Benefits of targeting both pericytes and endothelial cells in the tumor vasculature with kinase inhibitors.

By G. Bergers, Steven Song, Nicole Meyer-Morse, E. Bergsland, D. Hanahan. Journal of Clinical Investigation, 2003

1,419 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology, Neurology

View Paper: https://www.semanticscholar.org/paper/fd08f26631a4adbe96df386b67b8d37f7905e9c8

How researchers see this paper

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

In Cancer Research

1. N. Ferrara
2. Rakesh K. Jain
3. J. Joyce
4. D. Hanahan
5. Peter Carmeliet
6. A. Adamis
7. R. Kerbel
8. G. Bergers

In Molecular Biology

1. N. Ferrara
2. Rakesh K. Jain
3. J. Joyce
4. D. Hanahan
5. Peter Carmeliet
6. A. Adamis
7. R. Kerbel
8. G. Bergers

In Neurology

1. D. Hanahan
2. N. Ferrara
3. J. Joyce
4. G. Bergers
5. R. DePinho
6. N. Sharpless
7. Rakesh K. Jain
8. Helmut Kettenmann

Citations in the corpus

• Ten years of anti-vascular endothelial growth factor therapy (2016, background): “…(PNET) — highly vascularized malignancies that develop in pancreatic endocrine cells — could potentially benefit from anti-angiogenic therapy 118 Monotherapy with the VEGFR RTKI pazopanib has proved efficacious in locally advanced or metastatic renal cell carcinoma 120 (TABLE 1) , and it…”
• PDGF-C mediates the angiogenic and tumorigenic properties of fibroblasts associated with tumors refractory to anti-VEGF treatment. (2009, background): “Previous studies suggested that a combination of VEGF antagonists with PDGFR inhibitors, such as imatinib, might be a particularly effective anticancer strategy (Bergers et al., 2003; Erber et al., 2004; Jo et al., 2006).”
• Angiogenesis in life, disease and medicine (2005, background): “Combined administration of RTKIs, targeting VEGFRs and PDGFRβ, increases the anti-angiogenic effect, even in the often-intractable late stage of solid tumour”
• Combined inhibition of VEGF‐ and PDGF‐signaling enforces tumor vessel regression by interfering with pericyte‐mediated endothelial cell survival mechanisms (2004, background): “The findings of our study are in agreement with a previous report on the beneficial effects of targeting endothelial cells and pericytes using SU6668 and SU5416 (37).”
• Antiangiogenic therapy elicits malignant progression of tumors to increased local invasion and distant metastasis. (2009, background): “), which effectively inhibits both VEGFR and PDGFR signaling, a combination that we previously demonstrated to have potent efficacy and added benefit over singular inhibition of VEGFR, by targeting both endothelial cells and their supporting pericytes (Bergers et al., 2003; Pietras and Hanahan, 2005”
• Gene Expression Signature of Fibroblast Serum Response Predicts Human Cancer Progression: Similarities between Tumors and Wounds (2004, background): “), and platelet-derived growth factor is one of the principal molecular signals and mitogenic factors in serum. Platelet-derived growth factor receptor and cyclooxygenase 2 are inhibited by imatinib mesylate and nonsteroidal anti-inflammatory agents, respectively—two drugs with established efficacy ”
• Angiogenesis as a therapeutic target (2005, background): “Withdrawal of VEGF-A leads to endothelial apoptosis and vascular regressio”
• Drug resistance by evasion of antiangiogenic targeting of VEGF signaling in late-stage pancreatic islet tumors. (2005, methodology): “…growth in an endogenous mouse model of islet cell carcinogenesis, where the functional importance of VEGF signaling has been previously documented, via gene knockout of VEGF-A (Inoue et al., 2002) and pharmacological inhibition of VEGF receptors with small molecules (Bergers et al., 2000, 2003).”
• Cellular abnormalities of blood vessels as targets in cancer. (2005, background): “However, inhibitors of VEGF signaling not only stop angiogenesis but also cause regression of some tumor vessels and may reduce tumor size [42,43,44 ,45 ].”
• Pericytes: developmental, physiological, and pathological perspectives, problems, and promises. (2011, background): “Probably, the majority of the mural cells in the head region, including all parts of the CNS, are neural crest derived, as demonstrated in chick-quail chimeras (Bergwerff et al., 1998; Etchevers et al., 2001; Korn et al., 2002) and indicated by marker expression in mice (Heglind et al.”