Background: Thrombospondin-1 (TSP-1) is an extracellular matrix component glycoprotein, which is known to be a potent inhibitor of angiogenesis and may be important in cancer invasiveness. We examined the TSP-1 expression in correlation with conventional clinicopathological parameters to clarify its prognostic significance in bladder cancer. In addition, the possible correlation of TSP-1 expression with microvessel count, VEGF expression, p53 expression as well as with the expression of the extracellular matrix components was studied to explore its implication in vascularization and tumour stroma remodeling.
We report a case of a 55-yr-old man with malignant melanoma of scrotum. He was referred to our Hospital with a complaint of gradual focal enlargement of the scrotum in a period of 3 yr. On physical examination, a pigmented, poorly marginated mass, with central necrosis was observed. A fine-needle aspiration (FNA) of the lesion was performed. Cytological examination revealed highly cellular smears, containing malignant cells, dispersed or arranged in loose aggregates. Cellular morphology and characteristics were identical to those of malignant melanoma arising elsewhere in the skin. The immunocytochemical study revealed positivity of neoplastic cells for anti-melanoma monoclonal antibody (HMB-45) antigen. Histological confirmation finally was provided after wide excision of the lesion. We emphasize the difficulties in differential diagnosis considerations and diagnostic pitfalls of scrotal lesions.
BACKGROUND.Patients with resected breast carcinoma who received granulocyte-colony-stimulating factor (G-CSF)-supported adjuvant chemotherapy exhibited an increase in their serum CA 15-3 levels. The authors investigated the role of G-CSF-induced neutrophil MUC1 expression in this setting. METHODS.Twenty-two patients with resected early breast carcinoma and 6 patients with high-grade lymphoma received chemotherapy cycles with or without G-CSF support. When given, G-CSF was administered for either 5 or 10 days per cycle. Immunocytochemical staining and flow cytometric analysis of peripheral blood neutrophils and bone marrow myeloid cells for MUC1 epitopes were performed during treatment. RESULTS.At baseline, the median serum CA 15-3 was 16 U/mL, with weak MUC1 expression in peripheral neutrophils (median immunocytochemical score [ICCS] ϭ 40, flow cytometric score [FCS] ϭ 211 antibody molecules per neutrophil). For patients receiving chemotherapy cycles with 5-day G-CSF support, median CA 15-3 levels increased moderately (median ϭ 28 U/mL; P ϭ 0.016) and absolute neutrophil counts (ANC) did not increase, whereas ICC staining showed a moderate increase (median ICCS ϭ 105; P ϭ 0.015). For patients receiving chemotherapy cycles with 10-day G-CSF, serum CA 15-3 levels increased 2-4-fold from baseline levels and reached abnormal levels (median ϭ 47; P Ͻ 0.0005) and the ANC increased (median ϭ 21,400/mm 3 ; P ϭ 0.007), whereas significant induction of MUC1 expression occurred in the cell membrane and mostly in the cytoplasm of neutrophils (median ICCS ϭ 162; P ϭ 0.001). Flow cytometry detected increased cytoplasmic, but not surface, neutrophil MUC1 expression in the 10-day G-CSF group only (baseline median FCS ϭ 3975, 4th cycle median ϭ 6327 molecules per cell; P ϭ 0.028). In the bone marrow, induction of MUC1 expression was observed in the 10-day G-CSF group only in band forms and neutrophils, but not in more immature myeloid cells. Serum CA 15-3 levels and ICC score were found to demonstrate a linear relation. When ICCS and ANC were incorporated in a combined score, its relation with serum CA 15-3 levels demonstrated a parabolic (cubic) pattern. Serum CA 15-3 levels, ANC, and neutrophil MUC1 staining returned to baseline after the completion of therapy. No excess of malignant recurrences were observed. CONCLUSIONS.Women with resected breast carcinoma who received G-CSFprimed chemotherapy showed serum CA 15-3 elevation due to an increase in peripheral blood neutrophil number and induced neutrophil cytoplasmic MUC1 expression, which was caused by G-CSF. Physicians should be aware of this interaction.
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