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Hirsutism was characterized by excessive terminal hair growth in a male pattern on androgen-dependent areas of the female body, and it could occur in both men and women. The condition was commonly associated with polycystic ovary syndrome, idiopathic hyperandrogenemia, and other endocrine disorders. Diagnostic guidelines primarily focused on premenopausal women, but evaluations for underlying endocrinopathies in postmenopausal women and men were also necessary. Management strategies included eliminating causative drugs, assessing hypothalamic-pituitary-gonadal axis dysregulation, and identifying androgen-secreting tumors. Treatment options involved pharmacotherapy with estrogens-progestins, antiandrogens, and other agents, while surgical excision was considered for certain adenomas.

The study used transgenic mice with targeted expression of spermidine/spermine N1-acetyltransferase (SSAT) in hair follicle keratinocytes to investigate susceptibility to skin cancer. These K6-SSAT transgenic mice, bred onto a tumor-resistant C57BL/6 background, showed a 10-fold increase in epidermal tumors when exposed to a carcinogenesis protocol involving 7,12-dimethylbenz[a]anthracene and 12-O-tetradecanoylphorbol-13-acetate. The transgenic mice exhibited elevated SSAT activity and protein levels, along with increased putrescine and N1-acetylspermidine, indicating enhanced polyamine catabolism. The study concluded that this activation of polyamine catabolism might play a crucial role in chemically induced skin cancer, as evidenced by the early onset and progression to carcinomas in the transgenic mice.

The study demonstrated that YAP and TAZ proteins were crucial for skin homeostasis, particularly in the basal layer of the skin, where they were found in the nucleus and increased during wound healing. Deleting YAP and TAZ in the skin of adult mice resulted in slower cell proliferation, hair loss, and impaired wound regeneration. The nuclear localization of YAP/TAZ was regulated by Integrin-Src signaling, which was influenced by contact with the basal extracellular matrix. This mechanism was also observed in other squamous epithelia and squamous cell carcinomas. In contrast, columnar epithelia used a different mechanism involving Hippo signaling to keep YAP/TAZ in the cytoplasm. However, when columnar epithelial tumors lost their apical domain, YAP/TAZ became nuclear, making the tumors sensitive to the Src inhibitor Dasatinib.

In this study, researchers investigated whether overexpression of ornithine decarboxylase (ODC) was sufficient for tumor promotion in mouse skin. They used transgenic mice with high ODC expression in epidermal keratinocytes and found that these mice were more sensitive to carcinogen initiation compared to controls. Notably, mice with ODC overexpression in hair follicle keratinocytes developed tumors without the need for additional tumor promoters. The study concluded that ODC overexpression was sufficient to activate target cells in hair follicles, leading to clonal expansion and epidermal tumor formation, indicating that hair follicles are key sites for chemical carcinogen targeting in the skin.

The study investigated the carcinogenic effects of expressing a mutant H-ras oncogene in different epidermal cell populations of mice. It found that targeting the expression to follicular and interfollicular cells using a truncated keratin 5 gene promoter led to the development of acanthotic areas and carcinoma in situ in newborn mice, and papillomas and keratoacanthomas in adults. These benign tumors frequently progressed to malignancy, unlike those induced by other promoters, and did not require wounding or a tumor promoter for formation. The research concluded that the cell type in which tumor initiation occurs, particularly within the hair follicle, significantly influenced the malignant potential of the tumors.