High Intratumoral Expression Of Galectin-1 Correlates With Superior Outcome In Hiv-Associated Dlbcl

Introduction. HIV infected individuals have an increased risk of developing lymphoma even in the era of combined antiretroviral therapy. Galectin-1 (Gal-1) is known to promote various immunomodulatory functions, including Treg expansion (Dalotto-Moreno et al, Cancer Res 2013), promotion of tolerogenic dendritic cells (Ilarregui et al, Nat Immunol 2009) and apoptosis of fully-differentiated effector T-cells (Toscano et al, Nat Immunol 2007). In the context of cancer, Gal-1 is expressed on both tumor cells and cells in the tumor microenvironment, and is usually associated with immune privilege, tumor escape and hypoxia-driven angiogenesis (Juszczynski et al, Proc Natl Acad Sci 2007; Cedeno-Laurent et al, Blood 2012). Previously, high intratumoral Gal-1 levels have been suggested as an unfavorable outcome predictor in patients with classical Hodgkin lymphoma (cHL) (Kamper et al, Blood 2011). Furthermore, several in vitro studies revealed the benefit of Gal-1 inhibition with regards to overcoming treatment resistance e.g., after anti-VEGF and anti-CD20 therapy (Croci et al, Cell 2014; Lykken et al, Blood 2016). Thus, Gal-1 inhibition may prospectively be an important tool in lymphoma treatment. In this study, we have investigated the Gal-1 expression in pre-therapeutic tumoral tissue samples from patients with HIV-associated lymphoma and its correlation to clinicopathological features at lymphoma diagnosis.