ArticleBMC cancer2025
The Tie2 antagonist rebastinib reduces ovarian cancer growth in a syngeneic murine model.
Article in BMC cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
backgroundThe receptor tyrosine kinase TIE2 and its ligands, angiopoietins (ANGPTs), promote angiogenesis. In addition to expression on vascular endothelial cells, TIE2 is expressed on M2-like pro-tumorigenic macrophages. Thus, the TIE2 inhibitor rebastinib was developed as a potential therapy to address multiple cancers. The objective of this study was to determine the effects of rebastinib alone and combined with chemotherapy in a syngeneic murine model of ovarian cancer.
methodsFemale C57Bl6J mice were intraperitoneally injected with syngeneic ID8 ovarian cancer cells. Once tumors were established, mice were untreated (control) or treated with rebastinib, carboplatin plus paclitaxel (chemotherapy), or rebastinib plus chemotherapy. In one set of experiments, survival was followed for 140 days. In other experiments, ascites was harvested 24 h after the last treatment and analyzed by flow cytometry. In in vitro experiments, RNA sequencing was performed on ID8 cells and murine peritoneal macrophage cells (PMJ2R) after treatment with rebastinib, chemotherapy, or rebastinib plus chemotherapy.
resultsTumor-bearing mice treated with rebastinib plus chemotherapy had longer median survival than mice treated with chemotherapy (132.5 vs. 127 days, P < 0.01). Ascites from mice treated with rebastinib had more CD45 + macrophages (P < 0.03) and cytotoxic T cells (P < 0.0001) than ascites from mice treated with chemotherapy. Rebastinib had no significant effect on the numbers of regulatory T cells, Tie2 + macrophages, or Tie2 + M2 macrophages. In ID8 cells, in vitro, rebastinib treatment upregulated 1528 genes and downregulated 3115 genes. In macrophages, in vitro, rebastinib treatment upregulated 2302 genes and downregulated 2970 genes. Rebastinib differentially regulated ANGPT-like proteins in both types of cells, including several ANGPT-like genes involved in tumorigenesis, angiogenesis, and proliferation. ANGPTL1, an anti-angiogenic and anti-apoptotic gene, was increased tenfold in ID8 cells treated with rebastinib (P < 0.001) but was not altered in macrophages.
conclusionsRebastinib plus chemotherapy extends survival in a syngeneic murine model of ovarian cancer. Rebastinib alters proportions of immune cell subsets, increases cytotoxic T cells in ascites, and alters gene expression in tumor cells and macrophages.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.