Primary effusion lymphoma (PEL) is an unusual class of non-Hodgkin's lymphoma that develops in body cavities, without associated mass lesions. It has been linked to human herpes virus 8 (HHV-8), an etiological factor of Kaposi's sarcoma. Although PEL is a B-cell lymphoma, the neoplastic cells are usually of the "null" phenotype by immunocytochemistry. The relative infrequency of this entity, the absence of wide casuistic allowing a better characterization, and its unfavorable outcome, strongly support the need of a deeper knowledge. We report the clinico-biological findings of a 49-year-old male who was iatrogenically suppressed patient for 29 years because of renal transplantation. This case was diagnosed cytologically as peritoneal PEL and confirmed histologically on peritoneal biopsies. The immune status for both HHV-8 and Epstein-Barr virus (EBV) was evaluated and showed positive immunostaining only for the former. The combination of the immunocytochemistry results with the existence of a clonal rearrangement in the immunoglobulin heavy chain gene (identified by PCR) was compatible with the diagnosis of PEL. The presence of T-cell markers was consistent with the diagnosis of PEL with an aberrant T-cell phenotype.

In this study the EA.hy 926 endothelial cell line--simulating endothelial cells--was treated with imatinib in order to define a possible anti-angiogenic role for imatinib. Dose and time response experiments were performed. Cell morphology was studied, while migration efficiency, intercellular permeability and VE-cadherin expression were assayed, both in the presence and in the absence of imatinib. Imatinib-induced EA.hy 926 cell apoptosis was also examined. Results showed that imatinib reduced the endothelial cell population, changed cell monolayer morphology and reduced cell-to-cell cohesiveness. Migration efficiency was significantly decreased while intercellular permeability was 2.76-fold increased in the presence of imatinib. Indirect immunofluorescence microscopy showed nearly complete down-regulation of VE cadherin in imatinib-treated cells. Furthermore, apoptotic activity was detected in imatinib-treated cells. Altogether our results support an antiangiogenic profile for imatinib that possibly contributes to its therapeutic potential.

In women with an adnexal mass, ascites and elevated Ca-125 levels, ovarian carcinoma must be ruled out. However, several other conditions, including genital tuberculosis, may present similarly. A 41-year-old woman with weight loss, ascites and elevated levels of Ca-125 was evaluated for ovarian cancer. Computerized tomography revealed an adnexal mass, ascites and lymphnodes on the peritoneal surface. Paracentesis of the ascitic fluid revealed a lymphocytic exudate but failed to show any malignant cells. At laparotomy, frozen sections of tissue biopsies were negative for malignancy; however, a total hysterectomy plus adnexectomy was performed. Postoperatively histologic examination revealed typical features of genital tuberculosis. Antituberculosis treatment was effectively given to the patient. Serum levels of Ca-125 were undetectable 12 weeks after treatment. In conclusion, genital tuberculosis can be misdiagnosed and confused with ovarian cancer. Intraperitoneal tuberculosis should be considered in the differential diagnosis in cases in which ovarian cancer is suspected, even when malignancy-associated risk factors are present.

Apoptosis and cell proliferation increased as the grade of tumour increased in ovarian serous adenocarcinoma, suggesting a rapid turnover of the tumour cells in tumours of higher grade, and may play an important role in the growth and the extension of such cancer cells in the peritoneal cavity.

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