Introduction: Prior research has explored the relationship between inflammatory skin disorders and breast cancer (BC), yet the causality of this association remains uncertain.
Methods: Utilizing a bidirectional two-sample Mendelian randomization (MR) approach, this study aimed to elucidate the causal dynamics between various inflammatory skin conditions-namely acne, atopic dermatitis, psoriasis vulgaris, urticaria, and rosacea-and BC. Genetic variants implicated in these disorders were sourced from comprehensive genome-wide association studies representative of European ancestry. In the forward MR, BC was posited as the exposure, while the reverse MR treated each inflammatory skin disease as the exposure. A suite of analytical methodologies, including random effects inverse variance weighted (IVW), weighted median (WME), and MR-Egger, were employed to probe the causative links between inflammatory skin diseases and BC. Sensitivity analyses, alongside evaluations for heterogeneity and pleiotropy, were conducted to substantiate the findings.
Results: The MR analysis revealed an increased risk of acne associated with BC (IVW: OR = 1.063, 95% CI = 1.011-1.117, p = 0.016), while noting a decreased risk of atopic dermatitis (AD) in BC patients (IVW: OR = 0.941, 95% CI = 0.886-0.999, p = 0.047). No significant associations were observed between BC and psoriasis vulgaris, urticaria, or rosacea. Conversely, reverse MR analyses detected no effect of BC on the incidence of inflammatory skin diseases. The absence of pleiotropy and the consistency of these outcomes strengthen the study's conclusions.
Conclusion: Findings indicate an elevated incidence of acne and a reduced incidence of AD in individuals with BC within the European population.
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http://dx.doi.org/10.1111/srt.13782 | DOI Listing |
ACR Open Rheumatol
January 2025
Saint Louis University School of Medicine, St. Louis, Missouri.
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Department of Dermatology and Allergology, EB House Austria, Research Program for Molecular Therapy of Genodermatoses, University Hospital of the Paracelsus Medical University Salzburg, Salzburg, Austria.
Recessive dystrophic epidermolysis bullosa (RDEB) is caused by mutations in COL7A1, leading to loss or dysfunction of type-VII collagen (C7), a protein essential for skin stability. Clinically, patients suffer from severe skin blistering, chronic or recurrent wounds, and scarring, which predispose to early onset of aggressive squamous cell carcinoma. Previous studies showed that RDEB-keratinocytes (RDEB-KC) express high levels of matrix-metalloproteinase 9 (MMP-9), a molecule known to play a crucial role in wound chronification if dysregulated.
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January 2025
Institute of Pharmaceutical Research and Development, College of Pharmacy, Wonkwang University, Iksan, Jeonbuk, 54538, South Korea.
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View Article and Find Full Text PDFArch Dermatol Res
January 2025
Department of Dermatology, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, National Clinical Research Center for Dermatologic and Immunologic Diseases, 9 Dongdan 3rd Alley, Beijing, 100730, China.
Bullous pemphigoid (BP) is a debilitating autoimmune skin blistering disease, characterized by the deposition of specific autoantibodies at the dermal-epidermal junction. This leads to an inflammatory cascade involving the activation of complement proteins, mast cell degranulation, immune cell recruitment, and the release of proteases by granulocytes. While several cytokines and signaling pathways have been implicated in the pathogenesis of BP, the precise mechanism behind autoantibody production remains unclear.
View Article and Find Full Text PDFVet Sci
January 2025
Biosafety Research Institute and College of Veterinary Medicine, Jeonbuk National University, Iksan 54896, Republic of Korea.
Activated keratinocytes play a crucial role in skin inflammation through the production of multiple inflammatory mediators; however, little is known about cytokine secretion by activated keratinocytes in dogs. This study aimed to investigate the effects of the Th1 and Th2 types of cytokines on the production of keratinocyte-derived inflammatory mediators. Canine progenitor epidermal keratinocytes (CPEKs) were incubated with canine recombinant IL-4, IL-13, an IL4/IL13 mixture, IFN-γ, TNF-α, or an IFN-γ/TNF-α mixture for 24 h following 100% confluency.
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