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Perineural invasion (PNI) is one of the most potent interactions between tumors and nerves.
Perineural invasion (PNI) is one of the most potent interactions between tumors and nerves. According to Batsakis (1985), PNI is defined as “tumoral invasion in, around, and through the nerves” [11]. While this definition is widely accepted, it does have certain limitations. An alternative and broader definition, advocated by Liebig et al., includes tumors in close proximity to nerves involving at least 33% of the nerve circumference or the presence of tumor cells within the epineurium, perineurium and endoneurium of the nerve sheath [12]. Anything less than 33% represents focal abutment and not invasion [13]. PNI represents the pinnacle of tumor-nerve interaction, providing both tumor cells and nerves with a survival advantage.
PNI is a relatively novel histopathological feature associated with poor clinical outcomes and decreased survival in various malignancies, including pancreatic ductal adenocarcinoma (PDAC), head and neck squamous cell carcinoma (HNSCC), prostate cancer, gastric cancer, and CRC [9, 12, 14]. In most studies, the reported incidence of PNI in CRC patients ranges between 9% and 33% [15,16,17,18], which is significantly lower than that observed in PDAC. However, once confirmed, PNI is linked to rapid disease progression and unfavorable outcomes [19]. The New England Journal of Medicine has recognized PNI as pathological evidence of early metastasis, which is independently associated with decreased survival in CRC [20].
The interactions involving neural effects on other cells in the TME have garnered increasing attention [21]. Recently, an insightful perspective article discussed the relationship between the nervous system and the development of hallmark capabilities in tumors, emphasizing the role of neurons and axons as constituents of the TME that can facilitate the acquisition of hallmark features by tumors [22]. However, a comprehensive understanding of the interaction between PNI and the TME in CRC remains lacking. In this review, our aim is to elucidate the clinical relevance of PNI and provide in-depth overview of the specific molecules and cells within the TME that regulate PNI and promote cancer development. We hope that this endeavor will contribute to a deeper comprehension of the significance and underlying mechanisms of PNI in CRC.
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