Comments on “rhTNFR:Fc Suppresses the Development of Endometriosis in a Mouse Model by Downregulating Cell Proliferation and Invasiveness”

Antonio Simone Laganà, Francesca Maria Salmeri, Onofrio Triolo, Salvatore Giovanni Vitale, Roberta Granese, Vincenza Sofo
Reproductive sciences (Thousand Oaks, Calif.) · 2016 · vol. 25(7) , pp. 983–984 · doi:10.1177/1933719116653838 · PMID:27470149 · W2498355014
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⚙ AI-generated summary by claude@2026-06+body, 2026-06-07 ⓘ

This commentary discusses the findings of a study demonstrating that rhTNFR:Fc inhibits endometriosis development in mice by reducing cell proliferation and invasiveness.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 · read from full text ⓘ

This article is a brief “comments” piece on a previously published mouse study claiming that rhTNFR:Fc suppresses endometriosis development by downregulating cell proliferation and invasiveness. It does not present new experiments or original data in the provided text, and the only explicitly stated content is its bibliographic framing and contextual positioning relative to the earlier work it critiques. Because the excerpt lacks the comments’ substantive scientific arguments, key methods, results, and explicit limitations stated by the authors cannot be extracted here. This paper is centrally about endometriosis — it is a published set of comments on a study specifically focused on endometriosis in a mouse model.

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References Liu Y, Sun L, Hou Z, Mao Y, Cui Y, Liu J. rhTNFR: Fc suppresses the development of endometriosis in a mouse model by downregulating cell proliferation and invasiveness. Reprod Sci. 2015. pii: 1933719115620495. Laganà AS, Sturlese E, Retto G, Sofo V, Triolo O. Interplay between misplaced Mu¨ llerian-Derived stem cells and peritoneal immune dysregulation in the pathogenesis of endometriosis. Obstet Gynecol Int. 2013;2013:527041. Sturlese E, Salmeri FM, Retto G, et al. Dysregulation of the Fas/FasL system in mononuclear cells recovered from peritoneal fluid of women with endometriosis. J Reprod Immunol. 2011;92(1-2):74–81. Richter C, Messerschmidt S, Holeiter G, et al. The tumor necrosis factor receptor stalk regions define responsiveness to soluble versus membrane-bound ligand. Mol Cell Biol. 2012;32(13):2515–2529. Salmeri FM, Laganà AS, Sofo V, et al. Behavior of tumor necrosis factor-α and tumor necrosis factor receptor 1/tumor necrosis factor receptor 2 system in mononuclear cells recovered from peritoneal fluid of women with endometriosis at different stages. Reprod Sci. 2015;22(2):165–172. Othman ER, Hornung D, Hussein M, et al. Soluble tumor necrosis factor-alpha receptors in the serum of endometriosis patients. Eur J Obstet Gynecol Reprod Biol. 2016;20;200:1–5. doi:10.1016/j.ejogrb.2016.02.025. Author information Authors and Affiliations Corresponding author Rights and permissions About this article Cite this article Laganà, A.S., Salmeri, F.M., Triolo, O. et al. Comments on “rhTNFR:Fc Suppresses the Development of Endometriosis in a Mouse Model by Downregulating Cell Proliferation and Invasiveness”. Reprod. Sci. 25, 983–984 (2018). https://doi.org/10.1177/1933719116653838 Published: Version of record: Issue date: DOI: https://doi.org/10.1177/1933719116653838

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Condition tags

mesh:D004715endometriosis

MeSH descriptors

Endometriosis Animals Cell Proliferation Disease Models, Animal Female Humans Mice Receptors, Tumor Necrosis Factor

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

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