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In this study, lysocellin induced G1 phase arrest in human osteosarcoma cells, but diminished the cytotoxic efficacy of etoposide, while its derivative alopestatin may reduce etoposide-induced alopecia in a rat model.

This review highlights that genetically engineered mouse models are valuable for studying melanoma development and progression by mimicking human skin biology, revealing key signaling pathways and molecular mechanisms that contribute to melanoma heterogeneity and offering insights into potential therapeutic targets.

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 review explores the complex, context-dependent roles of tumor-secreted proteins and suggests that some proteins traditionally seen as tumor-promotive may act as tumor-suppressors in different environments, emphasizing the influence of cell fitness and treatment exposure.

This study observed that COX-2 overexpression in transgenic mice led to a significant reduction in skin tumor development compared to controls, challenging the expected role of COX-2 in promoting tumors.

Complex basal cell carcinomas need personalized treatment due to unique genetic mutations.

This study presents iSiMPRe, a method identifying protein regions enriched in mutations, revealing potential cancer-related genes and enhancing understanding of mutation effects across a wide range of cancer types.

This study found that inhibiting AP-1 activity in mice can induce lineage transdifferentiation between squamous and sebaceous tumors, suggesting AP-1's role in maintaining tumor cell identity.

This study found that overexpressing PKCδ in transgenic mice did not reduce squamous cell carcinoma development induced by UV radiation, despite its effectiveness against TPA-promoted cancer in these mice.

This study found that urokinase plasminogen activator (uPA) is elevated in hyperproliferative hair follicle keratinocytes in mice, and its inhibition significantly reduces their proliferation.

This article reviews the diverse roles of protein kinase C (PKC) isozymes in cancer biology, highlighting their potential as therapeutic targets, but reports no new experimental results.

This study found that overexpression of the enzyme ornithine decarboxylase in transgenic mice led to UVB-induced skin tumors, but this was prevented by the ODC inhibitor α-difluoromethylornithine.

This study found that inhibiting C/EBP transcription factors in mouse skin reduced papilloma formation and caused systemic hair loss, suggesting C/EBP may be a potential therapeutic target.

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.

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 study found that small molecule AP-1 inhibitors may selectively target SMO inhibitor-resistant basal cell carcinoma cells characterized by specific markers, potentially enhancing combinatorial cancer therapies.

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.

This study found that the development of Merkel cell carcinoma from hair follicles in mice can be driven by in vivo reprogramming with ATOH1 and relies on p53 loss for progression.

In this study, PKC ε transgenic mice exposed to ultraviolet radiation showed increased hair follicle stem cell frequency and altered gene expression compared to wild-type mice, suggesting a potential role in skin cancer susceptibility.

This study found that overexpressing the PML protein in transgenic mice decreased skin tumor occurrence and delayed their progression, highlighting PML's potential role in influencing keratinocyte growth and differentiation.

This study identified neuropilin-1 as the receptor for FOL-026 and showed that it stimulates angiogenesis and cell growth, suggesting potential for vascular repair and enhanced angiogenesis therapies.

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.

This study suggests that chronic treatment with TPA in mouse skin selectively expands a keratinocyte subpopulation hyperinducible for ODC, which may be a key target for neoplastic transformation.

This study reports that a clinical prognostic model based on immune-related genes improved survival prediction for patients with clear cell renal cell carcinoma, also identifying potential drugs targeting the gene DOCK8.

This study found that simultaneous inactivation of pRb and p53 genes in mice's epidermis accelerates aggressive squamous cell carcinoma development, highlighting p53 as a key tumor suppressor.

The researchers reported that the OVOL1-OVOL2 axis may play a role in hair follicle differentiation and tumorigenesis, and OVOL1 and OVOL2 are potential diagnostic markers for pilomatricoma and pilomatrix carcinoma.

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.

This study found that the simultaneous inactivation of pRb and p53 genes in mouse epidermis accelerated aggressive squamous cell carcinoma development via activation of the epidermal growth factor receptor/Akt pathway.

This study found that transgenic mice with keratinocyte-specific overexpression of CtBP1 exhibited abnormal hair follicle development, suggesting CtBP1 may play a pathogenic role in hair morphogenesis.