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This study found that mirex and TPA promote papilloma formation in CD-1 mouse skin through distinct populations of mutant Ha-ras cells, resulting in additive tumor yields.

This study found that despite carrying an activating Hras mutation, hair follicle stem cells integrate into normal skin without causing tumors, unlike similar mutations in the epidermis, suggesting unique tumor-suppressing mechanisms in hair follicles.

This study found that disrupting Stat3 in keratinocyte stem cells of mice reduced skin tumor formation by approximately 80%, suggesting Stat3's role in tumor initiation survival mechanisms.

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.

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 the Plcd3(mNab) mutation in mice worsens the alopecia caused by Plcd1 loss, suggesting synergistic effects between Plcd1 and Plcd3 on hair follicle health.

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 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.

In this study, basal cell carcinoma developed in Ptch-deficient mice only after chemical treatment, not skin wounding, suggesting a second unknown event is necessary for tumor formation.

This review discusses recent findings on molecular changes in cutaneous adnexal tumours and reports novel markers and pathways involved, highlighting the diverse oncogenic drivers and tumour suppressor alterations.

This study analyzed skin from 538 knockout mouse mutants and identified 50 with epidermal phenotypes, providing valuable insights into genetic conditions and systemic effects related to skin abnormalities.

This study suggests that biallelic loss of the Hedgehog signaling repressor Patched alone in Keratin 5+ epidermal cells is insufficient to drive basal cell carcinoma development unless exogenous stimuli trigger accumulation of BCC precursor cells.

This study found that NKIRAS2 expression affects skin tumor suppression and HRAS-driven transformation in mice, indicating its role in carcinogenesis depends on expression level and cellular context.

This review discusses recent findings on the plasticity and regulation of epithelial stem cells and reports no new experimental results.

This study found that overexpression of miR-214 in keratinocytes inhibits hair follicle development and cycling by targeting β-catenin in the Wnt signaling pathway.

This study found that Secretory Phospholipase A2-IIA (sPLA2-IIA) promotes proliferation through JNK/c-Jun signaling, distinctively affecting normal stem cells and cancer cells, suggesting it as a potential target for cancer treatment.

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 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.

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 synthesizes current evidence on the Warburg effect in anaplastic thyroid carcinoma and discusses potential therapeutic targets, but reports no new clinical results.

This review highlights the role of keratin mutations in epidermolysis bullosa simplex and the resulting chronic inflammation, but it presents no new experimental findings.

This study found that stem cells can temporarily act as non-professional phagocytes during hair cycle regeneration by clearing apoptotic cells through a process requiring local lipids and retinoids for activation, providing insights into their dual role in maintaining tissue integrity.

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

This research highlights that engineered mice lacking the vitamin D receptor show multiple health issues similar to human vitamin D deficiency, underscoring the widespread impacts of the vitamin D endocrine system.

This study found that quiescence in hair follicle stem cells acts as a tumor suppression mechanism for cutaneous squamous cell carcinoma, with Pten activity necessary to maintain this state.

This review provides an in-depth analysis of the structure and function of c-kit activation, and its role in both normal physiological and pathological conditions, with no new research findings reported.

In this study on adult-onset, whole body Spry1/2/4 triple knockout mice, researchers observed endocrine abnormalities and no increased tumor incidence, despite similar food intake and motor function.

In this study, researchers found that while blocking either glycolysis or glutaminolysis in cancer cells did not prevent tumor growth due to metabolic flexibility, simultaneous inhibition of both pathways hindered carcinoma development, indicating multiple interventions may be necessary for effective metabolic manipulation in cancer treatment.

This study found that in mice lacking EGFR, elevated Wnt signaling disrupts hair follicle development by affecting cell proliferation and differentiation, revealing a critical role for EGFR in regulating these processes.

In this study, CD4+ non-haematopoietic, skin-resident stem cell-like populations were identified in both murine and human epidermis, suggesting they may serve as potential basal cell carcinoma precursors.