Pancreatic cancer is an aggressive tumor with dismal prognosis. Neural invasion is one of the pathological hallmarks of pancreatic cancer. Peripheral nerves can modulate the phenotype and behavior of the malignant cells, as well as of different components of the tumor microenvironment, and thus affect tumor growth and metastasis. From a clinical point of view, neural invasion is translated into intractable pain and represents a predictor of tumor recurrence and poor prognosis. Several molecules are implicated in neural invasion and pain onset in PDAC, including neutrophins (e.g., NGF), chemokines, adhesion factors, axon-guidance molecules, different proteins, and neurotransmitters. In this review, we discuss the role of nerves within the pancreatic cancer microenvironment, highlighting how infiltrating nerve fibers promote tumor progression and metastasis, while tumor cells, in turn, drive nerve outgrowth in a reciprocal interaction that fuels tumor advancement. We outline key molecules involved in neural invasion in pancreatic cancer and, finally, explore potential therapeutic strategies to target neural invasion, aiming to both inhibit cancer progression and alleviate cancer-associated pain.
胰腺癌是一种侵袭性强、预后极差的恶性肿瘤。神经侵犯是其重要的病理学特征之一。外周神经能够调控恶性细胞的表型与行为，并影响肿瘤微环境中多种组分的功能，从而促进肿瘤生长与转移。从临床角度看，神经侵犯会导致顽固性疼痛，并预示肿瘤复发及不良预后。在胰腺导管腺癌中，多种分子参与神经侵犯与疼痛发生过程，包括神经营养因子（如神经生长因子NGF）、趋化因子、黏附因子、轴突导向分子、多种蛋白及神经递质。本文综述了神经在胰腺癌微环境中的作用，重点阐述浸润神经纤维如何促进肿瘤进展与转移，同时肿瘤细胞又如何驱动神经增生，形成促进肿瘤发展的双向交互作用。我们系统梳理了参与胰腺癌神经侵犯的关键分子，并最终探讨了靶向神经侵犯的潜在治疗策略，旨在同时抑制癌症进展并缓解癌性疼痛。
肿瘤(癌症)患者之家