ArticleBreast cancer research : BCR2026
Vascular abnormalization confers tumor resistance to antiangiogenic therapy via downregulating angiostatic factors.
Article in Breast cancer research : BCR, 2026. 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
11 authors.
Funding
Abstract
backgroundAngiogenesis is a hallmark of cancer. However, the efficacy of antiangiogenic therapy is hindered by drug resistance. The underlying mechanisms are complex and multifactorial, and the practical strategies to overcome resistance remain limited.
methodsBy establishing single cell clones (SCCs) from EO771 breast tumor cell line, we classified SCCs as resistant and sensitive to Anlotinib, a new antiangiogenic agent. Resistant and sensitive SCCs were then mixed in different ways to uncover novel mechanisms of antiangiogenic resistance by integrating orthotopic tumor models, RNA sequencing (RNA-seq), immunohistochemistry, blocking antibodies, and recombinant proteins.
resultsIncreasing the diversity and quantity of sensitive SCCs overcame the influences of resistant SCCs and improved Anlotinib efficacy. Sensitive SCC tumors exhibited a more normalized vasculature and increased intratumoral CD8+ T cells compared to resistant SCC tumors. Moreover, elevated vessel perfusion was significantly correlated with better Anlotinib efficacy. RNA-seq data revealed upregulation of dual-function genes (e.g., Ifng, Cxcl9, and Vcam1) linking angiostasis and immune activation. Strikingly, the addition of an angiostatic factor (e.g., recombinant murine IFN-γ or Endostar) converted resistant breast tumors to sensitive to Anlotinib treatment and induced vascular normalization, whereas neutralizing IFNγ, a key angiostatic factor in sensitive SCC tumors, impeded their responses to Anlotinib.
conclusionsThe downregulation of angiostatic factors promotes breast tumor vascular abnormalization and resistance to antiangiogenic therapy. Therefore, integrating angiostatic factors with pro-angiogenic blockers may overcome resistance, offering a translatable approach to improve antiangiogenic outcomes in breast cancer.
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.