Cardiac plasma cell granulomas: response to oral steroid treatment.

Plasma cell granulomas are lesions of uncertain histogenesis arising in a variety of locations, most commonly the lung. Treatment for these lesions is complete surgical excision if possible. Unresectable pulmonary lesions respond to oral corticosteroids and radiation therapy. We report the long-term outcome of two unusual pediatric cases of cardiac plasma cell granulomas originating within the right ventricle and posterior aspect of the left ventricle. The limited literature reports advocate surgical resection for this entity, with no discussion of alternative treatment strategies for unresectable lesions. We prospectively evaluated the response to postoperative oral steroid therapy, as complete surgical excision was not possible in either case. Sequential echocardiography demonstrated additional significant reduction in the size of the masses and the patients remain asymptomatic at 9 and 5.5 years follow-up, without evidence of obstruction or recurrence. Oral corticosteroids should be considered as a treatment option for any unresectable plasma cell granuloma.

Thrombospondin-1, vascular endothelial growth factor and fibroblast growth factor-2 are key functional regulators of angiogenesis in the prostate.

BACKGROUND: Prostate cells secrete many molecules capable of regulating angiogenesis; however, which of these actually function as essential regulators of neovascularization is not yet clear. METHODS: Functional angiogenic mediators secreted by normal and diseased prostate cells were identified using an in vitro angiogenesis assay. These factors were quantified by immunoblot or ELISA and localized in tissue by immunohistochemistry. RESULTS: Normal prostate epithelial cell secretions were anti-angiogenic due to inhibitory thrombospondin-1 (TSP-1) whereas this inhibitor was decreased in the pro-angiogenic secretions derived from benign prostatic hyperplasia (BPH) and cancer cells. This pro-angiogenic activity depended primarily on fibroblast growth factor-2 (FGF-2) and/or vascular endothelial growth factor (VEGF) whose secretion was increased. Immunolocalization studies confirmed that the changes detected in vitro also occurred in vivo. CONCLUSIONS: During disease progression in the prostate, production of TSP-1, the major inhibitor, is down-regulated while that of stimulatory FGF-2 and/or VEGF rise, leading to the induction of the new vessels necessary to support tumor growth.

Genetic analysis of prostatic atypical adenomatous hyperplasia (adenosis).

Atypical adenomatous hyperplasia (AAH) of the prostate, a small glandular proliferation, is a putative precursor lesion to prostate cancer, in particular to the subset of well-differentiated carcinomas that arise in the transition zone, the same region where AAH lesions most often occur. Several morphological characteristics of AAH suggest a relationship to cancer; however, no definitive evidence has been reported. In this study, we analyzed DNA from 25 microdissected AAH lesions for allelic imbalance as compared to matched normal DNA, using one marker each from chromosome arms 1q, 6q, 7q, 10q, 13q, 16q, 17p, 17q, and 18q, and 19 markers from chromosome 8p. We observed 12% allelic imbalance, with loss only within chromosome 8p11-12. These results suggest that genetic alterations in transition zone AAH lesions may be infrequent. This genotypic profile of AAH will allow for comparisons with well-differentiated carcinomas in the transition zone of the prostate.