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This study identified gene expression patterns in a mouse model that may influence tumor susceptibility and tissue functions related to inflammation and cell proliferation, highlighting Lgr5 and the vitamin D receptor as key regulators.

This study found significantly higher P-Smad2 levels in both lesional and nonlesional skin of organ transplant recipients, suggesting elevated TGF-β signaling might contribute to their increased cancer susceptibility.

In this study, researchers demonstrated that the expression of the oncogene SmoM2 leads to basal cell carcinoma in the ear epidermis of mice but not in the back skin, with differences in susceptibility linked to the composition of the extracellular matrix.

This study found that mice lacking the vitamin D receptor (VDR) developed skin tumors more rapidly than those with normal VDR activity, regardless of 1,25-dihydroxyvitamin D(3) presence.

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.

Ducks can get the Rous sarcoma virus if infected shortly after birth, leading to tumors and disease spread.

This study found that mice lacking the glucocorticoid receptor in their epidermis showed increased susceptibility to chemical-induced skin cancer, highlighting the receptor's role in skin carcinogenesis.

This study found that ACE2 and TMPRSS2 genes were more highly expressed in tumors of elderly male cancer patients compared to healthy individuals, with notable differences across age and gender.

This study reported that heterozygosity for FHIT affects mice's susceptibility to spontaneous alopecia areata and to certain preneoplastic lesions induced by benzo[a]pyrene, but does not change how they respond to budesonide and N-acetyl-L-cysteine.

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 case study suggests that genetic susceptibility to PCOS and rare syndromes, such as Trichorhinophalangeal syndrome Type 1, should be considered in young men with unexplained hyperandrogenism.

This study found that overexpression of PKCepsilon in mouse epidermis was associated with increased susceptibility to metastatic squamous cell carcinoma, potentially through a mechanism involving tumor necrosis factor-alpha.

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.

This research describes mouse models to explore Kindlin-1's role in skin disorders, including Kindler syndrome, revealing novel integrin-independent pathways potentially leading to skin tumors.

This study found that IL-4 VNTR intron 3 and TNF-α (rs1799964) gene polymorphisms do not have a significant association with alopecia areata susceptibility in the Egyptian population.

This review discusses the role of tumor suppressors in controlling tumor-associated inflammation and suggests that targeting this inflammation may counteract the effects of tumor suppressor loss.

The study observed that the tumor suppressor activity of bone morphogenetic proteins in mouse skin epithelium depends on Noggin levels, inhibiting Wnt and Shh signaling pathways to prevent tumor initiation and progression.

Fgfr2b helps maintain healthy skin and prevent cancer.

This review examines cell senescence pathways in melanocytes, highlighting the involvement of telomere attrition, the p16/RB pathway, and cAMP signaling in the context of melanoma development, but reports no new findings.

This article reviews the roles of lesser-known secreted phospholipase A2 isoforms in various biological processes, such as immune suppression, metabolic regulation, epidermal hyperplasia, and male reproduction, without reporting new clinical findings.

This review discusses autoimmune blistering diseases across species and highlights new treatment efficacy findings and ongoing trials, but it reports no new clinical results.

This study analyzed pexidartinib-associated adverse events from FDA data and reported common events such as hepatic issues and systemic reactions. It highlighted sex-specific susceptibilities and reinforced the need for risk mitigation and long-term monitoring in tenosynovial giant cell tumor management.

This study identified a genetic locus associated with rhabdomyosarcoma susceptibility in mice and found that specific differentiation markers are linked to the regression of basal cell carcinoma.

This review found substantial data suggesting that heavy metals may influence tumor development and progression in cancers such as breast, lung, prostate, and gastric, though noted limitations and gaps in research data require further investigation.

This review reports that transgender individuals undergoing hormonal therapy for gender transition face increased risks of cardiovascular disorders, brain tumors, changes in bone density, metabolic disorders, and other health issues, while highlighting the necessity of this therapy for gender transformation.

In this study, animal model observations suggested that GLI1 expression may reduce cSCC initiation but is not involved in the tumor's aggressiveness.

This protocol details a method for inducing skin cancer in mice through chemical carcinogenesis, which studies cutaneous malignancies but does not report new findings.

This workshop review discusses the dual role of cellular senescence in cancer, highlighting both its anticancer effects and pro-tumorigenic potential, while reporting no new research results.

This review discusses the side effects of iodotherapy for thyroid cancer treatment, including various physical symptoms and impacts, and emphasizes the need for further research and pharmacological support; it reports no new experimental results.

This study found that the cell of origin in mouse skin affects melanoma phenotype and response to therapies, despite the presence of the same genetic mutations.