[Varying characteristics of subcutaneous and dermal leiomyosarcomas. Two case reports and literature review]. / Unterschiedliche Charakteristika subkutaner und dermaler Leiomyosarkome. Zwei Fallbeobachtungen und Literaturübersicht.

Cutaneous leiomyosarcomas (LMS) originating from smooth muscle of the skin are rare malignant neoplasms. Preferential sites are hair-bearing areas, especially the legs. We report two patients in their 5th and 7th decade, in whom leiomyosarcomas were encountered in the lower leg and the capillitium, respectively. Histologically, the former was found to be a dermal leiomyosarcoma with subcutaneous infiltration, the latter an exclusively dermal tumor. The LMS of the lower leg had been excised three years previously in a different institution and had been diagnosed as a leiomyoma. Both lesions were excised with adequate safety margins in our institution and within a two-year postoperative observation period no recurrences were encountered. Dermal leiomyosarcomas have a 33% recurrence rate while that of subcutaneous leiomyosarcomas show is 50%. In contrast to exclusively dermal tumors, subcutaneous LMS show a tendency for hematogenic and lymphogenic metastases. Therapy of choice is excision with wide safety margins.

CDKN2A/p16 inactivation is related to pituitary adenoma type and size.

p16 (CDKN2A, MTS1, INK4A) status at genomic and protein levels was analysed and correlated with clinico-pathological features in 72 pituitary adenomas. Methylation of CpG islands of promoter/exon 1 sequences was found in most gonadotroph, lactotroph, plurihormonal, and null cell adenomas (36 of 44, 82%), but it was rare in somatotroph (1 of 13 cases, 8%) and corticotroph adenomas (1 of 15 cases, 7%). Homozygous CDKN2A deletion was restricted to rare somatotroph (15%) and corticotroph adenomas (13%). Immunohistochemical p16 protein expression was observed in the normal adenohypophysis, whereas it was absent in 60 of 72 (83%) tumours and reduced in another ten (14%) tumours. Staining for p16 was only seen in 5 of 15 (33%) corticotroph, 3 of 13 (23%) somatotroph, 3 of 5 (60%) plurihormonal, and 1 of 19 (5%) null cell adenomas. p16 immunonegativity without CDKN2A methylation or deletion occurred in 22 tumours, including most somatotroph and corticotroph adenomas (15 of 28, 54%). Both CDKN2A alterations and p16 negativity were related to larger tumour size. Patients with p16-negative tumours were older than patients with p16-positive tumours. These data suggest that p16 down-regulation is common in all adenoma types. The mechanisms of p16 down-regulation probably involve CDKN2A methylation in most types, but remain to be determined in somatotroph and corticotroph adenomas. These findings also suggest that p16 down-regulation is usually not an initial event, but is acquired during adenoma progression.