ArticleOncology reports2011
Effects of bevacizumab in mouse model of endometrial cancer: Defining the molecular basis for resistance.
Article in Oncology reports, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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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.
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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.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- Efficacy and Safety of Bevacizumab-Combined Chemotherapy for Advanced and Recurrent Endometrial Cancer: A Systematic Review and Meta-analysis.Balkan medical journal · 2021Pooled it
- Serum HE4 and polymorphisms in MMP9 and MMP13 associated with survival outcome in patients with endometrial carcinoma: a retrospective cohort study and nomogram development.Future science OA · 2026Article
- Global expression analysis of endometrial cancer cells in response to progesterone identifies new therapeutic targets.The Journal of steroid biochemistry and molecular biology · 2023Article
- Paclitaxel anticancer activity is enhanced by the MEK 1/2 inhibitor PD98059 in vitro and by PD98059-loaded nanoparticles in BRAFInternational journal of pharmaceutics · 2021Article
- Advantages of Tyrosine Kinase Anti-Angiogenic Cediranib over Bevacizumab: Cell Cycle Abrogation and Synergy with Chemotherapy.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Mutated p53 portends improvement in outcomes when bevacizumab is combined with chemotherapy in advanced/recurrent endometrial cancer: An NRG Oncology study.Gynecologic oncology · 2021Article
- Re-expression of miR-200c suppresses proliferation, colony formation and in vivo tumor growth of murine claudin-low mammary tumor cells.Oncotarget · 2017Article
- Inhibitory effects of Arhgap6 on cervical carcinoma cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Identification of a multi-cancer gene expression biomarker for cancer clinical outcomes using a network-based algorithm.Scientific reports · 2015Article
- Molecular cues on obesity signals, tumor markers and endometrial cancer.Hormone molecular biology and clinical investigation · 2015Review
- Role of bevacizumab in colorectal cancer growth and its adverse effects: a review.World journal of gastroenterology · 2013Review
- Dichloroacetate reverses the hypoxic adaptation to bevacizumab and enhances its antitumor effects in mouse xenografts.Journal of molecular medicine (Berlin, Germany) · 2013Article
- Systemic administration of bevacizumab prolongs survival in an in vivo model of platinum pre-treated ovarian cancer.Oncology letters · 2012Article
- Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Endometrial cancer is the most frequent gynecologic cancer in women. Long-term outcomes for patients with advanced stage or recurrent disease are poor. Targeted molecular therapy against the vascular endothelial growth factor (VEGF) and its receptors constitute a new therapeutic option for these patients. The goal of our study was to assess the potential effectiveness of inhibition of VEGF/VEGFR signaling in a xenograft model of endometrial cancer using bevacizumab (Avastin, a humanized antibody against VEGFA). We also aimed to identify molecular markers of sensitivity or resistance to this agent. We show that bevacizumab retards tumor growth in athymic mice by inhibiting molecular components of signaling pathways that sustain cell survival and proliferation. We also demonstrate that resistance to bevacizumab may involve up-regulation of anti-apoptotic genes and certain proto-oncogenes. We propose that down-regulation of ARHGAP6 and MMP15 transcripts indicates that tumors are sensitive to bevacizumab whereas inhibition of PKCδ- or S6K-dependent signaling and up-regulation of TNFRS4 or MMP13 and MMP14 mark a developing resistance to bevacizumab therapy. Interestingly, the significant activation of c-Jun oncogene detected in bevacizumab-treated tumors suggests that, in endometrial cancers, the c-Jun-mediated pathway(s) contribute to bevacizumab resistance.
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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.