Targeting the ANG2/TIE2 axis inhibits tumor growth and metastasis by impairing angiogenesis and disabling rebounds of proangiogenic myeloid cells.
By R. Mazzieri, F. Pucci, David Moi, E. Zonari, Anna Ranghetti, A. Berti, L. Politi, B. Gentner, Jeffrey L. Brown, L. Naldini and 1 more. Cancer Cell, 2011
633 citations recorded by the source corpus.
Subfields: Cardiology and Cardiovascular Medicine, Immunology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/b72e07a9f6b5ac7c838d45a137d440dd3c5d1aab
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Immunology
- A. Mantovani
- Lisa M. Coussens
- P. Allavena
- R. Weinberg
- B. Ruffell
- Zena Werb
- D. Gabrilovich
- G. Germano
In Molecular Biology
- Zena Werb
- Lisa M. Coussens
- R. Weinberg
- P. Allavena
- Hugo Gonzalez
- M. C. Simon
- A. Mantovani
- Bryan L. Krock
Citations in the corpus
- Tumor Metastasis: Molecular Insights and Evolving Paradigms (2011, background): “Conversely, Angpt2 appears to facilitate the metastatic colonization of mammary and pancreatic carcinomas by promoting the capacity of infiltrating myeloid cells to support the vascularization of metastatic nodules (Mazzieri et al., 2011).”
- The interaction of anticancer therapies with tumor-associated macrophages (2015, background): “In mouse tumor models and in cancer patients, refractoriness to antiangiogenic therapies is associated with higher numbers of CD11b+ cells or TEMs infiltrating tumor tissues (Mazzieri et al., 2011; Lu-Emerson et al., 2013; Gabrusiewicz et al., 2014).”
- Accessories to the crime: functions of cells recruited to the tumor microenvironment. (2012, neutral): “In regard to targeting tumor-promoting IICs, there are both encouraging examples (Denardo et al., 2011; Giraudo et al., 2004; Mazzieri et al., 2011; Pietras et al., 2008; Shree et al., 2011), and sobering cases of adaptive resistance, including substitution of a targeted subtype by another with…”
- Progress in tumor-associated macrophage (TAM)-targeted therapeutics (2017, neutral): “demonstrated that therapeutic blockade of ANG2 with an anti-ANG2 antibody reduced angiogenesis and tumor growth in mammary and pancreatic tumor models by preventing association between TEMs and angiogenic blood vessels as well as suppressing expression of TIE2 in TEMs [121].”
- The nature of myeloid-derived suppressor cells in the tumor microenvironment (2016, background): “A distinct subset of monocytes, angiopoietin receptor Tie-2 monocytes, was shown to migrate to the tumor and differentiate into TAM in mammary carcinoma [74,75].”
- Differential Macrophage Programming in the Tumor Microenvironment (2012, positive): “, MMTV-PyMT mice [49], a property that has thus far not been observed in tumors following blockade of TAM infiltration [50], or by myeloidspecific Vegfa ablation [37], thus hinting at a unique mode of action either downstream or parallel to VEGFA bioactivity [48].”
- Role of macrophage targeting in the antitumor activity of trabectedin. (2013, background): “…therapeutic settings. ancer Cell 23, 249–262, February 11, 2013 ª2013 Elsevier Inc. 249 Several mouse and human studies have shown that high TAM density is mostly associated with poor patient prognosis and resistance to therapies (DeNardo et al., 2011; Mazzieri et al., 2011; Steidl et al., 2010).”
- Basic and therapeutic aspects of angiogenesis. (2011, neutral): “Expression of ANG2 by tumor ECs activates TEMs to stimulate angiogenesis (Mazzieri et al., 2011).”
- Tumor-associated macrophages: from basic research to clinical application (2017, background): “Tie2 TAMs are closely associated with tumor vasculature and have been found crucial for angiogenesis in orthotopic and transgenic tumor models [46], which depend on endothelial cellproduced angiopoietin-2 (ANG2) and Tie2 receptors on TAMs along the vasculature (Fig.”
- Angiopoietins in angiogenesis. (2013, background): “genesis and metastasis in mouse models of spontaneous carcinogenesis, including metastatic breast cancer [115].”