Epithelioid sarcoma: clinical, MR imaging and pathologic findings.

OBJECTIVE: To report and describe the MR imaging features of eight new cases of this rare soft tissue sarcoma and correlate them with the clinical and histologic findings. DESIGN AND PATIENTS. Retrospective analysis was carried out for the MR imaging characteristics and histologic findings of eight patients with pathologically proven epithelioid sarcoma and the literature was reviewed. Findings were correlated in each case with the patient's clinical presentation and eventual outcome. RESULTS: The patients, whose primary tumors ranged from 2.5 cm to 19 cm in maximum dimension, were 1 to 90 years of age. Tumors involved the extremities ( n=5), the scalp ( n=2) and the paraspinal muscles ( n=1). Five tumors presented as well-defined, frequently painful, deeply situated masses and three as subcutaneous nodules or cutaneous ulcers with no palpable mass. Four patients had associated regional lymphadenopathy and one had distant metastases at diagnosis. MR imaging showed tumor infiltration of adjacent tissues in seven patients. Signal characteristics reflected varying degrees of cellularity, and the presence of necrosis, hemorrhage, fibrosis, hyalinization and inflammation. Bone marrow involvement was demonstrated in one patient. Clinical outcomes were generally poor. CONCLUSIONS: Epithelioid sarcoma is an aggressive soft tissue sarcoma with a varied clinical presentation, growth pattern, MR signal characteristics and histologic picture. The tumor favors the distal extremities and is commonly infiltrative and accompanied by enlarged regional lymph nodes. This neoplasm may present as an intramuscular mass but should also be suspected in patients with ulcerating cutaneous nodules with or without regional lymphadenopathy.

Factors affecting adoptive transfer of resistance to Schistosoma mansoni in the snail intermediate host, Biomphalaria glabrata.

We examined potential variables affecting adoptive transfer of resistance to Schistosoma mansoni in Biomphalaria glabrata implanted with amebocyte-producing organs (APOs) from resistant snails. Transplants of 7 tissues other than the APO (heart, kidney, mantle, albumin gland, brain, digestive gland, and gonad) did not transfer resistance, suggesting a unique property of this structure. Only APOs from donors previously exposed to miracidia transferred resistance, although whether this is evidence for a priming effect or merely the elimination of susceptible donors is not known. Variability in the donor and in the implant itself apparently was unimportant, inasmuch as implants from small or large snails or from 2 separate donors all conferred similar levels of resistance. Recipients of APOs from 2 additional resistant strains of B. glabrata, 10-R2 and Salvador, also displayed resistance. However, no resistance was transferred by APOs from schistosome-refractory B. obstructa. Histological examination of implants removed from recipients that either did or did not show transferred resistance revealed no differences in mitotic activity. Furthermore, implanted APOs from B. obstructa displayed no mitotic activity. Finally, reexposure of snails with transferred resistance to a large dose of miracidia caused infection in 70%, suggesting that either transferred resistance is transitory or it can be overwhelmed.

Killing of Schistosoma mansoni sporocysts in Biomphalaria glabrata implanted with amoebocyte-producing organ allografts from resistant snails.

Schistosome-susceptible National Institutes of Health (NIH) albino Biomphalaria glabrata were implanted with the amoebocyte-producing organ (APO) from 4 types of donors: (1) exposed-resistant (eR), i.e., schistosome-resistant 13-16-R1 snails that had been exposed to miracidia of Schistosoma mansoni 30 or more days previously in order to verify their resistance, (2) exposed-susceptible (eS), i.e., NIH albino snails that had been similarly exposed to miracidia, (3) unexposed-resistant (uR), and (4) unexposed-susceptible (uS). Allograft recipients, along with unimplanted NIH albino and 13-16-R1 controls (cS and cR, respectively), were then challenged with 100 miracidia each of Schistosoma mansoni at 14-15 days postimplantation. Histological sections of tentacles fixed at 3 days postchallenge (PC) showed significantly fewer normal sporocysts and more numerous developmentally retarded sporocysts in cR snails than in the other 5 treatment groups, and significantly more killed sporocysts in both cR snails and recipients of eR APOs than in the other 4 groups. In addition, the histological condition of eR allografts in both unchallenged (at 1, 3, 7, 10, and 14 days postimplantation) and schistosome-challenged (at 3 days PC) NIH albino recipients was examined. Viable hematopoietic cells were found in 96% of implants, and in 86% of implants low numbers of mitotic figures were found among these cells, although no increased mitotic activity occurred in challenged recipients. These data suggest that lowered susceptibility to infection with S. mansoni in recipients of APO allografts results primarily from hemocyte-mediated resistance.

Transfer of resistance to Schistosoma mansoni in Biomphalaria glabrata by allografts of amoebocyte-producing organ.

Allografts of amoebocyte-producing organ (APO) were implanted heterotopically into the schistosome-susceptible NIH albino stock of Biomphalaria glabrata from either 13-16-R1 (a schistosome-resistant stock) or NIH albino donors. At 3, 7-8, 14-15, 21, 28-33, or 47-71 days postimplantation (PI), allograft recipients were exposed to 50 miracidia each of Schistosoma mansoni and subsequently monitored for development of sporocysts and cercariae. Relative to untampered snails and recipients of NIH albino APOs, recipients of 13-16-R1 APOs showed significantly lower infection rates from 7 days PI until the end of the experiment. The mechanism for this apparent transfer of resistance is unknown, but hypothetically it may involve chimerism, i.e., production of hemocytes with the resistant phenotype by implanted 13-16-R1 APOs, or synthesis by the implant of soluble "resistance factors" that induce cytotoxicity in recipient hemocytes, or both.