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This review highlights REV7's crucial roles in maintaining genome stability, its implication in several cancers, and its association with poor prognoses and treatment resistance, while also noting that REV7 suppression may improve chemotherapy sensitivity.

In this study, researchers found that deleting TNFα in PKCε transgenic mice reduced the development of cutaneous squamous cell carcinomas induced by UV radiation or a chemical protocol.

This study found that TPA was significantly more effective than mezerein in inducing dark basal keratinocytes in mouse skin, which may be important in early tumor promotion stages.

This laboratory study found that PI extract, along with its metabolites Ang and Mac, inhibited cell proliferation and protein expression linked to pathways involved in BPH, suggesting potential for therapeutic use, although the Ang-Mac combination showed no significant effect on apoptosis through the p53 pathway.

This study found that deleting the transcription factor Twist1 in keratinocytes significantly reduced UVB-induced skin carcinogenesis in mice, suggesting a potential target for preventing cutaneous squamous cell carcinoma.

In this study, sequences upstream of the TGM3 gene were found to regulate epithelial-specific gene expression in keratinocytes, suggesting potential applications in gene therapy.

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

This study found that normal human melanocytes can be protected from apoptosis through both PI 3-kinase/Akt-dependent and independent pathways, with insulin and TPA offering nearly complete protection.

The research found that while Dnmt3a and Dnmt3b are not necessary for skin homeostasis in mice, the loss of Dnmt3a increases squamous tumor formation from carcinogens, and combined deletion of both results in more aggressive and metastatic tumors.

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.

In this study, researchers identified a highly reactive, isozyme-specific sequence for TGase 3, contributing to understanding its distinct functional role and activity distribution in the mouse epidermis.

This study found that keratin K1014chim expression in mice did not reduce epidermal cell proliferation but increased susceptibility to benign tumors, challenging previous beliefs about K10's role in inhibiting tumor development.

In this study, PKCepsilon transgenic mice showed increased TNFalpha shedding during skin tumor promotion, which may contribute to the development of metastatic squamous cell carcinoma.

This study found that CTIP2 is highly expressed in mouse skin during embryogenesis and adulthood, suggesting it may play a role in skin development and homeostasis.

In this study, researchers found that contrary to expectations, keratin 10 domains did not reduce cell proliferation and instead increased tumor development in genetically modified mice.

This study suggests that activation of polyamine catabolism in K6-SSAT transgenic mice may significantly increase skin tumor development and progression to carcinomas following chemical induction.

This study found that Rap1 deficiency in mice may lead to telomere shortening, DNA damage, and impaired mitochondrial function, contributing to cardiac aging and dysfunction.

This study found that the transcription factor p63 is crucial for horizontal basal cell differentiation in the olfactory epithelium, suggesting a p63-dependent mechanism activates reserve stem cells after injury.

This study demonstrates that mice with ectopic expression of the human GLI-1 gene in their skin developed tumors resembling human basal cell carcinoma, suggesting that GLI-1 is central to tumor development without additional p53 or Ha ras mutations.

This review discusses the role of TGM3 in skin and hair follicle biology, human tumor pathology, and genetic abnormalities, and reports no novel results; the authors highlight its potential as a cancer diagnostic biomarker.

This study found that in thin cutaneous melanomas, tumor regression is associated with a higher risk of sentinel lymph node involvement.

In this study, Meis1 was found to regulate epidermal homeostasis and act as a proto-oncogenic factor in skin tissues, with differences in expression patterns between normal and tumor cells.

This study found that HPV8-induced actinic keratoses may mechanistically involve Lrig1+ hair follicle keratinocyte stem cells, with the E6 gene promoting downstream STAT3 activity in a mouse model.

This study found that telomere shortening disrupts BMP/pSmad/P63 signaling, leading to skin atrophy via Follistatin up-regulation, and suggests potential therapeutic targets.

This study found that patients with the MITF p.E318K variant are more likely to develop multiple primary melanomas and dysplastic nevi with uncommon dermoscopic patterns compared to non-carriers.

This study found that Stat3 deletion in certain skin cells led to increased differentiation and altered stem cell behavior, suggesting its significant role in skin tumor development and keratinocyte migration.

This study observed that disrupting the Pnkp gene in adult mice resulted in a premature aging-like phenotype, suggesting PNKP's vital role in maintaining normal growth and survival of certain progenitor cell populations.

This study reported that UVR induced PKCε phosphorylation of Stat3 in transgenic mice, suggesting a role in enhancing sensitivity to UVR-related skin cancer development.

This review discusses the role of the CXXC5 protein as a transcription factor and signaling coordinator, noting its involvement in embryonic development, tissue homeostasis, and diseases such as tumorigenesis, but reports no new experimental findings.

This study reviews the role of the zinc finger protein CXXC5 in cellular signaling and its implications for cancer, discussing how its dysregulation is linked to various physiological and pathological processes, as well as potential therapies targeting CXXC5.