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A 67-year-old man presented to ear, nose and throat department complaining of nasal congestion and recurrent epistaxis for 5 months. Nasal endoscopy revealed a pigmented polyp obstructing the right nasal cavity. MRI with contrast agent showed a right nasal cavity polypoid mass with hyper signal intensity (SI) both in non-enhanced T1-w and diffusion imaging, marked hypo SI in T2-w sequences and avidly contrast enhancement characterised by rapid wash-in without significant wash-out on dynamic perfusion imaging. Histological specimen showed epithelioid and spindle cells with focal intense pigmentations and immunohistochemical features compatible with primary melanotic sinonasal mucosal melanoma (SNM). As melanotic SNM shows MRI pathognomonic high non-enhanced T1-w SI, this case underlines the crucial role of MRI not only in assessing the local tumour extension/recurrence but also in increasing the diagnostic confidence of detecting melanotic SNM. Thus, MRI should be always performed in case of clinical–endoscopic suspicion of SNM.

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(ALCANZA) : an international, open-label, randomised, phase 3, multicentre trial. Lancet 2017; 390:550-66 Funding sources: none.

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Macrophages (MΦs) and reactive oxygen species (ROS) are implicated in carcinogenesis. The oxidative stress sensor, transient receptor potential ankyrin 1 (TRPA1), activated by ROS, appears to contribute to lung and breast cancer progression. Although TRPA1 expression has been reported in melanoma cell lines, and oxidative stress has been associated with melanocytic transformation, their role in melanoma remains poorly known. Here, we localized MΦs, the final end-product of oxidative stress, 4-hydroxynonenal (4-HNE), and TRPA1 in tissue samples of human common dermal melanocytic nevi, dysplastic nevi, and thin (pT1) and thick (pT4) cutaneous melanomas. The number (amount) of intratumoral and peritumoral M2 MΦs and 4-HNE staining progressively increased with tumor severity, while TRPA1 expression was similar in all samples. Hydrogen peroxide (H2O2) evoked a TRPA1-dependent calcium response in two distinct melanoma cell lines (SK-MEL-28 and WM266-4). Furthermore, H2O2 induced a TRPA1-dependent H2O2 release that was prevented by the TRPA1 antagonist, A967079, or Trpa1 gene silencing (siRNA). ROS release from infiltrating M2 MΦs may target TRPA1-expressing melanoma cells to amplify the oxidative stress signal that affects tumor cell survival and proliferation.