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SPRY1 deficiency in skin cells causes stem cells to move to the skin surface, leading to increased pigmentation.

In this study, overexpression of ornithine decarboxylase accelerated basal cell carcinoma in Ptch1+/– mice under UVB exposure, while its inhibition reduced tumor induction, suggesting potential chemoprevention strategies in humans.

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 that dihydrotestosterone (DHT) regulates the degradation of p27 in MCF-7 breast cancer and OVCAR-3 ovarian cancer cells, involving SKP2 as a key factor.

This study demonstrated that de novo designed bifunctional proteins can target and degrade BCL-xL, leading to cell apoptosis, suggesting a new approach to targeted protein degradation therapy.

In this study, TC-1 cells, resembling stromal cells formed by epithelial-mesenchymal transition, significantly affected the behavior of normal human keratinocytes, supporting the role of stromal cells in tumor progression.

In this study, silencing P-cadherin in human scalp hair follicles reduced melanogenesis and associated protein expression, suggesting P-cadherin is crucial for normal hair pigmentation via GSK3β-mediated Wnt signaling.

The researchers reported that in mice, the type of tumor suppressor deleted along with oncogenic Kras activation in HFSCs influenced the specific squamous cell carcinoma phenotype that developed.

In this study, crossing mice overexpressing antizyme with MEK mutants significantly delayed tumor development and reduced tumor frequency, likely by slowing cell growth in skin tumors.

This study found that deleting Smad2 and Smad3 in murine skin leads to severe skin abnormalities and cancerous lesions, similar to but more severe than those seen in Smad4 mutants, indicating the critical role of TGF-β signaling in skin development.

This study suggests that chronic treatment with TPA in mouse skin selectively expands a keratinocyte subpopulation hyperinducible for ODC, which may be a key target for neoplastic transformation.

This study found that integrin alpha-6 and p63 may play a role in hair loss, with variable expression patterns in different types of alopecia observed in scalp biopsy samples.

In this study, researchers found that selectively disabling ribonucleotide excision repair in mouse epidermis caused DNA damage, skin inflammation, and led to skin cancer, suggesting a potential role for this repair mechanism in tumorigenesis.

This phase I study reported that ETC-159, targeting Wnt signalling, showed tolerable safety profiles at doses that inhibit its pathway, though bone turnover markers increased, warranting early and regular monitoring. No tumor responses were observed, but two patients achieved stable disease for several cycles.

In this study, mice lacking the Mcpip1 gene in their myeloid cells did not develop SCC-like tumors but instead showed increased melanocyte activity and hair loss, indicating a distinct role for myeloid Mcpip1 in skin cancer development compared to keratinocyte Mcpip1.

This study found that epigallocatechin-3-gallate (EGCG) may reduce paclitaxel-induced apoptosis in human dermal papilla cells by regulating microRNA expression related to apoptosis and cell proliferation.

This study found that the expressions of CDK inhibitors p21waf1/cip1 and p27kip1 were higher during the anagen phase compared to telogen, suggesting a role in follicular epithelial cell differentiation.

New hair regrowth model introduced, imiquimod kills skin cancer cells, T-cadherin loss makes skin cancer more invasive, no strong link between PTCH1 gene and skin cancer after transplant, and male teens more likely to have hereditary hair loss.

This review discusses genome maintenance mechanisms critical for preventing age-related diseases by preserving stem and progenitor cell potential, but reports no new empirical findings.

In this study, researchers found that YAP and TAZ, when localized in the nucleus of basal layer cells, are crucial for skin regeneration and hair growth, with their loss leading to slower cell proliferation, hair loss, and impaired wound healing in mice.

Blocking the JAK/STAT pathway may help reduce skin sensitivity in Xeroderma pigmentosum.

This study found that Malt1, particularly its protease activity, plays a crucial role in maintaining Treg cell function and homeostasis, with its inactivation leading to autoimmune diseases and altered immune responses in mice.

In this study, researchers found that deleting the Bmi1 gene in murine melanocytes caused premature hair greying and loss of melanocyte lineage cells, highlighting BMI1's role in protecting melanocyte stem cells from stress and oxidative damage.

This study suggests that activating AMPK to phosphorylate ZDHHC13 may enhance MC1R function and reduce melanoma risk in individuals with red hair.

In this case report, researchers described a female child with total alopecia due to a mutation in the SNRPE gene, emphasizing the need for updated genetic testing as knowledge advances to avoid diagnostic delays in hereditary nonsyndromic hypotrichosis.

This study suggests that finasteride may upregulate BTG2 and CD244 gene expression through differential methylation, indicating potential as a treatment avenue for medulloblastoma.

CTP-543 is generally safe for treating alopecia areata.

Caspase-3 helps control cell growth and organ size by activating YAP.

In this study, the researchers observed that transfecting hair follicle cells with an amino-terminal truncated beta-catenin gene significantly increased cell proliferation, potentially by enhancing c-myc gene expression.