Normalization of Tumor Vasculature: An Emerging Concept in Antiangiogenic Therapy

By Rakesh K. Jain. Science, 2005

5,585 citations recorded by the source corpus.

Subfields: Biotechnology, Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/b1d9abee6ee485df7d730de0b5ec99421b5c4573

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Citations in the corpus

Antiangiogenic agents can increase lymphocyte infiltration into tumor and enhance the effectiveness of adoptive immunotherapy of cancer (2010, neutral): “Although the inhibition of growth of tumor vessels seems to play a role, there is considerable evidence that normalization of the properties of the tumor vasculature can substantially enhance drug penetration into tumors (22, 23).”
VEGF in Signaling and Disease: Beyond Discovery and Development (2019, background): “These effects are expected to reduce tumor interstitial pressure and lead to enhanced uptake of cytotoxic agents and antibodies by the tumor (Jain, 2005; Willett et al., 2004).”
Stem cell-related "self-renewal" signature and high epidermal growth factor receptor expression associated with resistance to concomitant chemoradiotherapy in glioblastoma. (2008, result): “This is in accordance with the concept suggesting that antiangiogenic agents may temporarily lead to “normalization” of aberrant tumor vasculature, resulting in more efficient delivery of drugs and oxygen to the tumor.(39,40) In a recent trial, addition of the antiangiogenic integrininhibitor cileng”
The Enhanced Permeability and Retention (EPR) Effect: The Significance of the Concept and Methods to Enhance Its Application (2021, background): “Since the tumor vascular formation is mainly attributed to the effects of vascular endothelial growth factor (VEGF), the application of VEGF antibodies antagonizes the effect of VEGF and temporarily normalizes tumor vasculature [35].”
Angiogenesis in Cancer (2006, neutral): “…expression of the VEGF family and their receptors in 80 cases of ovarian carcinoma, revealed the presence of VEGF-A, VEGF-C, VEGFR-2, and VEGFR-3 in the cytoplasm of tumor cells, and also of endothelial cells of the blood and lymph vessels in the stroma adjacent to tumor nests (Nishida et al 2004).”
The role of hypoxia in cancer progression, angiogenesis, metastasis, and resistance to therapy (2015, background): “tumor; however, at the same time induce more aggresive and metastatic tumor phenotype.(71,72)”
Causes, consequences, and remedies for growth-induced solid stress in murine and human tumors (2012, background): “Specifically, the decreased vascular permeability would decrease IFP and increase blood flow in previously static blood vessels, thereby increasing drug delivery and treatment efficacy of a number of therapies (1, 21, 22).”
M1 and M2 macrophages derived from THP-1 cells differentially modulate the response of cancer cells to etoposide (2015, background): “[40] showed that when primary macrophages were incubated in direct co-culture with MCF-7 cells, they produced TNF-α that induced MCF-7 cell apoptosis.”