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Using cell size, cell density, and microscopic growth pattern, 20 duodenal stromal tumors were initially separated into benign and malignant categories. The 10 histologic benign tumors had uniform spindle cells, low cellularity, and an organoid pattern. All had round eosinophilic collagen blobs scattered among the spindle cells, were 4.5 cm or less in maximum diameter, and had two or fewer mitoses per 50 high-power fields (HPF). None metastasized or recurred during a median follow-up of 7 years. In contrast, the 10 histologically malignant tumors were highly cellular, all had two or more mitoses per 50 HPF, and all but one had diameters of 4.5 cm or greater, the exception being 4 cm. Eight cases also had benign-appearing areas, usually submucosal. Eight patients died with disease a median of 31 months after resection, almost all with liver metastases. One patient is alive with metastasis at 13 years. The patient with the 4-cm malignant tumor is disease free at 49 months. All 15 cases were strongly vimentin positive, 11 had S-100 protein, and seven had the CD34 marker. None were desmin or actin positive. No immunophenotype separated benign from malignant. The proliferation marker, proliferating cell nuclear antigen, correlated with histologic diagnosis and clinical outcome, but Ki-67 did not. Based on light microscopic features alone, benign and malignant duodenal stromal tumors can be separated from each other. Tumors with large cells and an organoid pattern are predictably benign; in this study, these tumors measured 4.5 cm or less in diameter and had fewer than 2 mitoses per 50 HPF. Highly cellular tumors with small cells and little or no organoid pattern are malignant. They usually have a diameter greater than 4.5 cm and more than two mitoses per 50 HPF, and they are usually fatal. Immunostaining for cytoplasmic proteins and proliferation markers offers no additional prognostic information to the light microscopic appearances. These conclusions apply only to duodenal tumors; whether they also apply to stromal tumors of the jejunum and ileum is not known.
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PMID:Stromal tumors of the duodenum. A histologic and immunohistochemical study of 20 cases. 752 72

One hundred and twenty-four localized prostate cancer patients operated on at Johns Hopkins Hospital (JHH) since 1975 were identified. The sample was optimized for evaluation of prostate cancer progression. Based upon accurate clinical histories, these radical prostatectomy patients included 50 progressors and 74 non-progressors using appearance of serum PSA as an indication of recurrence (mean follow-up = 8.6 +/- 1.8 years, range 7-15 years). All patients included in the study had no involvement of their seminal vesicles or lymph nodes at the time of prostatectomy. Average time to progression was 3.6 +/- 2 years, range of 1-8 years. Using paraffin-embedded specimens, several five micron sections were cut and placed on Probe-On slides; one slide was H&E-stained and the other was Feulgen-stained. The H&E and Feulgen-stained slides were screened and "dotted" by pathologists at JHH and CytoDynostics, Inc. A CAS-200 Image analysis system (Cell Image Systems, Elmhurst, IL) equipped with a Cell Measurement Program version 1.2 beta, was used to capture the Feulgen-stained images and to perform the calculations. From the "dotted" areas, 150 cancer cells were selected for measurement of DNA content and 27 nuclear morphometric shape and size factors, including 21 Markovian chromatin texture variables. Additional sections were used for immunochemistry staining with an alkaline phosphatase streptavidin-biotin complex stain to detect and quantitate cancer cells binding monoclonal antibodies directed against proliferating cell nuclear antigen (PCNA) and HER-2/neu antigen. All data were entered into a statistical program (STATA) for further analysis and univariate and multivariate statistical analysis was performed using logistic regression and its stepwise variant. The biomarkers of greatest utility to detect progressors when analyzed univariately included post-operative Gleason score (p = < 0.0001), HER-2/neu antigenicity (p = 0.0147), CAS-200 DNA ploidy (p = 0.008), and twelve Markovian nuclear texture and shape features (p = < 0.0001), whereas PCNA (p = 0.160) failed. The optimal set of nuclear morphometry progression tumor features were selected using backward stepwise logistic regression estimate analysis which drops variables due to collinearity. Although post-operative Gleason score is a strong univariate predictor of progression, DNA ploidy and HER-2/neu contributed significantly to further stratification of higher risk groups within the low Gleason score subpopulation. The best Markovian features combined with post-operative Gleason score generated sensitivity = 90%, specificity = 96%, positive predictive value = 94%, negative predictive value = 93% and the area under the receiver operator curve was 0.975.
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PMID:Quantitative nuclear morphometry, Markovian texture descriptors, and DNA content captured on a CAS-200 Image analysis system, combined with PCNA and HER-2/neu immunohistochemistry for prediction of prostate cancer progression. 752 56

Surrogate endpoint biomarkers (SEBs) are needed in clinical chemoprevention trials to avoid the excessively long study periods and high costs associated with the use of cancer incidence reduction as an endpoint, particularly with relatively slow-growing tumors such as prostatic adenocarcinoma. SEBs should be directly associated with the evolution of neoplasia, and develop with high frequency in abnormal cells of susceptible individuals. If SEBs can be modified by a particular intervention regimen in short-term studies, the rationale for carrying out long-term studies may be strengthened. The consensus panel identified a small and manageable group of biomarkers measured in tissue or serum as the most promising in prostate cancer chemoprevention, including (1) prostate specific antigen (PSA); (2) morphometric markers, such as nuclear size and roundness; (3) proliferation markers, such as MIB-1 and PCNA; (4) nuclear DNA content (ploidy); (5) oncogene c-erbB-2 (HER-2/neu) expression; (6) angiogenesis; and (7) high-grade prostatic intraepithelial neoplasia (PIN). Information regarding many of these and other biomarkers is limited, calling for further investigation. Also, these factors, chosen chiefly for their proven or proposed utility as prognostic factors, may be less useful as SEBs. It was agreed that concurrent study of numerous markers rather than single markers allows comparison of their relative utility, including assessment of ease of quantitation and the sensitivity, specificity, and positive and negative predictive value.
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PMID:The most promising surrogate endpoint biomarkers for screening candidate chemopreventive compounds for prostatic adenocarcinoma in short-term phase II clinical trials. 752 57

Tumour-associated cell-surface glycoprotein is associated with tumour progression in gastric cancer. We investigated the biological significance of tumour-associated cell-surface glycoprotein, determined by the binding of Helix pomatia agglutinin (HPA), with regard to survival time and to the malignant potential of cancer cells in serosally invasive gastric cancer in 119 patients. HPA was positively stained in 75 of 119 patients (63.0%) with gastric cancer with serosal invasion. In patients with HPA-positive tissue, the tumour was larger than in HPA-negative cases and was frequently located in the middle third of the stomach. The incidence of lymph node metastasis was higher than in patients with HPA-negative tissue. There were no differences between the cases staining negatively and positively with HPA with respect to the other factors examined. Gastric cancer tissues with HPA-positive staining revealed a higher positive rate of abnormal p53 staining and a higher concentration of proliferating cell nuclear antigen (PCNA) labelling. The survival time of the patients with HPA positive staining was shorter than for those whose tissues were HPA negative. Thus, tumour-associated cell-surface glycoprotein is apparently closely related to the malignant potential of serosally invasive gastric cancer.
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PMID:A tumour-associated cell-surface glycoprotein accompanying p53 overexpression and higher growth potential for gastric cancer. 753 20

An epizootic of pigmented subcutaneous spindle cell tumors affected nearly 25% of the adult gizzard shad (Dorosoma cepedianum) sampled from Lake of the Arbuckles in central Oklahoma over a 2 year period. Grossly, the tumors were primarily distributed over the head, trunk and fins as superficial raised masses that were almost always darkly pigmented. Histologically, they were located in the dermis, had a variable amount of connective tissue, and consisted of cells in a variety of forms and arrangements. Most tumors were composed of fusiform or spindle cells arranged in wavy bundles, whirling patterns or interwoven fascicles. Pigmentation was attributed to large dense deposits of melanin or to scattered individual melanin-containing cells. Immunohistochemical detection of proliferating cell nuclear antigen revealed a high proliferative activity in the spindle cells. Electron microscopy showed that the tumors were composed of several cell types, including host reactive cells, melanocytes in stages of maturity, and fibroblast-like cells. Tumor cells had neither cell-to-cell junctions nor an external lamina. Although the cell of origin of the tumors was not identified, evidence points toward melanocytes or, possibly, nerve sheath cells. However, an origin from fibroblasts or some other poorly differentiated cell cannot be ruled out. The etiology of the tumors was not determined. Fractionation of lake water and sediment samples followed by GC-MS analysis revealed no carcinogenic compounds. A retroviral etiology is unlikely because assays for reverse transcriptase in tumor homogenates were negative, and no evidence of viral particles was found in specimens examined by electron microscopy.
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PMID:Pigmented subcutaneous spindle cell tumors in native gizzard shad (Dorosoma cepedianum). 754 76

To assess the histological grade in benign and malignant cartilage tumors of bone by more objective methods, we examined the differentiation and proliferative activity of tumor cells in six enchondromas, five chondroblastomas, and 13 chondrosarcomas immunohistochemically. A variable number of cells in all tumors showed S-100 protein and vimentin immunoreactivity. In fully differentiated cartilage of enchondromas and low grade chondrosarcomas, tenascin, which is an extracellular matrix glycoprotein, was present in small amounts or absent but was increased at the periphery of tumor lobules and even in the matrix throughout the high grade chondrosarcomas. Higher rate and intensity of proliferating cell nuclear antigen (PCNA) reactivity were found in chondrosarcomas, especially in spindle-shaped cells of high grade tumors, than in enchondromas. The distribution of PCNA-positive cells almost corresponded to the regions with tenascin reactivity. One tumor of high grade chondrosarcoma showed p53 protein immunoreactivity. Aberrant expression of cytokeratin was observed in four chondroblastomas. The expression of desmin was identified in relatively large proportions of enchondromas and chondrosarcomas, regardless of their benign or malignant nature and histological grade. Smooth muscle or muscle-specific actins also were present in a smaller number of tumors. Based on these findings, it is concluded that unusual staining characteristics were present, in addition to those of a chondroblastic nature, in the cartilage tumors of bone. Tenascin and PCNA positivity of various degrees in all chondroblastomas may suggest that they are chondrogenic tumors having a relatively high proliferative activity, albeit their benign clinical course. Proliferative activity of tumor cells in enchondromas and chondrosarcomas correlated well with their histological grade. Tenascin may play a role in promoting tumor cell proliferation of cartilagenous neoplasms and, on the other hand, the alterations of extracellular matrix involving tenascin synthesis seem to be a result of tumor development.
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PMID:Differentiation and proliferative activity in benign and malignant cartilage tumors of bone. 754 39

Tumour growth depends on neovascularisation and tumour cell proliferation. Factor VIII-related antigen (F-VIII RA) localises to vascular endothelium. Expression of proliferating cell nuclear antigen (PCNA) is correlated with cell proliferation. We investigated the correlation between the expression of these antigens and prognosis in gastric carcinoma. A total of 108 specimens resected from patients with gastric carcinoma were investigated by staining with monoclonal antibodies against F-VIII RA and PCNA. Microvessel count (MVC; the mean number of microvessels in the five areas of highest vascular density at 200 x magnification) and PCNA labelling index (PCNA LI; percentage of positive cells in more than 500 tumour cells) were determined. The results showed that prognosis was significantly worse in patients who had a tumour with a high MVC (16 or greater) or a high PCNA LI (42% or greater) than in those patients who had a tumour with a low MVC (less than 16) or a low PCNA LI (less than 42%). Furthermore, MVC was significantly associated with the risk of hepatic recurrence. In conclusion, both MVC and PCNA LI may be good prognostic indicators in patients with gastric carcinoma.
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PMID:Tumour angiogenesis and tumour cell proliferation as prognostic indicators in gastric carcinoma. 754 71

Cell proliferation and vascularization play an important role in the metabolic functions of normal and malignant tissues. Tumor cell proliferation and density of microvessels (DM) in 33 specimens of oral squamous cell carcinoma (SCC) were assessed by immunohistochemical staining of proliferating nuclear cell antigen (PCNA) and JC/70A, respectively. Their staining patterns were compared to the clinicopathologic findings. The PCNA labeling index (LI) showed significantly higher values in advanced carcinomas (T3 and T4) (mean, 20.19 +/- 12.79) than in early carcinomas (T1 and T2) (mean, 9.58 +/- 4.01; P < 0.01). The DM (mean, 105.92 +/- 22.65) and PCNA LI (mean, 25.69 +/- 13.32) of tumors with lymph node metastasis were significantly higher than in tumors without nodal involvement (DM, mean, 72.6 +/- 24.30; P < 0.01) (PCNA LI, mean, 10.25 +/- 3.99; P < 0.001). Marginal DM values were significantly correlated and directly proportional to the mode of tumor invasion. Evaluation of PCNA and DM at the periphery of the tumor may help to identify oral SCC that have higher malignant potential.
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PMID:Cell proliferation and tumor angiogenesis in oral squamous cell carcinoma. 754 66

To evaluate the prognostic significance and clinicopathologic correlation of proliferative activity in patients with hepatocellular carcinoma, Ki-67 antigen expression was examined using immunohistochemical staining with monoclonal antibody MIB1. Seventy-two patients (65 men, 7 women; age range 24-77 years, mean, 52 years) having hepatocellular carcinoma surgically resected were studied. Tumor and nontumorous tissues were stained with monoclonal antibody MIB1 with microwave oven pretreatment. Tumor and nontumor MIB1 (T-MIB1 and NT-MIB1) scores were assessed by counting the positive staining nuclei per 1,000 cells. The T-MIB1 score ranged from 5-630 per 1,000 cells (mean +/- standard deviation [SD] = 145 +/- 162). It was found to be significantly higher in less well-differentiated tumors (Edmondson's grades III and IV) than in well-differentiated ones (Edmondson's grades I and II) (P = .017). The T-MIB1 score was also higher in nonencapsulated tumors than in encapsulated ones, although it did not reach statistical significance (P = .069). It had no influence on tumor size, tumor invasiveness, the background disease in the nontumorous livers, patients' HBsAg status, or serum alpha-fetoprotein levels. Diseases in the nontumorous livers or patients' HBsAg status had no influence on the NT-MIB1 scores. When the tumors were stratified into two groups with T-MIB1 score < or = 20 and T-MIB1 score > 20, those patients with score < or = 20 had significantly longer disease-free survival (DFS) than those with scores > 20 (median DFS: 34 months and 4.7 months, respectively; P = .011). In addition, MIB1 and PCNA were closely correlated (P < .01). The authors conclude that proliferative activity in hepatocellular carcinoma, as defined by MIB1 immunohistochemical analysis, is significantly related to tumor cellular differentiation. It is also a potentially valuable prognostic factor in patients with this tumor.
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PMID:Ki-67 antigen expression in hepatocellular carcinoma using monoclonal antibody MIB1. A comparison with proliferating cell nuclear antigen. 754 66

Eicosanoids have been implicated in colon carcinogenesis, but their role remains unclear. The levels of PGE2 are elevated in colon cancer tissues and in blood draining colon tumors. The effect of eicosanoids on the proliferation of colonic cells is unknown. We studied the effect of several prostaglandins (PGs) and leukotriene (LT)B4 on the proliferation rate of the human colon adenocarcinoma cell lines SW1116 and HT-29 and of 16,16-dimethyl PGE2 (dmPGE2) on the colon of BALB/c mice. PGs E2, F2 alpha, I2, the methyl ester of PGE2, dmPGE2, and LTB4 (10(-10), 10(-8), 10(-6) M), administered for up to 72 h, stimulated cell proliferation in SW1116 cells and all but PGF2 alpha and PGI2 stimulated proliferation in HT-29 cells. The proliferative effect was time- and concentration-dependent. However, in SW1116 cells the response to PGs was 'bell-shaped', being maximal at 10(-8) M, with the 10(-10) and 10(-6) M concentrations being less effective. In HT-29 cells, the addition of methyl groups to the PGE2 molecule increased the proliferative effect. None of these eicosanoids affected the distribution of these cells in the cell cycle or their rate of programmed cell death (apoptosis). dmPGE2 stimulated 3.6-fold the proliferation of colonocytes in normal BALB/c mice. This was determined by bivariate flow cytometric analysis of the expression of proliferating cell nuclear antigen (PCNA) in virtually pure populations of mouse colonocytes. dmPGE2 did not alter the cell cycle distribution of these cells. We conclude that several PGs as well as LTB4 stimulate the proliferation of human colon carcinoma cells in vitro, while dmPGE2 has a similar effect on mouse colonocytes in vivo. These findings raise the possibility that eicosanoids may contribute to colonic carcinogenesis by stimulating the proliferation rate of tumor cells in the colon.
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PMID:Selected eicosanoids increase the proliferation rate of human colon carcinoma cell lines and mouse colonocytes in vivo. 754 86

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