ArticleCancer gene therapy2013
Combining virotherapy and angiotherapy for the treatment of breast cancer.
Article in Cancer gene therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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
16 citing papers in PubMed, 34 citations in OpenAlex.
- Angiogenic cytokines and their influence on circulating tumour cells in sera of patients with the primary diagnosis of breast cancer before treatment.BMC cancer · 2016Trial
- Development and preclinical evaluation of a decoy DLL4-encoding oncolytic HSV-1 for high-grade glioma.Oncogene · 2026Article
- Vascular Endothelial Growth Factor/Angiopoietin-2 Bispecific Antibody-Induced Vascular Normalization: From Basic Mechanisms to Therapeutic Applications in Breast Cancer.Immunity, inflammation and disease · 2026Review
- Review
- The role of viruses in cancer development versus cancer therapy: An oncological perspective.Cancer medicine · 2023Review
- Article
- VCN-01 disrupts pancreatic cancer stroma and exerts antitumor effects.Journal for immunotherapy of cancer · 2021Article
- High-background parenchymal enhancement in the contralateral breast is an imaging biomarker for favorable prognosis in patients with triple-negative breast cancer treated with chemotherapy.American journal of translational research · 2021Article
- Strategies to Develop Potent Oncolytic Viruses and Enhance Their Therapeutic Efficacy.JCO precision oncology · 2021Review
- Oncolytic virus immunotherapies in ovarian cancer: moving beyond adenoviruses.Porto biomedical journal · 2018Article
- Recent advances in oncolytic adenovirus therapies for cancer.Current opinion in virology · 2016Review
- Polymeric Cups for Cavitation-mediated Delivery of Oncolytic Vaccinia Virus.Molecular therapy : the journal of the American Society of Gene Therapy · 2016Article
- From Benchtop to Bedside: A Review of Oncolytic Virotherapy.Biomedicines · 2016Review
- Role of Recombinant DNA Technology to Improve Life.International journal of genomics · 2016Review
- Promising oncolytic agents for metastatic breast cancer treatment.Oncolytic virotherapy · 2015Review
- The tumor-associated marker, PVRL4 (nectin-4), is the epithelial receptor for morbilliviruses.Viruses · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
A breast cancer-selective oncolytic adenovirus was engineered to express antagonists of vascular endothelial growth factor (VEGF) and Notch signaling to combine direct anticancer activity with disruption of tumor-associated angiogenesis. Replication of the parental virus, AdEHE2F, is stimulated by estrogen receptor (ER), E2F1 and hypoxia, and it mediates selective lysis of breast cancer cells in vitro and in vivo. Here, we encoded soluble Flt-1 (sFlt1) and soluble Dll4 (sDll4) under control of the E3 promoter. sFlt1 (the extra-cellular domain of VEGF receptor 1) binds VEGF-A and inhibits stimulation of VEGFR2, decreasing angiogenic stimulus. Conversely, sDll4 (the extracellular domain of Delta-like 4) antagonizes Notch signaling to prevent endothelial maturation. We hypothesized that these agents might show additive or synergistic activity. In vitro, sFlt1 inhibited endothelial cell proliferation and sprouting, whereas sDll4 increased the number of vascular branchpoints. In ER-positive ZR75.1 tumors in vivo AdEHE2F showed the potent direct virotherapy with no augmentation owing to sFlt1 or sDll4; however, in ER-negative MDA-231 tumors efficacy was enhanced by encoding sFlt1 or sDll4, with survival time extending to double that of controls. There was also a dramatic decrease in the total number of tumour blood vessels, as well as the number of perfused vessels, suggesting that improved efficacy reflects combined anti-tumour and anti-vascular effects.
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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.