ArticleNorth American journal of medical sciences2011
Overexpression of linker for activated T cells, cyclooxygenase-2, CD1a, CD68 and myeloid/histiocyte antigen in an inflamed seborrheic keratosis.
Article in North American journal of medical sciences, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- Psoriasis and Seborrheic Keratoses: Insights from Biologic Therapy and Skin Imaging.Life (Basel, Switzerland) · 2025Article
- MicroRNA-146b-3p regulates the development and progression of cerebral infarction with diabetes through RAF1/P38MAPK/COX-2 signaling pathway.American journal of translational research · 2018Article
- Endothelin-1 enhances the melanogenesis via MITF-GPNMB pathway.BMB reports · 2013Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
contextInflamed seborrheic keratoses are generally associated with the accumulation of variable numbers of lymphocytes and histiocytes in the superficial dermis. The precise immunologic mechanism of this histologic phenomenon is not known CASE REPORT: A 62-year-old male presented with a patch on the right neck with additional features of inflammation. Skin biopsies for hematoxylin and eosin examination, as well as for immunohistochemistry analysis were performed.
resultsH&E staining demonstrated classic features of an inflamed seborrheic keratosis. Overexpression of LAT, COX-2, CD1a, and CD68 was noticed in the inflammatory infiltrate. A strong presence of CD1a was also seen in the epidermis suprajacent to the inflammation. Myeloid/histiocyte antigen was strongly expressed by the keratinocytes
conclusionA complex immune response seems to be involved in the pathophysiology of an inflamed seborrheic keratosis.
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