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Lentigo maligna (LM) is an in situ form of melanoma which can progress into invasive lentigo maligna melanoma (LMM). Variations in the pigmentation and thus visibility of the tumour make assessment of lesion borders challenging. We tested hyperspectral imaging system (HIS) in in vivo preoperative delineation of LM and LMM margins. We compared lesion margins delineated by HIS with those estimated clinically, and confirmed histologically. A total of 14 LMs and 5 LMMs in 19 patients were included. HIS analysis matched the histopathological analysis in 18/19 (94.7%) cases while in 1/19 (5.3%) cases HIS showed lesion extension not confirmed by histopathology (false positives). Compared to clinical examination, HIS defined lesion borders more accurately in 10/19 (52.6%) of cases (wider, n=7 or smaller, n=3) while in 8/19 (42.1%) cases lesion borders were the same as delineated clinically as confirmed histologically. Thus, HIS is useful for the detection of subclinical LM/ LMM borders. Key words: lentigo maligna; lentigo maligna melanoma; tumour margin assessment; hyperspectral imaging. peerReviewed

Amelanotic lentigo maligna melanoma (ALMM) is an infrequent presentation of lentigo maligna melanoma, less than thirty cases having been reported to date. Hypopigmented or erythematous macules on the face of older women, resembling Bowen's disease or eczema, are the most common clinical presentation. We report a case of ALMM in a 73-year-old woman. Therapeutic trials with cryotherapy, 5-fluorouracil, and azelaic acid were unsuccessful, and the lesions were eventually cured by surgical excision. ALMM requires early clinical suspicion and histopathologic confirmation of diagnosis in every patient presenting with a slowly enlarging erythematous or hypopigmented macule, especially when located on the face of an older woman with a light complexion.

Growth hormone (GH) exerts its regulatory functions in controlling metabolism, balanced growth and differentiated cell expression by acting on specific receptors, which trigger a phosphorylation cascade resulting in the modulation of numerous signalling pathways, and dictate gene expression. Immunohistochemical techniques were used to demonstrate the presence of growth hormone receptors in 126 formalin-fixed, paraffin-embedded melanocytic tumours comprising melanocytic naevi, superficial spreading melanoma, nodular melanoma, lentigo maligna melanoma and metastatic melanomas. The relative proportion of positive cells and intensity of staining was higher in neoplastic cells, compared to normal cutaneous cells. Of the 76 cases of common melanocytic naevi (CMN) studies, 46 were weakly reactive with MAb 263. Heterogeneity of immunoreactivity was found in primary melanoma lesions with a variable range of positive cells. Of 37 cases studied, 34 were moderately to strongly positive. Immunoreactivity showed subcellular localization of the GH-receptor in cell membranes, was predominantly cytoplasmic, but strong nuclear immunoreaction was also apparent in many instances. The nuclear localization of immunoreactivity is the result of nuclear GH-receptor/binding protein, identically to the cytosolic and plasma growth hormone binding protein. Intense immuno-reactivity was also observed in the cellular Golgi area of established cell lines and cultured tissue-derived cells in exponential growth phase, indicating cells are capable of GH-receptor synthesis. In the primary lesions, dermal tumour cells tended to be more immunoreactive relative to those seen in the dermal region. Metastatic lesions in various organs also expressed growth hormone receptors in secondary tumour cells and all of the metastatic cases were positive. The expression of GH-receptors in human melanoma cells means that these cells are directly responsive to GH action and that GH may stimulate local production of IGF-I, which then acts in an autocrine mechanism.

IT HAS been stated that diagnosis of cutaneous malignant melanoma is comparable to writing the death certificate of the patient. An exception to this gloomy prognosis is the malignant melanoma arising from the pigmented lesion that Hutchinson * first described as senile freckle or infective melanotic freckle, later termed by Darier and by Dubreuilh lentigo malin des vieillards and still later by Dubreuilh 3 melanose circonscrite precancereuse . We believe this disease is too briefly discussed in the usual textbooks of dermatology to afford comprehensive understanding of the pathologic process and differentiation from the more serious malignant melanoma arising from the pigmented dermoepidermal nevus (junction type nevus). Such differentiation is of importance from the standpoint of prognosis and of treatment. Discussion of these features is the object of this report. Since Hutchinson's * brief description of the disease relatively few comprehensive reports have been published. Notable exceptions