Deficient expression of HLA class-I molecules observed in many cancers is suggested to influence both disease progression and potential efficacy of T cell-mediated immune therapy. Previous studies have attempted to correlate either primary breast cancer tumor grade with HLA class-I levels or the presence of HLA class-I-deficient cells in metastatic lesions with survival. In this study we evaluated the HLA class-I status of matched primary and secondary breast cancer lesions in order to ask the question: is metastasis of breast cancer associated with down-regulation of HLA class-I expression? Immunocytochemistry analysis shows a definitive correlation between diminished HLA class-I expression and dissemination of breast cancer to tumor-draining lymph nodes: both the total number of HLA class-I+ cells per sample and the levels of expression are dramatically decreased in secondary versus primary tumor lesions.
View Article and Find Full Text PDFContext: Medullary carcinoma (MC) is a special type of breast cancer that has a better prognosis than atypical medullary carcinoma (AMC) and high-grade invasive ductal carcinoma (HGIDC) with prominent lymphocytic infiltrates. What accounts for the different clinical courses of these carcinomas, despite their similar histology, is unknown. To address this issue, we performed a comparative study of amplification and overexpression of HER-2/neu and expression of several other important biochemical markers (p53, MIB1, and estrogen receptor [ER]/progesterone receptor [PR]) in these 3 cancer groups.
View Article and Find Full Text PDFObjective: Matrix metalloproteinase (MMP) activity is essential for remodeling of ischemic tissue. The murine hindlimb ischemia model exhibits tissue remodeling including revascularization in part due to angiogenesis. MMP-2 and -9 are type IV collagenases necessary for basement membrane degradation as a part of extracellular matrix remodeling and angiogenesis.
View Article and Find Full Text PDFBackground: Acute limb ischemia initiates a systemic inflammatory response, including pulmonary polymorphonuclear leukocyte (PMN) sequestration and acute lung injury. Lung injury is partly attributed to release by PMN's of extracellular matrix (ECM) modifying metalloproteinases (MMPs). We hypothesized that acute hindlimb ischemia (HI) would increase MMP activity in the lung and other organs and that systemic neutrophil depletion before HI would block this effect.
View Article and Find Full Text PDFHepatic stellate-cell lipidosis due to hypervitaminosis A can lead to cirrhosis, which can be averted by restricting vitamin A intake. Other causes, including the use of synthetic retinoids, have been postulated. We studied the frequency and etiology of stellate-cell lipidosis in patients undergoing liver biopsy for reasons other than vitamin A abuse.
View Article and Find Full Text PDFContext: Placental transmogrification of the lung is a term introduced to describe a peculiar histologic pattern characterized by formation of placental villuslike structures in the lung parenchyma. It has been reported to occur in association with bullous emphysema and lipomatosis.
Objectives: To study the relationship between placental transmogrification and pulmonary hamartomas.
Amplification of Her-2/neu in breast carcinoma is associated with poor prognosis, short disease-free interval, and short survival time in both node-negative and -positive patients. Little is known about the starting point of amplification of Her-2/neu and how it progresses from benign to malignant breast lesions. We attempted to address these questions by evaluating amplification of Her-2/neu in benign, premalignant, and malignant lesions using fluorescence in situ hybridization (FISH).
View Article and Find Full Text PDFMolecular markers of ordinary invasive ductal carcinoma of the breast have been extensively studied and their prognostic significance has been assessed. A common variant of breast cancer, tubular carcinoma, has an excellent prognosis as judged from several clinicopathologic studies. One would assume that tubular carcinomas have "favorable" molecular markers, however, published series of tubular carcinomas do not include molecular markers.
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