Effect of imatinib on growth of experimental endometriosis in rats
Imatinib, along with anastrozole, suppressed experimental endometriosis growth in rats by reducing endometriotic tissue and ovarian follicles, likely through inhibition of angiogenesis and cell proliferation.
One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works
Abstract
My notes (saved in your browser only)
Condition tags
MeSH descriptors
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.
References (40)
- A Novel Angiogenesis Inhibitor Bevacizumab Induces Apoptosis in the Rat Endometriosis Model via crossref
- An update on the pharmacological management of endometriosis via crossref
- A potential role for colony-stimulating factor 1 in the genesis of the early endometriotic lesion via crossref
- BAY 1002670: a novel, highly potent and selective progesterone receptor modulator for gynaecological therapies via crossref
- Could statins constitute a novel treatment for endometriosis? Systematic review of the literature via crossref
- Danazol treatment of endometriosis-associated pain via crossref
- Dienogest is a selective progesterone receptor agonist in transactivation analysis with potent oral endometrial activity due to its efficient pharmacokinetic profile via crossref
- Effect of Vascular Endothelial Growth Factor Inhibition on Endometrial Implant Development in a Murine Model of Endometriosis via crossref
- Effects of aromatase inhibitors on proliferation and apoptosis in eutopic endometrial cell cultures from patients with endometriosis via crossref
- Effects of Pazopanib, Sunitinib, and Sorafenib, Anti-VEGF Agents, on the Growth of Experimental Endometriosis in Rats via crossref
- Endometriosis and Subfertility: Is the Relationship Resolved? via crossref
- Endometriosis: cost estimates and methodological perspective via crossref
- ENMD-1068, a protease-activated receptor 2 antagonist, inhibits the development of endometriosis in a mouse model via crossref
- Gonadotropin-releasing hormone agonist induces apoptosis and reduces cell proliferation in eutopic endometrial cultures from women with endometriosis via crossref
- Kisspeptin antagonists via crossref
- Novel agents for the medical treatment of endometriosis via crossref
- Progestogens for endometriosis: forward to the past via crossref
- Recent patents on new steroid agents targeting the steroidogenesis for endocrine cancer treatments via crossref
- Regression of endometrial explants in a rat model of endometriosis treated with the immune modulators loxoribine and levamisole via crossref
- Sorafenib inhibits growth, migration, and angiogenic potential of ectopic endometrial mesenchymal stem cells derived from patients with endometriosis via crossref
- Studies on the surgical induction of endometriosis in the rat via crossref
- The effect of dinitrosyl iron complexes with glutathione and S-nitrosoglutathione on the development of experimental endometriosis in rats: A comparative studies via crossref
- The Efficacy of Bevacizumab, Sorafenib, and Retinoic Acid on Rat Endometriosis Model via crossref
- Vascular endothelial growth factor (VEGF) in endometriosis via crossref
- doi:10.1530/rep.1.00978 via crossref
- doi:10.1016/j.leukres.2011.09.025 via crossref
- doi:10.1016/j.fertnstert.2005.07.1296 via crossref
- doi:10.1530/rep.1.00868 via crossref
- doi:10.1016/j.leukres.2011.11.003 via crossref
- doi:10.1111/j.1365-2605.2007.00755.x via crossref
- doi:10.1016/j.reprotox.2008.03.004 via crossref
- doi:10.1210/en.2008-0349 via crossref
- doi:10.1056/nejm200411113512024 via crossref
- doi:10.1056/nejmc0707841 via crossref
- doi:10.1038/nm.2033 via crossref
- doi:10.1200/jco.2014.59.7344 via crossref
- doi:10.2174/1872213x113079990021 via crossref
- doi:10.1086/677359 via crossref
- doi:10.1016/j.tips.2015.04.005 via crossref
- doi:10.1095/biolreprod.106.051516 via crossref
SciLite annotations
chemicals 9
organisms 4
Source provenance
- crossref
- last seen: 2026-06-20T06:34:59.460456+00:00
- europepmc
- last seen: 2026-09-17T06:16:55.786923+00:00
- pubmed
- last seen: 2026-05-13T22:21:19.813018+00:00
- scilite
- last seen: 2026-05-18T04:26:01.642840+00:00
- unpaywall
- last seen: 2026-09-17T06:32:46.214484+00:00
Courtesy of the U.S. National Library of Medicine