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This study found that the KrasG12D mutation alters ERK signal dynamics in hair follicle stem cells, leading to tissue deformation, and suggests a collective effect of mutant cells is necessary for disruption.

In this study, the researchers developed a quantum algorithm, QuantAnts machines, which identified complexes of CD9, CD34, and CD74 as potential targets for certain cancers involving the RAS pathway.

This review examines the origins and mechanisms of tumor initiation in common skin cancers, but does not present new experimental findings; it emphasizes the need for further research on cancer stem cells.

This review discusses the genetic pathways involved in melanoma and suggests that targeting these pathways with pharmacological inhibitors may provide a new therapeutic approach, though clinical results have been disappointing so far.

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 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 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.

This study found that keratin 15 expressing cells from the hair follicle contribute to the development and long-term persistence of cutaneous papillomas in transgenic mice, with a subset showing the Ha-ras mutation.

This review suggests that bendamustine, alone or in combination, shows effectiveness in treating indolent non-Hodgkin lymphoma and chronic lymphocytic leukemia, with recent studies highlighting its benefits especially in combination therapies, while balancing efficacy with a favorable toxicity profile.

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.

In this transgenic mouse study, preliminary findings suggest that overt melanocyte hyperplasia may require prior keratinocyte hyperplasia, indicating a potential role for keratinocyte mutation in early melanoma development.

This research found that activating a KrasG12D mutation in mice led to skin thickening, papillomas, and hair growth issues, suggesting that even rare KRAS mutations can mimic human RAS/MAPK syndrome symptoms.

This study observed distinct differences in hair characteristics between individuals with cardio-facio-cutaneous syndrome and Costello syndrome, highlighting the role of the RAS pathway in these RASopathies and aiding clinical diagnosis.

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 identified hair follicle stem cells as a source of squamous cell carcinoma in an inducible mouse model and proposes targeting these for future cancer therapies.

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

This study found that VEGF-deficient keratinocytes can form tumors using different aneuploidy and signaling patterns, highlighting VEGF's role beyond angiogenesis in tumor cell growth and survival.

This study found that loss of the DNA methyltransferase Dnmt3a, but not Dnmt3b, increased carcinogen-induced squamous tumors in murine epidermis, with combined deletion leading to more aggressive and metastatic carcinomas.

This study found that H-Ras activation in aged mouse skin leads to increased dysplasia and progression to in situ squamous cell carcinoma, highlighting an age-linked connection between immune changes, senescence, and cancer risk.

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.

Ets2 gene is crucial for placental development in mice.

This study identified that a deficiency in the palmitoyl transferase enzyme, due to a mutation in the Zdhhc13 gene, led to severe physiological abnormalities in mice, including skin, bone, and systemic amyloid issues.

This review summarizes how genetic studies using conditional β-catenin loss- and gain-of-function mice have advanced understanding of canonical Wnt signaling's role in embryonic development, adult stem cell maintenance, and cancer modeling.

In this study, peptide-based nanoparticles were successfully used to deliver the CRISPR-Cas9 system into cancer cells, effectively targeting and editing KRAS mutations, suggesting promising therapeutic potential for cancer treatment.

In this study, activation of oncogenic K-ras in a mouse model caused the oral mucosa to rapidly progress from squamous hyperplasia to carcinoma within 14 days, demonstrating its acute sensitivity.

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