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Targeting Galectin-1 in pancreatic cancer: immune surveillance on guard

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Article: e952201 | Received 04 Jun 2014, Accepted 05 Jun 2014, Published online: 29 Oct 2014

Figures & data

Figure 1. Role of Gal1 in stroma remodeling and immune escape in pancreatic cancer: implications in anti-Gal1 blockade therapy. Galectin-1 (Gal1) is highly expressed in the stroma of pancreatic tumors (see immunohistochemistry on the left). Gal1 promotes angiogenesis and is involved in pancreatic stellate cell activation and proliferation. Thus, Gal1 functionally contributes to the intense stromal reaction commonly occurring in pancreatic tumors (right, upper panel). Moreover, Gal1 impairs neutrophil recruitment and induces T-cell apoptosis, and favors a T helper type 2 (Th2) anti-inflammatory environment, thus resulting in tumor immune evasion (right, upper panel). Blocking Gal1 in pancreatic tumors hampers tumor progression by reducing angiogenesis, stromal activation and restoring immunosurveillance, leading to reduced tumor growth (right, lower panel).

Figure 1. Role of Gal1 in stroma remodeling and immune escape in pancreatic cancer: implications in anti-Gal1 blockade therapy. Galectin-1 (Gal1) is highly expressed in the stroma of pancreatic tumors (see immunohistochemistry on the left). Gal1 promotes angiogenesis and is involved in pancreatic stellate cell activation and proliferation. Thus, Gal1 functionally contributes to the intense stromal reaction commonly occurring in pancreatic tumors (right, upper panel). Moreover, Gal1 impairs neutrophil recruitment and induces T-cell apoptosis, and favors a T helper type 2 (Th2) anti-inflammatory environment, thus resulting in tumor immune evasion (right, upper panel). Blocking Gal1 in pancreatic tumors hampers tumor progression by reducing angiogenesis, stromal activation and restoring immunosurveillance, leading to reduced tumor growth (right, lower panel).

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