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This commentary discusses how microphthalmic-associated transcription factor levels in circulating tumor cells correlate with melanoma progression and suggests the factor may be up-regulated in vivo, but it reports no new clinical results.

In this study, researchers found that overexpressing SOX2 in colorectal cancer cell lines can cause DNA damage and cell death, while repressing it reduces tumor growth and cell aggressiveness.

This study found that the absence of Ctip2 in epidermal keratinocytes led to impaired wound healing in mice, affecting cell migration, proliferation, and hair follicle stem cell maintenance.

This article reviews the connection between PI3K-AKT-mTOR pathway mutations and heritable skin diseases characterized by tissue overgrowth, but it reports no new clinical results.

This study found that induced TERT expression in mouse skin epithelium rapidly transitions hair growth from the resting to active phase by promoting stem cell proliferation through a non-telomere related mechanism.

This review highlights the potential of PROTACs to transform cancer treatment by selectively degrading oncogenic proteins, overcoming drug resistance, and reducing toxicity; it also discusses challenges in optimizing these therapies for personalized applications.

This study found that trichohyalin is expressed in cancerous tongue epithelial cells, while plectin-1 expression may indicate malignancy.

This study reported that the novel AKT inhibitor CCT128930 demonstrated significant antitumor activity in human cancer cell lines and xenografts, highlighting its potential as an anticancer therapy.

This review discusses managing prostate cancer in patients with high-risk germline mutations and highlights the need for more research and consensus guidelines, reporting no new clinical results.

This study found that the E3 ligases NEDD4 and NEDD4L regulate intestinal stem cell priming by degrading the LGR5 receptor, and their loss leads to increased Wnt activation and crypt proliferation, which in turn accelerates intestinal tumor progression in mice.

Long-standing benign tumors can become cancerous, especially in people with weakened immune systems.

In this study, a synthetic antagonist of the p75 neurotrophin receptor was found to significantly inhibit hair follicle regression in murine skin cultures, suggesting a potential role in treating hair disorders characterized by premature catagen entry.

This review discusses how increased gene copy number for telomerase components may contribute to telomerase up-regulation in cancer cells, although the exact mechanisms are not fully understood.

In this study, the disruption of Gh/tissue transglutaminase in mice did not affect viability but reduced thymocyte viability and fibroblast adhesion, suggesting its role in cell stabilization and extracellular matrix interactions.

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 study reports that miR-22 promotes cancer progression and metastasis by maintaining Wnt/β-catenin signaling and cancer stem cell function.

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.

This study suggests that the expression of VLCFA biosynthesis genes is suppressed in skin hyperplasia and cancer, which could influence keratinocyte function.

This study found that deleting the vitamin D receptor from specific stem cells in mouse hair follicles disrupts their ability to regenerate the epidermis after injury, suggesting an essential interaction with the transcription factor p63.

This study suggests that TIP39 and its receptor PTH2R, identified in human epidermis, may play a role in keratinocyte function and influence skin differentiation.

This study found that overexpression of parathyroid hormone-related peptide in transgenic mice skin disrupted normal hair follicle development, suggesting a role for the peptide in the early stages of follicle formation.

This study found that mice with a homozygous knockout of the Ten1 gene, developed through CRISPR-Cas9-mediated exon 3 deletion, exhibited telomere shortening and symptoms consistent with accelerated aging, such as reduced lifespan, skin changes, aplastic anemia, and cerebellar hypoplasia.

This study found that STAT3 directly inhibited the activity of the sheep FST gene promoter, consequently reducing cell proliferation and promoting a better understanding of hair follicle development mechanisms.

Results are not reported in this study, which investigated the effects of radiation on hair follicles and evaluated various cellular responses and signaling pathways, particularly focusing on WNT signaling and the impact of Wnt3a treatment.

In this study, the presence of the HPV11-E2 protein in transgenic mice was found to increase and vary the expression of a reporter gene in hair follicle bulge regions.

This study found that P144 (Disitertide) significantly reduced collagen deposition and improved muscle organization in a rabbit model of post-radiotherapy fibrosis, suggesting potential antifibrotic effects.

In this study, activation of c-MycER in adult mouse epidermis rapidly induced proliferation and disrupted keratinocyte differentiation, causing changes similar to precancerous lesions, which regressed once c-MycER was deactivated.

This study found that mutations in the TMPRSS6 gene affect the ability of matriptase-2 to inhibit hepcidin, which may impact the molecular pathogenesis of iron-refractory iron-deficiency anemia.

In liver cancer cells, this study found that upregulating hsa_circ_0002980 inhibits cell proliferation, metastasis, and EMT by modulating the miR-1303/CADM2 axis, suggesting it as a potential therapeutic target.

This study found that transgenic mice with keratinocyte-specific overexpression of CtBP1 exhibited abnormal hair follicle development, suggesting CtBP1 may play a pathogenic role in hair morphogenesis.