A novel noninvasive model of endometriosis for monitoring the efficacy of antiangiogenic therapy

Christian M. Becker, Becker CM, Wright RD, Renee D. Wright, Ronit Satchi-Fainaro, Ronit Satchi‐Fainaro, Tae Funakoshi, Funakoshi T, Folkman J, Judah Folkman, Andrew L. Kung, D'Amato RJ, Robert J D'Amato, Robert J. D’Amato
The American Journal of Pathology · 2006 · vol. 168(6) , pp. 2074–2084 · doi:10.2353/ajpath.2006.051133 · PMID:16723720 · PMC1606629 · W2036759587
Lab / animal OA: bronze CC0 ⤵ 63 in-corpus citations
📄 Open PDF View on OpenAlex View on PubMed View at publisher
⚙ AI-generated summary by gemini-2.5-flash-lite, 2026-06-07 ⓘ

This paper describes a novel noninvasive model of endometriosis in mice designed to assess the efficacy of antiangiogenic therapies.

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

Abstract

Endometriosis, the presence of ectopic endometrial tissue, is a common disease associated with high morbidity and socioeconomic problems. Angiogenesis, the formation of new blood vessels, plays an important role in the formation and growth of endometriotic lesions. We have created a novel, noninvasive model to monitor the growth of these lesions and the associated angiogenesis in vivo. First, we generated luciferase-expressing transgenic mice by inserting the human ubiquitin C promoter coupled to the firefly luciferase reporter. Injection of luciferin in these mice causes full-body bioluminescence, which can be detected using a low-light CCD camera. Endometrial tissue from these transgenic mice was surgically implanted into nonluminescent recipients. Bioluminescence of lesions was noninvasively imaged after intravenous or intraperitoneal injection of luciferin. Transabdominal luminescence compared well with the location of the transgenic endometriotic lesions, and lesion size correlated with the intensity of luminescence. Systemic treatment with the angiogenesis inhibitors caplostatin and endostatin peptide mP-1 delayed and suppressed the onset and intensity of the luminescent signal. Caplostatin suppressed the growth of endometriotic lesions by 59% compared with controls. This novel, noninvasive model of endometriosis provides a means to study early angiogenesis in vivo and to monitor endometriotic growth and the efficacy of systemic antiangiogenic therapy.

My notes (saved in your browser only)

Condition tags

endometriosis

MeSH descriptors

Endometriosis Neovascularization, Pathologic Neovascularization, Pathologic Angiogenesis Inhibitors Angiogenesis Inhibitors Angiogenesis Inhibitors Animals Animals Cyclohexanes Cyclohexanes Disease Models, Animal Disease Models, Animal Endometriosis Endometriosis Endometriosis Endometrium Endometrium Endometrium Female Female

Citation neighborhood (2-hop)

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. Outer rings show 2-hop neighbours — papers reached through the immediate citers/citees. [ collapse to 1-hop ]

References (81)

Cited by (50)

Source provenance

europepmc
last seen: 2026-10-15T06:08:49.021275+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-10-08T21:03:51.313027+00:00
License: CC0 · commercial use OK