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Oncogene-driven immunosuppression via glyco-immune checkpoint modulation in pancreatic ductal adenocarcinoma.

Project description

Glycosylation and immune evasion in pancreatic cancer

Pancreatic ductal adenocarcinoma (PDAC) is known for its resistance to treatment and a highly immunosuppressive tumour microenvironment. Recent evidence underscores the role of sugar moieties on proteins in helping tumours evade immune attack. Cancer cells often change the glyco-codes on their surface proteins and, following recognition by glycan-binding proteins (GBPs) on immune cells, they suppress immune responses. With the support of Marie Skłodowska-Curie Actions programme, the DiscoverableTumor project aims to understand how common PDAC mutations, especially in the KRAS oncogene, influence glycan structures and their interaction with GBPs. The discovery of new oncogene-driven immune evasion mechanisms in PDAC may fuel the development of promising therapeutic strategies for this aggressive disease.

Objective

Pancreatic ductal adenocarcinoma (PDAC) stands out as one of the most aggressive tumors, ranking as the third leading cause of cancer-related death. Glycosylation has emerged as a critical regulatory mechanism contributing to tumor progression and immunosuppression, a hallmark of PDAC tumor microenvironment (TME). Recent studies have shown that tumor immune evasion programs can be facilitated by the activation of immunosuppressive glyco-immune checkpoints (GICs), governed by interactions between cell-surface glycans and glycan-binding proteins (GBPs). While oncogene mutations are known to have immunosuppressive effects and impact protein glycosylation, their effect on GIC modulation remains unexplored. This project aims to investigate how oncogene mutations affect GBP-glycan interactions acting as GICs in PDAC, potentially identifying new therapeutic targets. To identify relevant GICs, I will examine how the most frequent KRAS oncogene mutations in PDAC affect glycosylation and GBP activity, leading to the creation of immunosuppressive functions. Using co-culture experiments with primary pancreatic duct epithelial cells and key TME cellular components, such as cancer-associated fibroblasts, as well as lymphoid and myeloid immune cells, I intend to uncover alterations in the cell surface glycome and changes in GBP binding activity that contribute to immunosuppressive pathways. I will employ unbiased glycan-targeted proximity labeling techniques to uncover novel oncogene-driven GBP-glycan axes and simultaneously analyze the activities of GBPs previously associated with cancer and immune evasion, such as galectins (galectins 1/3/9) and siglecs (particularly Siglecs 7/9/15). The findings will be validated using cellular and organoid models of PDAC to assess candidate GICs as therapeutic targets for this challenging disease.

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HORIZON-TMA-MSCA-PF-EF - HORIZON TMA MSCA Postdoctoral Fellowships - European Fellowships

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Call for proposal

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(opens in new window) HORIZON-MSCA-2024-PF-01

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Coordinator

AGENCIA ESTATAL CONSEJO SUPERIOR DE INVESTIGACIONES CIENTIFICAS
Net EU contribution

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€ 209 914,56
Address
CALLE SERRANO 117
28006 MADRID
Spain

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Comunidad de Madrid Comunidad de Madrid Madrid
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Research Organisations
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