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This chapter examines how toxins such as inorganic arsenic, dioxin, and bacterial toxins can disrupt the balance of keratinocyte stem cell regeneration and differentiation, affecting skin barrier maintenance.

This symposium reported that DNA damage accumulation in aging stem cells affects genome integrity, highlighting novel mechanisms like Bmi1's role in DNA repair and the involvement of BATF in lymphoid differentiation.

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 reported that reconstructed skin models can be useful for studying the effects of non-water-soluble topical products on xenobiotic metabolism, particularly in enzyme activities like EROD and GST.

This study found that AHCC significantly reduced alopecia caused by Ara-C in neonatal rats and improved liver function affected by 6-MP and MTX in mice.

This study found that activating CXCR2 on ras-transformed keratinocytes promotes migration and tumor development in a mouse skin model.

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 study found that TCDD significantly reduced EGF receptor binding in various animal models, linked to toxic symptoms like weight loss and developmental delays, with receptor phosphorylation persisting several days.

This study found that transgenic mice expressing IGF-1 in their skin showed significant skin changes, early hair follicle generation, and a higher propensity to develop tumors after chemical promotion, suggesting IGF-1's role in skin carcinogenesis.

The study introduced an advanced skin model, ImmuSkin-MT, which effectively distinguished between different strengths of skin sensitizers by mimicking the interaction of immune cells in skin tissue.

This study demonstrated that metabolomics could identify persistent biomarkers distinguishing between heavy ion and γ radiation exposures, offering a potential tool for assessing long-term radiation risk for intestinal pathologies.

This study demonstrated that switching aE-catenin to aT-catenin in murine skin substantially rescued hyperproliferative and pre-cancerous conditions, but led to partial baldness, indicating potential functional discrepancies.

This study reports that A132, a hair dye ingredient, induces phototoxicity and photogenotoxicity via mitochondrial apoptosis when exposed to sunlight, suggesting potential risks of oxidative stress and hair damage.

This study found that long-term smoking was associated with increased mitochondrial DNA deletions in hair follicles, especially among smokers with low plasma glutathione S-transferase activity.

In this study, SMR-2 and SMR-6, retinoid analogs, were found to be approximately 100 times more toxic than retinoic acid in male mice, primarily affecting skin, immune, and reproductive systems.

This study found that selective inactivation of ribonucleotide excision repair in mouse epidermis led to spontaneous DNA damage, skin inflammation, and the development of squamous cell carcinoma, suggesting potential implications for cancer development in humans.

The study created a test that found hormonal and toxic effects in plant and fungal extracts using prostate cancer cells.

This study found that EGFR and MEK inhibitors may induce acneiform skin toxicities by interacting with the skin bacterium Cutibacterium acnes to increase IL-36γ and IL-8 production in keratinocytes.

This study elucidates a mechanism for acne-like skin toxicity caused by EGFR/MEK inhibitors, involving an interaction with skin bacteria to trigger inflammation, which supports existing antibiotic treatment practices.

This article reviews evidence suggesting that vitamin D and its metabolite may help protect against nonmelanoma skin cancer, but reports no new empirical findings.

In this study, researchers found that the NUDT15 R139C gene variant is a significant genetic risk factor for azathioprine-induced severe myelotoxicity in Japanese patients with dermatological conditions, suggesting that screening for this variant may help prevent adverse reactions in East-Asian populations.

This study discovered that DNA damage independently induces IL-19 and IL-24 cytokines, which regulate senescence-associated secretory phenotype factors, suggesting potential pathways for treating cancer and age-related diseases.

This study found no evidence that the tested hair dye ingredients undergo hepatic metabolism to reactive oxidized metabolites in human liver microsomes and hepatocytes.

This article discusses dermatologic adverse events associated with topoisomerase inhibitors and anthracyclines, such as alopecia and hand-foot syndrome, but reports no new clinical results.

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 chapter reviews studies on the side effects of cytostatics and immunosuppressive drugs, detailing various toxicities such as cardiovascular, pulmonary, and neurotoxicity, but provides no new clinical results.

In this study, γ-ray irradiation in mice during the first telogen phase led to decreased hair follicle density and pigmentation anomalies, suggesting damage to stem cells and progenitors for keratinocytes and melanocytes.

This study found that mutations in the TULP3 gene are associated with progressive degeneration of the liver, kidney, and heart in adults, highlighting the importance of early detection and management.

In this study, the reconstructed skin epidermal model derived from hair follicles showed gene expression and enzyme functionality consistent with native human skin, suggesting its viability for studying skin metabolism and potential toxicity of dermo-cosmetic ingredients.

This study found that using a recombinant adenoassociated virus to induce survivin expression protected normal tissues from radiation damage in mice, reducing side effects compared to controls.