediated NFkappaB/AP-1 activation, with JNK-dependent Bcl-2 phosphorylation also playing a critical role.

This study found that TPA induces apoptosis in pig renal epithelial cells by affecting cell cycle proteins, and activated ras can prevent this process.