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This study observed that deleting PTEN in mouse facial motoneurons enhanced peripheral axon regeneration but also led to physiological changes and potential hyperplasia in older mice.

In this study, conditional inactivation of the Mad2l1 SAC gene in mice led to aggressive and lethal acute lymphoblastic leukemia and hepatocellular carcinoma, demonstrating a link between chromosomal instability and cancer development.

This study reported that genetic changes in trichilemmal carcinoma resemble those in other skin cancers, with TP53 mutations associated with aggressive clinical outcomes.

This study found that trichilemmal carcinoma shares genetic changes with other skin cancers, suggesting a similar pathogenesis, particularly in those with aggressive clinical courses linked to TP53 mutations.

This study reported genetic mutations in trichilemmal carcinoma similar to those found in other skin cancers, including TP53 mutations associated with aggressive disease.

In this study, the deletion of Smad4 and PTEN genes in mice was associated with rapid and invasive squamous cell carcinoma formation in the forestomach, modeling human esophageal cancer progression.

In this study with mice, simultaneous inactivation of Smad4 and PTEN genes led to rapid development of invasive forestomach squamous cell carcinomas, mirroring human esophageal SCCs.

This study found that quiescence in hair follicle stem cells acts as a tumor suppression mechanism for cutaneous squamous cell carcinoma, with Pten activity necessary to maintain this state.

This study by Flores and colleagues found that the type of tumor that develops in a specific subset of epidermal stem cells is influenced by which tumor suppressor gene is deleted.

This article discusses the complex role of TGFβ in cancer progression, highlighting its dual function as both a tumor suppressor in early stages and a promoter in later stages, without reporting new results.

This article reviews the role of exosomes in promoting axonal regeneration and discusses recent findings on how exosome-borne molecules might influence the PTEN-mTOR pathway in injured neurons; it reports no new experimental results.

In this study, the researchers found that vitamin D and calcium signaling in keratinocytes are essential for normal skin regeneration after wounding, with deficiencies significantly delaying wound closure and re-epithelialization in mice.

This study found that disrupting Smad4 signaling in young mice led to overactivation of follicle stem cells, causing hyperplasia and depletion of the stem cell niche.

This study found that PTEN regulates the number and genomic stability of hair follicle stem cells in the skin, with its deficiency leading to increased stem cell accumulation and senescence through interactions with BMAL1 and BMI-1.

This study found that loss of the Pten gene in Lgr5+ hair follicle stem cells promoted squamous cell carcinoma formation through the Akt/β-catenin signaling pathway.

This study explored the immune environment of the hair follicle's bulge region and suggested that its unique signaling may prevent melanoma formation by lacking necessary proinflammatory signals for full oncogenic transformation, indicating potential strategies for melanoma prevention by replicating this immune-privileged environment.

This review discusses the role of oxidative stress in hair greying and suggests that understanding melanocyte susceptibility at different follicular locations may help develop therapies for preventing and reversing the process; it reports no new experimental results.

This review examines regulatory mechanisms of quiescent stem cells in tissue homeostasis, drawing on observations from the intestine and other self-renewing tissues, without presenting new data.

This study found that among young women in West Bengal, India, co-occurring PCOS and related conditions like estrogen resistance and leptin receptor insufficiency are common, with notable genetic variations identified, including impairments in leptin signaling and insulin resistance.

This study found that deleting the Mad2l1 gene in mice leads to rapid onset of acute lymphoblastic leukemia and liver cancer due to induced chromosomal instability.

This study in mice found that WWP2 facilitates odontoblast differentiation and dentin formation by targeting PTEN for degradation, thereby enhancing KLF5 activity, which may suggest its crucial role in dental development.

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.

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 astilbin downregulates effector CD4+ T cell activities through the CYP1B1/ROS/PPARγ pathway, suggesting its potential use in treating inflammation.

This review discusses the role of YAP/TAZ proteins in skin cancer physiology and tumorigenesis, and the potential of targeting these proteins in skin cancer treatments, but presents no new experimental findings.

This study found that deleting Stim1 and Stim2 in mature T regulatory cells disrupts Ca 2+ signaling, preventing their differentiation and leading to severe autoimmune disorders in mice.

In this study, researchers identified a new dominant mutation in Hairless mice, called Pied, resulting from a deletion in the Adam10 gene, which causes freckle-like skin pigmentation by inhibiting melanocyte expansion.

This study found that UV radiation-induced fibroblast depletion in the skin is primarily due to a deregulated inflammatory response, with T cells aiding fibroblast survival under stress.

This study found that platelet-derived growth factor signaling is crucial for maintaining the hair follicle dermal stem cell pool and supporting their regenerative capacity.

In this study, researchers used a murine model of irritant contact dermatitis to reveal that hair follicle regions serve as key sites for neutrophil transepidermal migration, which requires MMP-9 expression stimulated by dermal monocytes.