Journal of Shanghai Jiao Tong University (Medical Science) ›› 2022, Vol. 42 ›› Issue (6): 833-838.doi: 10.3969/j.issn.1674-8115.2022.06.020

• Review • Previous Articles    

Advances in cytological mechanism of neural invasion in pancreatic ductal adenocarcinoma

ZHANG Xiuqi(), SHEN Baiyong()   

  1. Pancreatic Center, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China
  • Received:2022-02-25 Accepted:2022-05-22 Online:2022-06-28 Published:2022-08-19
  • Contact: SHEN Baiyong;


Pancreatic ductal adenocarcinoma (PDAC) is the most common type of pancreatic malignant tumor, and the incidence of neural invasion of PDAC is as high as 80%?98%, far higher than any other solid tumor. Its neural invasion is defined as the discovery of PDAC cells in the nerve adventitia, perinerve and neurointima surrounding the nerve/nerve sheath. Many studies have shown that the occurrence of neural invasion in PDAC is closely related to faster disease progression, higher local recurrence rate and worse prognosis. The neural invasion of PDAC is related to the behavior/interaction of various types of specific/non-specific immune cells and glial-related cells in the pancreatic tumor microenvironment. These behaviors run through the progression of PDAC. Studies show that Schwann cells, pancreatic stellate cells, tumor-associated macrophages and even T cells, are related to the occurrence of neural invasion of PDAC, which is based on the cell-cell interaction of the above cells and a series of intracellular signal pathways. This review summarizes and introduces the research progress in the field of cytological mechanism of PDAC neural invasion in recent years. Detailed studies of its mechanism may contribute to the discovery of new targets and treatment methods, provide a theoretical basis for controlling or even reversing the neural invasion process of PDAC in the future, and make it possible to improve the prognosis of patients with PDAC.

Key words: pancreatic ductal adenocarcinoma (PDAC), neural invasion, tumor immune microenvironment, cytological mechanism, tumor metastasis

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