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Pain is an essential signal of danger and provides motivation to seek treatment, facilitating early diagnosis of disease. Pancreatic cancer is particularly lethal and has a 5-year survival rate below 5%. This is mainly due to delayed perception of visceral pain resulting in late diagnosis, by which time the tumour has metastasised.1 This sobering statistic highlights the need for rapid detection and the importance of understanding pain mechanisms in pancreatic cancer. Patients with pancreatic cancer who report more intense pain have shorter survival times, indicating pain intensity is prognostic for disease progression.2 Further, neuropathies including pancreatic nerve damage, neuritis and cancer cell invasion are typical features of pancreatic cancer, and the degree of neuropathy correlates with the severity of pain highlighting the importance of cancer–nerve interactions.2 ,3 This marked neural plasticity is supported by peripheral glial cells (Schwann cells) which have immune cell-like functions and also high affinity for pancreatic cancer cells. Schwann cells initiate and mediate neural interactions with cancer cells, particularly in the early stages of pancreatic cancer. In this issue of Gut, Demir et al 4 undertook a comprehensive investigation of Schwann cell involvement in human and mouse pancreatic cancer which revealed that interleukin-6 (IL-6) secreted by activated Schwann cells inhibits pain signalling in the early stages of pancreatic cancer. This novel mechanism has dire implications, as inhibiting pain signalling would delay treatment seeking behaviour and therefore early detection of cancer.
Demir et al …