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Both periodic acid-Schiff and Congo red staining were negative, excluding fungal infection and amyloid deposits, respectively. Upon further dermatological examination, the patient had an asymmetrically and darkly pigmented 0.8 ! 0.6 cm macula behind his right ear which was excised and diagnosed as malignant melanoma Clark level III, invasion 0.9 mm ( fig. 1 b). Another skin biopsy taken parasternally demonstrated a well-differentiated squamous cell carcinoma. No other classical cutaneous manifestations of MEN1-like angiofibroma, collagenoma or lipomas were found, nor were they reported by the patient to have been present before. In 1999, MEN1 had been diagnosed in the patient and his son. For several years, the patient had suffered from bilateral nephrolithiasis caused by hyperparathyroidism. In addition, he had an euthyroid goiter; as a result, he underwent parathyroidectomy and thyroidectomy. Following persistent abdominal pain in 1999, a pancreatic tumor was suspected. There was no evidence of acromegaly, a gastrinoma or insulinoma. On computerized tomography, a 3-cm pancreatic tumor was seen. Subsequently, the pancreas and spleen were surgically removed. Histologically, a neuroendocrine tumor of the pancreas was diagnosed, with liver metastases, in 2001, which were found by ultrasound, computerized tomography, scintigraphy with 111 In-labeled octreotide, and subsequent liver biopsy. Complete blood count, electrolytes (including calcium), liver function and renal function tests were normal. Serum gastrin, serotonin, prolactin, and insulin-like growth factor-1 were within the normal range. Because of the absence of clinical complaints and any evidence of hormonal activity, as well as the slow progression, the liver metastases of the pancreatic neuroendocrine tumor were not treated. The coding region (exons 2–10) of the MEN1 gene on chromosome 11 was analyzed for germline mutations. A heterozygotic deletion of 13 bp was found at the verge of intron 5 to exon 6 covering nucleotides 5,290–5,302. Because of the multiple underlying diseases, no systemic therapy of papillomatosis confluens et reticularis was initiated, though it was the initial cause for presentation to the hospital. The melanoma and squamous cell carcinoma were excised with no apparent signs of metastasis. Microdissection of tumor tissue (well-differentiated squamous cell carcinoma, melanoma) and normal skin tissue (sebaceous gland, lymphocytes, epidermis) was performed as previously described [12] . To search for loss of heterozygosity in the tumor tissue at the MEN1 locus, microdissected tumor and normal DNA were amplified with the polymerase chain reaction using the polymorphic DNA markers/primers D11S480, D11S449 and PYGM which map to the MEN1 gene locus at 11q13, as described by McKeeby et al. [3] . Primer sequences read for exon 5/6 forward: TCC CTG TTG GTT CTG ACC, and for exon 5/6 reverse: CGC CCG CCG CGC CCC GCG CCC GTC CCG CCG CCC CCG CCC GTG CCT CAG CCA CTG TTA GG.

Combination of Multiple Skin Malignancies with Multiple Endocrine Neoplasia Type 1: Coincidental or Pathogenetically Related?