Dynamics of the immune reaction to pancreatic cancer from inception to invasion.

By Carolyn E. Clark, S. Hingorani, R. Mick, C. Combs, D. Tuveson, R. Vonderheide. Cancer Research, 2007

938 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/f5883891039552884cc5b7e8fe5e979381d9418f

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Citations in the corpus

Tumor-derived granulocyte-macrophage colony stimulating factor regulates myeloid inflammation and T cell immunity in pancreatic cancer (2012, background): “…in patients with the same disease—the role of these cells remains controversial particularly with regard to the in vivo relevance of the T cell suppressive qualities that are typically demonstrated in vitro (Andreu et al., 2010; Clark et al., 2007; Melani et al., 2003; Stairs et al., 2011).”
Oncogenic Kras-induced GM-CSF production promotes the development of pancreatic neoplasia (2012, background): “…and CD4+Foxp3+CD25+ regulatory T cells (Tregs), compared with normal pancreas and spleen (Figure 1D and Figures S1C and S1D) and in agreement with the reported increase in the abun- dance of these putative immunosuppressive cell populations during early pancreatic neoplasia (Clark et al., 2007).”
The Pancreas Cancer Microenvironment (2012, background): “A comprehensive analysis of the immune cell composition of PanIN and PDA in the LSL-Kras;Pdx1-Cre mice defined an important baseline for future studies (97).”
Phase 2 Trial of Single Agent Ipilimumab (Anti-CTLA-4) for Locally Advanced or Metastatic Pancreatic Adenocarcinoma (2010, background): “In this model, immunosuppressive cell types dominate early infiltrates and persist in invasive lesions.(22) In humans, a lymphocytic infiltrate predominates in the microenvironment of pancreatic adenocarcinoma, and T regulatory lymphocytes, which exert an immunosuppressive response to antigenic stim”
CXCR2 Inhibition Profoundly Suppresses Metastases and Augments Immunotherapy in Pancreatic Ductal Adenocarcinoma (2016, neutral): “Initially PDAC must overcome immune surveillance; indeed, both human and mouse pancreatic intraepithelial neoplasia (PanINs) and PDACare characterized by the infiltration of immune suppressor cells, suggesting tumor immunity is blocked early during tumorigenesis (Clark et al., 2007).”
Differential Macrophage Programming in the Tumor Microenvironment (2012, neutral): “It is important to note that the composition of the immune microenvironment [68, 90, 91] and the overall polarization state of TAMs becomes more favorable towards growth during tumor progression [92].”
RAS oncogenes: weaving a tumorigenic web (2011, background): “One possible mechanism by which oncogenic RAS expression may lead to a compromised antitumour immune response is through the recruitment of immunosuppressive regulatory T cells (T Regs ) and myeloid-derived suppressor cells (MDSCs) to the tumour sit”
Tumor-Derived Lactate Modifies Antitumor Immune Response: Effect on Myeloid-Derived Suppressor Cells and NK Cells (2013, background): “MDSCs also suppress immune effector function by generation of Tregs (11).”
Coordinated regulation of myeloid cells by tumours (2012, background): “Mice with autochthonous pancreatic cancer undergo progressive waves of myeloid cell recruitment after the initiation of the transforming programme driven by the Kras oncogen”
Stat3/Socs3 activation by IL-6 transsignaling promotes progression of pancreatic intraepithelial neoplasia and development of pancreatic cancer. (2011, result): “Thereby, our data extend previous findings implicating immune cells to include myeloid-derived suppressor cells, tumor-associated macrophages, and Treg in PDAC development (Clark et al., 2007).”
The Pancreatic Cancer Microbiome Promotes Oncogenesis by Induction of Innate and Adaptive Immune Suppression (2018, neutral): “PDA is invariably preceded by and associated with a robust inflammatory cell infiltrate that has profound influences on disease progression (18).”
Depletion of Carcinoma-Associated Fibroblasts and Fibrosis Induces Immunosuppression and Accelerates Pancreas Cancer with Diminished Survival (2014, neutral): “In summary, our study, together with other ongoing efforts to elucidate pancreatic tumor immunity and immunotherapy (Bayne et al., 2012; Clark et al., 2007; Hiraoka et al., 2006; Roberts et al., 2013; Vonderheide et al., 2013), will likely offer insights into potential efficacy of combination…”
Tumor‐associated macrophages (TAM) as major players of the cancer‐related inflammation (2009, neutral): “gressively [18].”
EMT and dissemination precede pancreatic tumor formation (2012, background): “The emergence of PanIN lesions is associated with the appearance of an inflammatory stroma characterized by activated fibroblasts andmyeloid-derived cells (Aguirre et al., 2003; Clark et al., 2007).”