ArticlePurinergic signalling2025
Reprogramming the tumor microenvironment by targeting cytidine deaminase in pancreatic ductal adenocarcinoma tumors: implications for the role of P2Y
Article in Purinergic signalling, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Immunotherapies, such as immune checkpoint inhibitors (ICI), anti-cancer vaccines and adoptive T cell transfer, are promising treatments for cancer patients. However, ICI have not shown therapeutic benefit for most mismatch repair-proficient colorectal and pancreatic ductal adenocarcinoma tumors (PDAC), which are aggressive and deadly (Li et al. in Biomedicines 12:2175, 2024). Tumor metabolism can enhance immunological tolerance, but hinder immune cell function. In a recent publication in Nature Cancer, Scolaro et al. (Scolaro et al. in Nature Cancer 5:1206-1226, 2024) showed that cytidine deaminase (CDA) upregulation may play a crucial role in shaping the immunosuppressive landscape of human PDAC and other tumors. CDA targeting in pancreatic cancer cell lines led to reduced tumor growth, weight and total regression after treatment aimed at the programmed cell death protein 1 receptor (PD-1) immune checkpoint protein. CDA inhibition, both genetically and pharmacologically, overcame immunotherapy resistance in PDAC models. CDA targeting in PDAC cells altered the tumor microenvironment (TME), enabling T cells to respond to anti-PD-1. In mice with sgNT and sgCda tumors receiving anti-PD-1 treatment, they reduced the number of CD8
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