Tumor refractoriness to anti-VEGF treatment is mediated by CD11b+Gr1+ myeloid cells

By F. Shojaei, Xiumin Wu, A. K. Malik, Cuiling Zhong, M. Baldwin, S. Schanz, G. Fuh, H. Gerber, N. Ferrara. Nature Biotechnology, 2007

887 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/bfef9fbbfaca4e0da183789fcf92a304747cbc18

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. A. Mantovani
2. A. Sica
3. P. Allavena
4. Xiumin Wu
5. Cuiling Zhong
6. L. Matrisian
7. A. Richmond
8. N. Vasudev

In Oncology

1. A. Mantovani
2. A. Sica
3. P. Allavena
4. C. Garlanda
5. F. Colotta
6. A. Richmond
7. C. Lewis
8. D. Hanahan

Citations in the corpus

• Accessories to the crime: functions of cells recruited to the tumor microenvironment. (2012, neutral): “…blockage (Casanovas et al., 2005), in others recruitment of additional or different subtypes of proangiogenic IICs or CAFs (Priceman et al., 2010; Shojaei et al., 2007), and in others shifting to heightened dependence on invasion and metastasis to co-opt normal tissue vasculature instead of…”
• Immunity, Inflammation, and Cancer (2010, neutral): “The recruitment of Gr1+ myeloid cells (presumably MDSC and TAM precursors) into tumors, curtails the effects of anti-VEGF therapy, presumably bypassing the requirement for local VEGF production by cancer cells for recruitment of TAM precursors (Shojaei et al., 2007).”
• Abrogation of TGF beta signaling in mammary carcinomas recruits Gr-1+CD11b+ myeloid cells that promote metastasis. (2008, background): “Gr-1+CD11b+ cells have also been implicated in tumor refractoriness to anti-VEGF treatment (Shojaei et al., 2007).”
• Overexpression of interleukin-1beta induces gastric inflammation and cancer and mobilizes myeloid-derived suppressor cells in mice. (2008, background): “MDSCs have been implicated in tumor refractoriness to anti-VEGF treatment and likely contribute to TGF-a-mediated metastasis (Shojaei et al., 2007a; Yang et al., 2008).”
• Myeloid derived suppressor cells (2013, background): “Further evidence for the importance of MMP-9 stems from studies investigating the reason for the failure of VEGF-inhibitors to suppress tumor growth, which found that anti-VEGF refractoriness was completely dependent on the tumor’s capacity for CD11b+Gr1+ MDSC recruitment.(53) Furthermore, when MDSC”