ArticleCancer biology & therapy2016
Chimeric Mouse model to track the migration of bone marrow derived cells in glioblastoma following anti-angiogenic treatments.
Article in Cancer biology & therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 20 citations in OpenAlex.
- Metastatic promoting role of mesenchymal stem cells in oral squamous cell carcinoma revealed by an improved bone marrow chimeric model.Scientific reports · 2026Article
- Central IRF4/5 Signaling Are Critical for Microglial Activation and Impact on Stroke Outcomes.Translational stroke research · 2024Article
- Engineered exosomes for studies in tumor immunology.Immunological reviews · 2022Review
- Review
- Changes in the tumor microenvironment and outcome for TME-targeting therapy in glioblastoma: A pilot study.PloS one · 2021Article
- CXCR2-Expressing Tumor Cells Drive Vascular Mimicry in Antiangiogenic Therapy-Resistant Glioblastoma.Neoplasia (New York, N.Y.) · 2018Article
- Major Challenges and Potential Microenvironment-Targeted Therapies in Glioblastoma.International journal of molecular sciences · 2017Review
- Optical clearing and fluorescence deep-tissue imaging for 3D quantitative analysis of the brain tumor microenvironment.Angiogenesis · 2017Article
- Canonical NFκB signaling in myeloid cells is required for the glioblastoma growth.Scientific reports · 2017Article
- Vascular mimicry in glioblastoma following anti-angiogenic and anti-20-HETE therapies.Histology and histopathology · 2017Article
- Tibial dyschondroplasia is highly associated with suppression of tibial angiogenesis through regulating the HIF-1α/VEGF/VEGFR signaling pathway in chickens.Scientific reports · 2017Article
- Activation of Myeloid TLR4 Mediates T Lymphocyte Polarization after Traumatic Brain Injury.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Taming immune suppressor: application of myeloid-derived suppressor cells in anti-cancer gene therapy.Translational cancer research · 2017Article
- p53 Mutation: Critical Mediator of Therapy Resistance against Tumor Microenvironment.Biochemistry & physiology · 2016Article
- Cancer Therapeutics Following Newton's Third Law.Biochemistry & physiology · 2016Article
- Anti-VEGFR2 driven nuclear translocation of VEGFR2 and acquired malignant hallmarks are mutation dependent in glioblastoma.Journal of cancer science & therapy · 2016Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Bone marrow derived cells (BMDCs) have been shown to contribute in the tumor development. In vivo animal models to investigate the role of BMDCs in tumor development are poorly explored. We established a novel chimeric mouse model using as low as 5 × 10(6) GFP+ BM cells in athymic nude mice, which resulted in >70% engraftment within 14 d. In addition, chimera was established in NOD-SCID mice, which displayed >70% with in 28 d. Since anti-angiogenic therapies (AAT) were used as an adjuvant against VEGF-VEGFR pathway to normalize blood vessels in glioblastoma (GBM), which resulted into marked hypoxia and recruited BMDCs to the tumor microenvironment (TME). We exploited chimeric mice in athymic nude background to develop orthotopic U251 tumor and tested receptor tyrosine kinase inhibitors and CXCR4 antagonist against GBM. We were able to track GFP+ BMDCs in the tumor brain using highly sensitive multispectral optical imaging instrument. Increased tumor growth associated with the infiltration of GFP+ BMDCs acquiring suppressive myeloid and endothelial phenotypes was seen in TME following treatments. Immunofluorescence study showed GFP+ cells accumulated at the site of VEGF, SDF1 and PDGF expression, and at the periphery of the tumors following treatments. In conclusion, we developed a preclinical chimeric model of GBM and phenotypes of tumor infiltrated BMDCs were investigated in context of AATs. Chimeric mouse model could be used to study detailed cellular and molecular mechanisms of interaction of BMDCs and TME in cancer.
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