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Cutaneous squamous cell carcinoma (cSCC) is the second most common nonmelanoma skin cancer, accounting for 20% of all skin cancers. The risk of the disease continues to rise annually with an estimated 50–200% increase in incidence within the last three decades. Although cSCC is one of the most common skin cancers, reported having 1 million cases per year in the United States, there is inconsistency with its reported metastatic rate. Research exploring cSCC metastasis found an overall rate of 1.2–5% but this range varies, and some dermatologists are finding cSCC's ability to spread more worrisome. This allows for clinical variation in the appropriate treatments and follow‐up guidelines when diagnosing a patient with cSCC. Poor prognosis in patients with a high metastatic potential makes cSCC clinically problematic. Clinician emphasis should be put on risk factors, anatomical site, tumor presentation, and histological features when evaluating cSCC's metastatic potential. In this review, specific skin conditions that predispose to cSCC and discrepancies in its reported metastatic potential will be discussed. [ABSTRACT FROM AUTHOR]

Capsaicin vanilloid receptor-1 mediates substance P release in experimental pancreatitis. Am J Physiol Gastrointest Liver Physiol 281: G1322-G1328, 2001.--We examined whether the capsaicin vanilloid receptor-1 (VR1) mediates substance P (SP) release from primary sensory neurons in experimental pancreatitis. Pancreatitis was achieved by 12 hourly injections of caerulein (50 [micro]g/kg ip) in mice. One group received capsazepine (100 [micro]mol/kg sc), a competitive VR1 antagonist, at 4-h intervals. Neurokinin-1 receptor (NK1R) internalization in acinar cells, used as an index of endogenous SP release, was assessed by immunocytochemical quantification of NK1R endocytosis. The severity of pancreatitis was assessed by measurements of serum amylase, pancreatic myeloperoxidase (MPO) activity, and histological grading. Caerulein administration caused significant elevations in serum amylase and pancreatic MPO activity, produced histological evidence of pancreatitis, and caused a dramatic increase in NK1R endocytosis. Capsazepine treatment significantly reduced the level of NK1R endocytosis, and this was associated with similar reductions in pancreatic MPO activity and histological severity of pancreatitis. These results demonstrate that repeated caerulein stimulation causes experimental pancreatitis that is mediated in part by stimulation of VR1 on primary sensory neurons, resulting in endogenous SP release. capsazepine; neurogenic inflammation; neurokinin-1 receptor; pancreatic acinar cells; primary sensory neurons

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