A 59-year-old man presented with a 10-cm × 8-cm tumoral plaque with a superficial nodule in the interscapular region of the back (Fig. 1). The lesion had been growing for 25 years. As a cystic lesion was suspected, the superficial nodule was biopsied. The histopathologic diagnosis was low-grade sarcoma with sclerosis. Two months after the initial biopsy, the lesion was completely excised, reaching the muscular fascia, with a 2-cm margin and with a free graft.Formalin-fixed paraffin-embedded samples were submitted to histologic and immunohistochemical study (4-µm paraffin sections); frozen tissue was submitted to electron microscopy.For histopathology, sections were stained with hematoxylin and eosin. Immunohistochemistry was performed following standard avidin-biotin immunoperoxidase procedures with primary antibodies for vimentin, CD34, smooth muscle-specific actin, bcl-2, S-100, desmin, myoglobin, factor VIII, p53 (all from DAKO, Copenhagen, Denmark), HHF-35 (Enzo Diagnostics, Farmingdale NY), cytokeratin (AE1/AE3) (Biogenex, San Ramon, CA), and factor XIIIa (Calbiochem Novabiochem Corporation, La Jolla, CA).At low magnification, the histologic study of the initial tumoral nodule revealed a poorly circumscribed mesenchymal proliferation, with fibroblastic-like neoplastic cells arranged in a fascicular and storiform pattern, admixed with extensive areas of sclerosis. At higher magnification, tumoral cells were spindle-shaped with hyperchromatic nuclei and scant cytoplasm. In some areas, sclerosis was so evident that a keloid-like pattern was seen (Fig. 2a).The surgical specimen showed a fibroblastic neoplastic proliferation infiltrating the dermis and hypodermis. In the dermis, cells were arranged in a storiform pattern, whereas in the hypodermis there was a honeycomb or lace-like pattern (Fig. 2b). There were also cellular areas alternating with sclerotic areas, with transitional zones in between, in both the dermis and hypodermis.The immunohistochemical study of the initial tumoral nodule and the surgical specimen showed that tumoral cells expressed vimentin, CD34 (Fig. 3), bcl-2, HHF-35, and smooth muscle actin. Neoplastic cells failed to show positivity with desmin, myoglobin, factor XIIIa, factor VIII, S-100, cytokeratin (AE1/AE3), and p53.
Peripheral T-cell lymphomas are uncommon, accounting for only 10% to 15% of all non-Hodgkin lymphomas and their classification has been controversial. We report a case of peripheral T-cell lymphoma with angiocentric growth pattern which presented as a paratesticular tumoral nodule in a 47-year-old-man. Formalin-fixed paraffin-embedded samples from the paratesticular tumor and non-infiltrated adjacent tissue were submitted to histological, immunohistochemical, polymerase chain reaction (PCR)-based and in situ hybridization analysis. Histopathologically, there was a lymphomatous infiltrate in the paratesticular soft tissue, composed of a variable mixture of medium-sized to large cells with large cytoplasm and irregular-shaped nuclei, together with blood vessel destruction, necrosis and karyorrhexis. Immunohistochemical study revealed a high p53 expression in neoplastic cells that showed T cytotoxic immunophenotype, failing to express the natural killer (NK)-cell antigen CD56. A monoclonal rearrangement of the T-cell receptor (TCR) gamma gene by a PCR technique was demonstrated. Type-A Epstein-Barr Virus (EBV) DNA was detected by PCR-based analysis. A combined in situ hybridization and immunohistochemical study revealed that most cells labeled positive for EBV RNA showed immunostaining with the CD45RO antibody. Based on the above results, the case reported was classified as extranodal peripheral T-cell lymphoma with cytotoxic phenotype and EBV associated. The present case does not fit neatly into any of the specific types of peripheral T-cell lymphomas of the REAL classification, so a diagnosis of peripheral T-cell lymphoma unspecified was made.
Rhabdomyosarcoma is a malignant mesenchymal neoplasm that rarely presents as primary skin tumor. So-called amianthoid fibers are hyalinized collagen mats that have been described in myofibroblastic tumors but not in rhabdomyosarcoma. A 65-year-old male developed a submandibular nodule 9 years after an oral squamous cell carcinoma, which had been treated with chemotherapy and radiotherapy. Histological examination of the nodule revealed a pleomorphic rhabdomyosarcoma with extracellular collagen deposits reminiscent of so-called amianthoid fibers. By immunohistochemistry, the tumor cells were positive for vimentin, desmin, smooth muscle actin (SMA), muscle-specific actin (MSA), CD10, CD56, CD99, β-catenin and D2-40. However, only 15-20% of the tumor cells were positive for myoglobin, MyoD1 and myf-4/myogenin. We describe first so-called amianthoid fibers harboring blood capillaries in a rhabdomyosarcoma, suggesting that they are rigid collagen structures that lead to tumor vascularization. The low expression for myogenic regulatory proteins and strong expression for other markers may be misleading and do not contribute to the diagnosis of rhabdomyosarcoma.
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