We conclude that LGALS1 possesses significant prognostic value for predicting ICI response in HNSCC. LGALS1 may represent a multimodal therapeutic target to sensitize tumors to immunotherapy, as its blockade simultaneously modulates tumor cells, myeloid cells, and CD8 T cells to overcome multi-layered resistance and promote robust anti-tumor immunity.

The mRNA expression levels of the transcription factors T-bet (TBX21), RORC2, and Foxp3 were analyzed in peripheral blood mononuclear cells (PBMCs) from colorectal cancer patients and healthy donors following co-culture with COLO 201 cells in the presence of galectin-1 inhibitor OTX 008, galectin-3 inhibitor GB1107, or both...Conversely, in healthy donor cells, galectin-3 blockade suppressed RORC2 and induced FOXP3 expression. Notably, the most pronounced downregulation of FOXP3 was achieved by simultaneously inhibiting both galectins.

Although in vitro lymphocyte proliferation was not observed, CD3+ cells increased in the metastatic lungs. These results suggest GGH and GGHS as immunostimulatory agents, with GGH as potential melanoma adjuvant therapy.

Approaches such as OTX008, anti-Gal1 monoclonal antibodies, and Gal1-targeted vaccines have demonstrated the ability to downregulate tumour progression by inhibiting Gal1 activity. These findings highlight the therapeutic promise of Gal1 not only as a novel target for cancer therapy but also as a potential prognostic biomarker, offering opportunities for the development of more effective and less toxic treatment strategies.

Treatment with OTX008, an LGALS1 inhibitor, markedly diminished the viability of primary malignant bone marrow cells from AML patients. Notably, LGALS1 expression was significantly reduced exclusively in AML-M5 patients after treatment, which may be due to its higher expression in AML-M5 subtype compared to other FAB subtypes. In summary, our findings indicate that LGALS1 could serve as an independent prognostic risk factor and a promising therapeutic target in AML, providing novel insights into AML pathogenesis and laying the foundation for the development of new therapeutic strategies.

Tci-gal-1 modulates apoptosis, degranulation, and production of cytokines by activated RBL-2H3 cells without detectable influence on gene transcription. This parasite protein is crucial for modulation of the protective immune response and the inhibition of chronic inflammation driven by mast cell activity.

Quantification of hemagglutination was shown to be optimal using U-bottom plates imaged and analysed with FIJI ImageJ rather than flat-bottom plates read for absorbance on an optical density plate reader. Galectin-3-induced red blood cell agglutination efficacy increased significantly from blood group O to A to B. However, for both the galectin-1 monomer and concatemer, a more comparable effect was observed between blood group B and O, but with more potent effects than in blood group A. Inhibition assays for both galectin-3 and galectin-1 induced-hemagglutination were able to demonstrate clear concentration responses and expected selectivity profiles for a set of small-molecule glycomimetics, confirming the historical profiles obtained in biochemical binding and functional cellular assays.

P2, N=0, Withdrawn, Providence Health & Services | N=92 --> 0 | Suspended --> Withdrawn

P1, N=36, Completed, Providence Health & Services | Active, not recruiting --> Completed | N=22 --> 36 | Trial completion date: May 2025 --> Oct 2022