CD40 Agonists Alter Tumor Stroma and Show Efficacy Against Pancreatic Carcinoma in Mice and Humans

By G. Beatty, E. Chiorean, Matthew P. Fishman, B. Saboury, U. Teitelbaum, Weijing Sun, R. Huhn, Wenru Song, Dongguang Li, L. Sharp and 3 more. Science, 2011

1,602 citations recorded by the source corpus.

Subfields: Immunology, Oncology

View Paper: https://www.semanticscholar.org/paper/45800100791bce89c0ce87e33f37d19290d3dd1b

How researchers see this paper

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

In Immunology

1. A. Mantovani
2. A. Sica
3. P. Allavena
4. C. Garlanda
5. F. Balkwill
6. G. Germano
7. M. Pittet
8. S. Jaillon

In Oncology

1. A. Mantovani
2. A. Sica
3. P. Allavena
4. C. Garlanda
5. F. Balkwill
6. G. Germano
7. Hans Clevers
8. A. Klein

Citations in the corpus

• The interaction of anticancer therapies with tumor-associated macrophages (2015, background): “In a mouse model of pancreatic cancer, anti-CD40 was found to modify macrophage phenotype with up-regulation of MHC class II and CD86 (Beatty et al., 2011).”
• Tumor-derived granulocyte-macrophage colony stimulating factor regulates myeloid inflammation and T cell immunity in pancreatic cancer (2012, background): “More likely in PDA, tumor-associated macrophages release IL-6 that directly affects the epithelium and promotes PanIN progression and PDA development in vivo (Beatty et al., 2011; Lesina et al., 2011).”
• Tumor associated macrophages and neutrophils in cancer. (2013, background): “Accordngly, several therapeutic strategies were proposed to inhibit their ecruitment, interfere with their survival, or reprogram them into M1 anti-tumoral phenotype (Beatty et al. 2011; Edwards and mens 2010; Germano et al. 2013; Rozel et al. 2009; Xin et al. 2009).”
• Progress in tumor-associated macrophage (TAM)-targeted therapeutics (2017, neutral): “However, in a KPC mouse model of pancreatic ductal adenocarcinoma (PDA), depletion experiments of different immune cell populations revealed that the anti-tumor effect of the antibody could be mediated in a T cell-independent manner, requiring only the tumor infiltration of macrophages [117].”
• Macrophage plasticity and polarization: in vivo veritas. (2012, positive): “In a model of pancreatic ductal adenocarcinoma, CD40 agonist antibodies promoted a remarkable antitumor effect and induced high expression of M1 markers (MHC class II and CD86) in macrophages (132).”
• Tumor-Associated Macrophages and Neutrophils in Tumor Microenvironment (2016, background): “CD40 agonist antibody [93] and TLR9 agonist (CpG-oligodeoxynucleotide) [94] have been shown to be effective in repolarizing M2-like protumoral macrophages.”
• Differential Macrophage Programming in the Tumor Microenvironment (2012, neutral): “The pathways that engage and mediate the maladaptive response of TAMs present attractive therapeutic targets, several of which have already shown promise in the preclinical arena, and to improve therapeutic responses to chemotherapy [37, 50, 120].”
• Role of macrophage targeting in the antitumor activity of trabectedin. (2013, background): “Strategies to exploit TAM as therapeutic target include re-education (Beatty et al., 2011; Duluc et al., 2009; Guiducci et al., 2005; Rolny et al., 2011), deletion by killing or blocking of recruitment (DeNardo et al., 2011; Qian et al., 2011; van Rooijen and van Kesteren-Hendrikx, 2003; Zhang et…”
• Epithelial-mesenchymal transition spectrum quantification and its efficacy in deciphering survival and drug responses of cancer patients (2014, neutral): “Although pancreatic carcinoma comprises a large fraction of stromal cells (Beatty et al , 2011), pancreatic carcinoma cell lines exhibit the same EMT spectrum as colon cells (Fig 3), supporting the notion that the EMT score still arises from the contributions of the pancreatic carcinoma cells not…”