胰管腺癌患者（PDAC）的分子分层具有指导治疗干预的临床决策的潜力。研究PDAC的不同分子亚型形成和发展机制将提高患者对现有治疗的反应，并有助于确定更具特异性的治疗方法。在《癌症研究》杂志的这个问题中，Faraoni和同事确定了CD73/Nt5e生成的腺苷作为胰管基底/鳞型PDAC免疫抑制的机制。利用针对胰腺泡状或导管细胞的关键基因突变的基因工程小鼠模型和一系列实验和计算生物学方法，作者发现腺苷信号通过受体ADORA2B诱导免疫抑制和肿瘤进展。这些数据展示了PDAC的分子分层结合有针对性的方法如何增强患者对这种致命癌症的治疗反应。请参阅Faraoni等人的相关文章，第1111页。©2023 American Association for Cancer Research。

Molecular stratification of patients with pancreatic ductal adenocarcinoma (PDAC) has the potential to guide clinical decision-making for therapeutic intervention. Investigating mechanisms by which different molecular subtypes of PDAC form and progress will improve patient responses to existing therapies and aid in identifying new, more specific therapeutic approaches. In this issue of Cancer Research, Faraoni and colleagues identified CD73/Nt5e-generated adenosine as a mechanism of immunosuppression specifically in pancreatic ductal-derived basal/squamous-type PDAC. Using genetically engineered mouse models targeting key genetic mutations to pancreatic acinar or ductal cells and an array of experimental and computational biology approaches, the authors found that adenosine signaling through receptor ADORA2B induces immunosuppression and tumor progression in ductal cell-derived tumors. These data demonstrate how molecular stratification of PDAC in combination with targeted approaches may enhance patient responses to therapy in this deadly cancer. See related article by Faraoni et al., p. 1111.©2023 American Association for Cancer Research.