Perineural invasion (PNI) as the fourth way for solid tumors metastasis and invasion has attracted a lot of attention, recent research reported a new point that PNI starts to include axon growth and possible nerve “invasion” to tumors as the component. More and more tumor–nerve crosstalk has been explored to explain the internal mechanism for tumor microenvironment (TME) of some types of tumors tends to observe nerve infiltration. As is well known, the interaction of tumor cells, peripheral blood vessels, extracellular matrix, other non-malignant cells, and signal molecules in TME plays a key role in the occurrence, development, and metastasis of cancer, as to the occurrence and development of PNI. We aim to summarize the current theories on the molecular mediators and pathogenesis of PNI, add the latest scientific research progress, and explore the use of single-cell spatial transcriptomics in this invasion way. A better understanding of PNI may help to understand tumor metastasis and recurrence and will be beneficial for improving staging strategies, new treatment methods, and even paradigm shifts in our treatment of patients.
The phenomenon that longstanding impaired olfactory function is associated with the decreased gustatory function was described in present studies, which was seems attributed to mutual chemosensory interactions. And the interaction between olfaction and gustation still needs more research to figure out. The objective of the study was to investigate how the taste was influenced by olfactory impairment in the central pathway. We tested 33 subjects with normal ( n = 19) or impaired ( n = 14) olfactory function for their gustatory event-related potentials (gERPs). Validated tests were used for olfactory and gustatory testing (Sniffin’ Sticks, gERPs, and three-drop test). This study reported an objective gustatory function decline in olfactory dysfunction participants. However, it also reported the increased gustatory event-related potentials of olfactory dysfunction participants, especially at the frontal electrode (F Z ) and electrode 16 (E16), and the reduced latency of P2 peak of them at electrode 21 (E21), while no obvious difference was observed at the centro-parietal electrode (P Z ). Inferior insula might be the main response area for the increase in gERPs, and this increase averaged amplitude of the P2 component may attribute to compensation of the secondary gustatory response that occurred in the gustatory processing of olfactory-impaired patients.
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