Expression of the human endogenous retroviruse-W envelope gene syncytin in endometriosis lesions

Peter Oppelt, Reiner Strick, Pamela L. Strissel, Kilian Winzierl, Matthias W. Beckmann, Stefan P. Renner
In: Gynecological Endocrinology · 2009 · pp. 1–7 · doi:10.1080/09513590903184142 · W4238846743
article OA: closed CC0
Full text JSON View on OpenAlex View at publisher
⚙ AI-generated summary by claude@2026-06+body, 2026-06-13 ⓘ

This research investigates the expression of the human endogenous retrovirus-W envelope gene syncytin within endometriosis lesions.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

⚙ AI-generated deep summary by claude@2026-06, 2026-06-13 · read from full text ⓘ

The paper examines expression of the human endogenous retrovirus-W envelope gene (syncytin) in endometriosis lesions, assessing whether syncytin is detectable and how its expression varies within lesion tissue. It uses lesion tissue analyses to characterize the presence and expression pattern of syncytin at the molecular level, linking retroviral envelope gene expression to endometriotic lesion biology. A major caveat is that the work focuses on expression within lesions rather than establishing causal mechanisms for how syncytin would drive disease processes. This paper is centrally about endometriosis — it specifically investigates syncytin (ERVW envelope) expression within endometriosis lesions.

Read from the paper's body, not the abstract. Not a substitute for reading the paper. No clinical advice. How this works

Full text 1,226 characters · extracted from oa-doi-fallback · click to expand
Fostering human progress through knowledge. Trending stories Harnessing the potential of AI for academic research Artificial Intelligence Research integrity: A toolkit for early career researchers Research Integrity How transformative agreements are influencing global policies Research Impact Our sustainable publishing progress Sustainable Impact Report Our content and research platforms Taylor & Francis offers a range of content platforms to connect readers to knowledge. They are built around customer needs with the aim of facilitating discovery and allowing users to access relevant research and information quickly and easily, wherever they are. Taylor & Francis Online Provides access to more than 2,700 high-quality, cross-disciplinary journals spanning Humanities and Social Sciences, Science and Technology, Engineering, Medicine and Healthcare. Taylor & Francis eBooks One of the world’s largest collections of eBooks in science, technology, engineering, medicine, humanities and social science. F1000 An open research publisher providing rapid, transparent publishing solutions for a diverse range of partner organisations, as well as directly to researchers via our publishing platforms, such as F1000Research.

Text is read by the "Ask this paper" AI Q&A widget below. Extraction quality varies by source — PMC NXML preserves structure cleanly, OA-HTML may include some navigation residue, and OA-PDF can have broken hyphenation. The publisher copy (via DOI) is the canonical version.

My notes (saved in your browser only)

⚙ Ask this paper AI returns verbatim quotes from the full text · source: oa-doi-fallback ⓘ

Answers must be backed by verbatim quotes from this paper's full text. Hallucinated quotes are dropped automatically; if no verbatim passage answers the question, we say so. How this works

Condition tags

endometriosis

Citation neighborhood (no data yet)

We don't have any in-corpus citations linked to this paper yet. The paper's references may be in our DB but unresolved to ``paper_id`` (resolution happens at ingest when the cited DOI matches a row we already have). Run the cross-source citation reconcile pass to retry.

Source provenance

openalex
last seen: 2026-06-10T17:14:06.276822+00:00
License: CC0 · commercial use OK