Report of an angiosarcoma mimic: Cutaneous aneurysmal fibrous histiocytoma
Department of Pathology, Loyola University Medical Center, Maywood, IL, USA.Apmis (Impact Factor: 2.04). 11/2006; 114(10):744-8. DOI: 10.1111/j.1600-0463.2006.apm_530.x
Aneurysmal fibrous histiocytoma is an unusual variant of the spectrum of fibrous histiocytomas with the peculiar morphologic appearance of a benign aneurysmal vasoformative process that ultimately culminates in multiple microhemorrhages within the tumor. It looks strikingly different from the usual cutaneous lesions encountered in clinical dermatology practice. A single report of a cutaneous aneurysmal fibrous histiocytoma in the skin of the back of a 60-year-old male is described with emphasis on the immunostaining pattern and review of the literature. There is a significant potential for confusion of this lesion with other cutaneous lesions, clinically as well as pathologically. In our case, the patient presented with a lesion that clinically resembled a hemangioma, was pathologically interpreted initially to be an angiosarcoma, and finally, the revised pathology was interpreted as an aneurysmal variant of a fibrous histiocytoma. Caution is warranted to avoid misinterpretation of cutaneous fibrohistiocytic tumors.
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ABSTRACT: RNA-sequencing of an aneurysmal benign fibrous histiocytoma with the karyotype 46,XY,t(3;11)(p21;q13),del(6)(p23)/46,XY showed that the t(3;11) generated two fusion genes: LAMTOR1-PRKCD and NUMA1-SFMBT1. RT-PCR together with Sanger sequencing verified the presence of fusion transcripts from both. In the LAMTOR1-PRKCD fusion, the part of PRKCD coding for the catalytic domain of the serine/threonine kinase is under control of the LAMTOR1 promoter. In the NUMA1-SFMBT1 fusion, the part of SFMBT1 coding for two of four malignant brain tumor domains and the Sterile alpha motif domain is controlled by the NUMA1 promoter. The data support a neoplastic genesis of aneurysmal benign fibrous histiocytoma and indicate a pathogenetic role for the two said fusion genes.Cancer Genetics 08/2015; DOI:10.1016/j.cancergen.2015.07.007 · 2.98 Impact Factor
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