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This study found that tissue transcriptomics and a normalization approach can effectively cluster nine inflammatory skin diseases and identify specific biomarkers, including PTEN as a marker for cutaneous lupus erythematosus.

This study found that COL17 plays a key role in regulating epidermal keratinocyte differentiation and proliferation, influencing the expression of differentiation markers and cellular growth in specific conditions.

This study suggests that KRTAP2-3 may serve as a novel biomarker to identify cells in the polyaneuploid cancer cell state, which is linked to therapy resistance and poor prognosis in prostate cancer.

This study found that PDCD4 protein expression is reduced in various skin cancers compared to normal skin, suggesting its potential role in preventing or treating certain skin cancers.

In this study on C3H/HeJ-engrafted mice, a single injection of BMD-1141 significantly increased anagen hair follicle counts and enhanced hair regrowth compared to daily high-dose ruxolitinib, suggesting it stimulates hair growth by influencing the hair cycle rather than altering immune response.

This study reported improvement in hair loss lesions in C3H/HeJ mice with alopecia areata following treatment with the CCR5 inhibitor maraviroc, alongside reduced infiltration of specific T cells in the lesions.

CD200 is not a reliable marker for identifying stem cells in all skin types.

This study found that the CD301b-expressing subpopulation of macrophages plays a crucial role in promoting reparative processes during the mid-stage of skin wound healing in a mouse model.

This study found that skin organoids derived from iPSCs with an HS-associated NCSTN mutation showed defects in hair follicle stem cell differentiation and increased expression of inflammatory proteins related to hidradenitis suppurativa.

This study found that topical treatment with 7DHC and BM15766 reduced hair growth in mice compared to those treated with Ethanol/DMSO, and hair did not recover after treatment ceased, alongside increased apoptotic cells and decreased expression of specific genes.

This study reports that the monoclonal antibody BKN-1 specifically stained basal cell epithelioma cells and certain normal skin structures, indicating a similarity in keratin expression between the tumor and follicular epithelium below the isthmus portion.

This study suggests that cultured hair follicle dermal sheath cup cells exhibit immune privilege properties, partly through the expression of PD-L1, which impacts co-cultured immune cells' behavior.

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 observed that NSG-hu-BLT mice developed graft-versus-host disease characterized by CD8+ T lymphocyte-related cell death in the skin and liver, which may affect their utility in other research areas.

This study reports that LL-37 treatment enhances cell proliferation, migration, and secretion of regenerative factors in adipose-derived stem cells, potentially promoting hair growth in vivo.

This study found that CRABP1, Nestin, and Ephrin B2 are expressed in both the tumor stroma and invasive front of skin adnexal tumors and basal cell carcinomas.

A new gene mutation may allow some piebaldism patients to regain skin color in white patches.

This study identified a monoclonal antibody, HKN-2, that recognizes specific cells in human skin and may indicate a common antigenic determinant between hair and other skin epithelial tissues.

CD34 is a marker for isolating stem-like cells in mouse hair follicles.

This article discusses junctional epidermolysis bullosa caused by COL17 deficiency, noting a lack of experimental therapies and the impact of nonsense mutations, but it reports no new clinical results.

In this phase I study, CT-707, a new ALK inhibitor, showed a 77% response rate among Chinese patients with advanced ALK-rearranged non-small cell lung cancer, suggesting clinical effectiveness despite some adverse events like diarrhea and liver enzyme elevation.

This study found that keratinocyte stem cells in mouse skin are closely related to side population or BCRP1-positive cells based on their localization and marker expression.

In this study, researchers analyzed skin tumors from patients with CYLD cutaneous syndrome and found that loss of CYLD function is linked to changes in cellular signaling pathways, particularly NF-κB signaling, and leads to increased secretion of specific extracellular matrix proteins.

This study suggests that mutation-targeted siRNA therapy could potentially treat keratitis-ichthyosis-deafness syndrome by selectively reducing harmful GJB2 mutant gene expression in patient-derived keratinocytes.

This study found that the development of Merkel cell carcinoma from hair follicles in mice can be driven by in vivo reprogramming with ATOH1 and relies on p53 loss for progression.

This study found that in alopecia areata, treatment with the oral JAK-inhibitor tofacitinib decreased clonally expanded CD8⁺ T cells in the scalp, but many expanded clones did not completely disappear, potentially leading to relapse after stopping treatment.

In this study, researchers documented the immunohistochemical distribution of CD34 in basal cell carcinoma and found distinct patterns of CD34 expression, with variations in CD34 positivity between different areas of BCC tumor stroma and adjacent skin regions.

This research developed new in vitro models for high-throughput screening of drugs that could protect or restore immune privilege in hair follicles, finding that Tofacitinib was effective in preventing inflammation-related marker upregulation, while Tacrolimus and αMSH worked specifically in outer root sheath keratinocytes.

Revertant cell therapy shows promise for treating type XVII collagen deficiency, but better cell selection methods are needed.

This study identified a novel G207E STING mutation causing a distinct phenotype involving alopecia, photosensitivity, and thyroid dysfunction, and suggests that common polymorphisms in TMEM173 and IFIH1 may influence disease presentation.