ArticleHuman pathology2019
ADAM3A copy number gains occur in a subset of conjunctival squamous cell carcinoma and its high grade precursors.
Article in Human pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- Update in the Diagnosis and Management of Ocular Surface Squamous Neoplasia (OSSN).Journal of clinical medicine · 2025Review
- The Management of Ocular Surface Squamous Neoplasia (OSSN).International journal of molecular sciences · 2022Review
- Article
- Maternal atopy and offspring epigenome-wide methylation signature.Epigenetics · 2021Article
- Update on the Management of Ocular Surface Squamous Neoplasia.Current ophthalmology reports · 2021Article
- Next-Generation Sequencing-Based Molecular Profiling of Conjunctival Squamous Cell Carcinoma and Its Potential Application for Therapy.Ophthalmology scienceArticle
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
Abstract
Conjunctival squamous cell carcinoma (cSCC) and its precursors are among the most frequent ocular surface neoplasms worldwide. Copy gain of 8p11.22 and ADAM3A overexpression have been recently identified in invasive cSCC. We sought to study copy number gains using fluorescent in situ hybridization (FISH) in cSCC and the spectrum of precursor lesions. A total of 54 cases conjunctival squamous intraepithelial neoplasia (CIN), carcinoma in situ (CIS), or cSCC were studied using FISH with an ADAM3A (8p11 locus) probe and a chromosome 8 (Chr 8) centromere reference probe. Eighty one percent (44/54) of the cases presented in men and 19% (10/54) in women. The age at presentation ranged from 12 to 94 years (mean 65.5 years). Severe CIN was diagnosed in 45% (24/54) of the cases, followed by CIS in 31% (17/54), moderate CIN in 15% (8/54), invasive cSCC in 7% (4/54), and mild CIN in 2% (1/54). Nine (of 54) (17%) cases harbored ADAM3A or Chr 8 gains, with one of these cases demonstrating high level amplification. All ADAM3A alterations were restricted to high-grade lesions, including 2/17 (12%) cCIS, 1/4 (24%) cSCC, 5/24 (20%) severe CIN and 1/8 (12%) moderate CIN. Monosomy 8 was detected in 2 (4%) cases. No ADAM3A alterations were detected in non-neoplastic controls. Gains of ADAM3A/chromosome 8 occur in a subset of cSCC and its precursors. Alterations were present in high-grade lesions, sparing non-neoplastic conjunctiva and absent in tested controls. Thus, the specificity of this alteration as a biomarker for ocular SCC deserves further study.
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