UMLS:C0027651 - FACTA Search

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Query: UMLS:C0027651 (tumor)
685,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The binding of urokinase-type plasminogen activator (u-PA) to a specific cell surface receptor (uPA-R) has been shown to enhance plasminogen activation, a process involved in extracellular matrix degradation and cell migration during angiogenesis and tumor growth. We investigated the expression of u-PA and uPA-R in renal cell carcinomas (n = 11). By immunohistochemistry using monoclonal and polyclonal anti-uPA-R antibodies, we found that tumoral capillary endothelial cells (von Willebrand factor and CD31 positive cells) overexpressed uPA-R, whereas vascular endothelial cells of the normal human kidney do not. In addition, tumor-associated macrophages (CD68-positive cells) strongly expressed uPA-R. In contrast, few tumoral cells and stromal fibroblasts expressed uPA-R. By in situ hybridization using a cDNA S35-labeled probe specific for uPA-R, we confirmed the local expression of uPA-R messenger RNA. We also detected the induction of u-PA in tumoral capillary endothelial cells and in tumor-associated macrophages. In two cases, tumoral cells themselves were also stained by anti-u-PA antibodies in focal areas. Finally tissue-type plasminogen activator (t-PA) was also overexpressed by tumoral capillary endothelial cells as compared with endothelial cells of normal human kidney vessels. These findings indicate an active invasive phenotype of endothelial cells in renal cell carcinoma and suggest a role for the plasminogen activation system in tumoral angiogenesis and invasion.
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PMID:Endothelial and macrophage upregulation of urokinase receptor expression in human renal cell carcinoma. 902 4

The pathological features of 11 nodules of early hepatocellular carcinoma (EHCC) were studied. Their macroscopic features resembled those of adenomatous hyperplasia and differed from those of advanced hepatocellular carcinomas (AHCC). The EHCC extended along the hepatic lobular structure and lacked expansive growth. The endothelial cells in the sinusoids of EHCC did not react to Ulex europaeus agglutinin 1 (UEA1) like adenomatous hyperplasia or other liver parenchyma, whereas the endothelial cells in the AHCC did react to UEA1. Immunohistochemically, CD68-positive Kupffer cells were noted in the sinusoids of EHCC, whereas in the AHCC Kupffer cells were not seen. Tumor emboli in the portal vein and intrahepatic metastases were not identified in EHCC, which seemed to be carcinoma-in-situ or a microinvasive stage of hepatocarcinogenesis.
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PMID:Early hepatocellular carcinoma macroscopically resembling adenomatous hyperplasia: pathological resemblance to carcinoma-in-situ. 905 92

Epithelioid hemangioendothelioma (EHE) is best considered a vascular neoplasm of intermediate malignancy. Although usually progressive, the clinical course is highly unpredictable. The present communication describes a case of extensive recurrent hepatic EHE, limited to the liver allograft and initially manifest as an insidious seeding of individual tumor cells in areas of perivenular inflammation associated with rejection. A detailed immunophenotypic characterization of this and a small series of EHE was carried out in an effort to highlight subtle disease recurrence and to gain possible insights into tumor biology associated with this intriguing disease. In a series of five cases of hepatic EHE, CD34 (QB-END/10) was found to be more sensitive than Factor VIII (F-VIII) for recognition of the disease, similar to previous reports. The former diffusely and distinctly stained both epithelioid and dendritic tumor cells, whereas staining for the latter was focal, indistinct, and showed a high background. Although the tumor cells were negative for some markers of dendritic or macrophage maturation, such as CD1a, S100 protein, Mac 387, CD68, and LN3, there was marked infiltration of hepatic EHE by factor XIIIa + (F-XIIIa), Mac 387+, CD68+, and LN3+ macrophages and dendrocytes, most of which were interpreted as reactive. The "reactive" macrophage and dendrocyte populations were present throughout the fibrotic stroma and intermingled with the epithelioid clusters of EHE. Interestingly, a small subset of tumor cells coexpressed CD34 or F-VIII and F-XIIIa, the last of which is normally restricted to cells of the monocyte/macrophage lineage and cytokine activated microvascular endothelium in vitro. The known association of F-XIIIa+ dendrocytes with granulation tissue, repair and fibrogenesis, and the modulation of F-XIIIa and F-VIII expression by inflammatory cytokines led us to speculate that EHE lesions may derive from primitive "reticuloenothelial" cells that can differentiate along endothelial and dendritic pathways. The EHE lesions may represent a neoplastic analogue of wound healing. Thus, the variability in F-VIII staining, the strong expression of CD34, the infiltration of EHE lesions with F-XIIIa+ dendrocytes, and the coexpression of CD34 and F-XIIIa on a subset of tumor cells may have an important biological basis.
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PMID:Hepatic epithelioid hemangioendothelioma: biological questions based on pattern of recurrence in an allograft and tumor immunophenotype. 906 May 95

Many of the antigens commonly investigated in histopathology can be enhanced by microwave pretreatment (MWPT) of formalin fixed, paraffin embedded tissue sections. We developed a double labeling method using microwave heating to detect otherwise undetectable nuclear antigens combined with immunohistochemistry (IHC) of cytoplasmic or membranous antigens that do not benefit from MWPT. We used the same primary antibody solutions used in single antibody IHC. The staining technique is based on the alkaline phosphatase anti-alkaline phosphatase (APAAP) and the labeled avidin-biotin (LSAB) methods. Four different protocols were tested, each modifying the sequence of MWPT, APAAP and LSAB staining. In this study Ki67, estrogen receptor, progesterone receptor, c-neu, CD68 and desmin primary antibodies were used in routinely formalin fixed, paraffin embedded tissues of 50 tumor specimens. MWPT followed by LSAB for microwave enhanced antigens and APAAP for antigens that cannot be enhanced by MWPT gave the best double staining results. This method improves characterization of tumor cell features from paraffin embedded tissue and should aid analysis of tumor differentiation, receptor status and nuclear proteins in the single cells in archival tissues.
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PMID:Immunohistochemical double staining of microwave enhanced and nonenhanced nuclear and cytoplasmic antigens. 906 4

The present study was to ascertain the immunomodulating and anti-tumor effects of Ganoderma (G.) lucidum. Polysaccharides (PS) from fresh fruiting bodies of G. lucidum (PS-G) were isolated and used to potentiate cytokine production by human monocytes-macrophages and T lymphocytes. Our results had shown that the levels of interleukin (IL)-1 beta, tumor necrosis factor (TNF)- alpha, and IL-6 in macrophage cultures treated with PS-G (100 micrograms/ml) were 5.1-, 9.8- and 29-fold higher, respectively, than those of untreated controls. In addition, the release of interferon (IFN)- gamma from T lymphocytes was also greatly promoted in the presence of PS-G (25-100 micrograms/ml). Furthermore, these cytokine-containing mononuclear cell-conditioned media (PSG-MNC-CM) were found to suppress the proliferation and clonogenicity of both the HL-60 and the U937 leukemic cell lines. DNA labeling and gel electrophoresis showed that treatment with PSG-MNC-CM markedly induced leukemic-cell apoptosis. Flow-cytometric analysis revealed that few (2.3 +/- 0.8%) apoptotic cells were seen in the control cultures, while PSG-MNC-CM treatment resulted in a significant increase in the apoptotic population both in the HL-60 (38.3 +/- 4.5%) and in the U937 (44.5 +/- 3.8%) cells. In addition, 40 to 45% of the treated leukemic cells were triggered to differentiate into mature monocytic cells expressing CD14 and CD68 surface antigens. However, PS-G alone had no such effects even at a higher dose of 400 micrograms/ml. Since untreated macrophages and T lymphocytes produced little or no cytokine, and normal MNC-CM did not suppress leukemic cell growth, it was suggestive that the anti-tumor activity of PSG-MNC-CM was derived from the elevated levels of cytokines. Antibody-neutralization studies further revealed that the anti-tumor cytokines in the PSG-MNC-CM were mainly of TNF- alpha and IFN- gamma, and these 2 cytokines acted synergistically on the inhibition of leukemic-cell growth.
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PMID:The anti-tumor effect of Ganoderma lucidum is mediated by cytokines released from activated macrophages and T lymphocytes. 909 52

CD34 and factor XIIIa (FXIIIa) antibodies delineate subsets of embryonic dendritic stromal stem cells that persist in adult mesenchyme. CD34 stains interstitial and adventitial dendritic cells that may function as multipotential precursor cells. FXIIIa+ dendrophages are tissue histiocytes active in tissue repair. Angiomatoid malignant fibrous histiocytoma (AMFH) is an enigmatic fibrohistiocytic tumor with limited vascular features. We examined an unusual soft tissue tumor from the nasolabial subcutis of a 57 year old man that showed histologic features of AMFH. Most of the tumor cells expressed CD34. 10-30% of the tumor cells were FXIIIa+ dendrophages. Sinusoidal areas were largely composed of FXIIIa+ cells that also expressed HLA-DR and CD68 suggesting macrophage differentiation. CD31 and Factor VIII antigen highlighted capillaries and single cells among the CD34+ tumor cells. The vessels had actin+ myopericytes and there were single actin+ tumor cells. Electron microscopy showed primitive dendritic cells and fewer histiocyte-like cells. The Ki 67 index was 15% including both FXIIIa+ and CD34+ cells. The patient is disease free three years after wide excision. We conclude that this AMFH-like neoplasm is a fibrohistiocytic tumor in which CD34+ fibroblast-like precursors and FXIIIa+ tissue dendrophages combine to build both sinusoidal tissue with endothelial and macrophage elements as well as capillary vascular tissue that is invested with myopericytes. Study of additional AMFH lesions from this standpoint is desirable.
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PMID:An unusual soft tissue tumor with features of angiomatoid malignant fibrous histiocytoma composed of bimodal CD34 and factor XIIIa positive dendritic cell subsets. CD34 and factor XIIIa in angiomatoid MFH. 911 73

We evaluated the occurrence, tissue distribution, and prognostic value of tumor-associated macrophages in 121 papillary thyroid carcinomas using immunohistochemical staining with anti-CD68 antibody in archival paraffin-embedded sections. Lymphocytic infiltration and dendritic cell presence were also evaluated. Three groups were identified according to the presence and characteristics of macrophages: 1) tumors without evidence of infiltrating macrophages: (n = 35); 2) tumors with infiltrating macrophages but no evidence of neoplastic cells phagocytosis (n = 68); and 3) tumors with infiltrating macrophages and in situ evidence of active neoplastic cell phagocytosis (n = 18). Neoplastic cell phagocytosis by macrophages was positively correlated with both lymphocytic infiltration and dendritic cells (P = 0.0000), whereas it was negatively correlated with vascular invasion (P = 0.0032). Distant metastases developed in none of the 18 tumors with neoplastic cell phagocytosis, but occurred in 15 of 103 of the remaining tumors (P = 0.0647) and were significantly and negatively associated with lymphocytic infiltration or dendritic cells. The present study indicates, therefore, that immune reaction, involving neoplastic cell phagocytosis by macrophages and lymphocytic infiltration, plays a role in the development of distant metastases in patients with papillary thyroid cancer.
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PMID:In situ evidence of neoplastic cell phagocytosis by macrophages in papillary thyroid cancer. 914 59

Inflammatory malignant fibrous histiocytoma (IMFH), consisting of large, atypical histiocyte-like cells set amidst an inflammatory backdrop of eosinophils, neutrophils, lymphocytes, and xanthoma cells, can be difficult to distinguish from Hodgkin's disease and non-Hodgkin's lymphoma, particularly of the Ki-1 anaplastic large-cell type in small biopsy specimens. This problem is becoming more prevalent with the use of needle biopsies guided by computed tomography for definitive diagnosis. For this reason, we studied the expression of a battery of leukocyte markers in IMFH to evaluate whether they could serve as an independently reliable means of distinguishing amongst the three neoplasms. Eight examples of histologically typical IMFH were stained with a number of leukocyte markers that included CD30 (BerH2), CD15 (leuM1), CD45/ CD45RB (2B11,PD7/26/16), CD43 (leu 22), CD45RO (A6), CD20 (L26), and CD68 (KPI). The large anaplastic tumor cells within IMFH consistently lacked CD30, CD15, CD45/CD45RB, CD43, CD45RO, and CD20. In one case, the anaplastic cells expressed CD68. Benign histiocytes within IMFH expressed CD68 and displayed variable expression of CD15, CD45/CD45RB, and CD43. The reactive lymphocytes consisted mostly of scattered small T cells with a few B cells, mainly within lymphoid aggregates. We conclude that the immunophenotypic profile of the anaplastic cells in IMFH (lack of CD15, CD30, CD43, CD45/CD45RB, CD45RO, CD20) differs from most cases of Hodgkin's disease (ICD30+, CD15+/-) and from Ki-1 anaplastic large cell lymphoma (CD30+, CD45/CD45RB+/-, CD43+/-, CD45RO+/-, CD20-/+). Immunohistochemistry is an important diagnostic adjunct, provided care is taken to exclude benign histiocytes and inflammatory cells from consideration.
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PMID:Inflammatory malignant fibrous histiocytoma: distinction from Hodgkin's disease and non-Hodgkin's lymphoma by a panel of leukocyte markers. 916 Mar 7

To examine the differentiation and proliferative activity of tumor cells, 30 osteosarcomas, including osteoblastic, chondroblastic, fibroblastic, malignant fibrous histiocytoma-like, telangiectatic, giant cell-rich low-grade central, and epithelioid types, were studied immunohistochemically. A variable number of tumor cells in all cases showed osteocalcin immunoreactivity. In four preparations of the frozen sections, osteoblastic, fibroblastic, and chondroblastic tumor cells were positive for bone-type alkaline phosphatase antibody 2D3. S-100 protein immunoreactivity was found not only in seven tumors of the chondroblastic type, but also in four of nine osteoblastic tumors and each of the low-grade central, giant cell-rich, and epithelioid types. A histiocytic marker, CD68, was negative for tumor cells in all cases. Some cells of 17 tumors were positive for desmin and/or alpha-smooth muscle actin; this was regarded as an indication of myofibroblastic differentiation. Tumor cells of the epithelioid type and those of two osteoblastic tumors expressed cytokeratin (CAM5.2) and epithelial membrane antigen. Proliferating-cell nuclear antigen (PCNA) reactivity was found in the cell nuclei of 22 tumors, most of which were high grade. Many cells in six high-grade tumors also showed the nuclear staining for p53 protein. Of these tumors, PCNA and p53 positivities tended to be more numerous in osteoblastic cells, atypical spindle-shaped, and bizarre giant cells than in well-developed chondroid cells. From these findings, osteosarcomas are concluded to be composed basically of osteoblastic cells, that are indispensable for diagnosis of osteosarcomas, with a variable number of chondroblastic, myofibroblastic, and, rarely, epithelioid cells, and this manifold cellular differentiation corresponds to the histological and clinical diversities. The osteoblastic, fibro- or myofibroblastic, and undifferentiated cells mainly participate in proliferation of osteosarcomas. The p53 gene alterations may play a part in the neoplastic transformation and proliferation of osteosarcomas.
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PMID:Histological and immunohistochemical diversities, and proliferative activity and grading in osteosarcomas. 916 46

Central giant cell granulomas (CGCGs) are jaw tumors of unknown origin that often exhibit an aggressive, though unpredictable, clinical course. The purpose of this study was to determine the immunoprofile of the mononuclear cells that seem to be responsible for the biologic behavior of these tumors. Numbers of cells in cell cycle were also determined and compared in clinically aggressive and non-aggressive CGCGs. Sixteen aggressive and 12 non-aggressive CGCGs were immunohistochemically stained with antibodies to CD34, CD68, factor XIIIa, alpha-smooth muscle actin, prolyl 4-hydroxylase, Ki-67, and p53 protein. Cell populations and numbers of cells in cell cycle were determined through microscopic quantitative assessment. CD34-positive cells were limited to support vessels. CD68-positive mononuclear cells constituted a small population of cells in all tumors. With two exceptions, factor XIIIa-positive cells were rarely seen. Alpha-smooth muscle actin staining was present in approximately half the tumors, and occasionally large numbers of positive cells were seen. Most mononuclear cells were positive for fibroblast-associated antigen. No phenotypic differences were detected between aggressive and non-aggressive tumors. P53 protein did not appear to be overexpressed in CGCGs. Ki-67 staining showed that only mononuclear cells were in cell cycle, and that there were no differences between aggressive and non-aggressive tumors. We conclude that CGCGs are primarily fibroblastic (and myofibroblastic) tumors in which macrophages appear to play a secondary role. Tumor cells show no differentiation toward endothelial cells or macrophage-related dendrocytes (factor XIIIa). Cellular phenotypes and numbers of cells in cell cycle are similar in both aggressive and non-aggressive tumors.
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PMID:Central giant cell granulomas of the jaws: phenotype and proliferation-associated markers. 917 89

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