tbuckley/cabot-search huggingface dataset:
Abstract P1-07-16: Liver derived epithelial cells as source of false positive circulating tumor cells in early breast cancer
Authors: L Habets, W Körber, B Frenken, M Danaei, M Kusche, U Peisker, T Kroll, K Pachmann
Journal: Cancer Research (2012)

Abstract The MAINTRAC technique as introduced by our coworkers from Jena (RBC lysis, fluorometric detection and analysis on Olympius ScanR) detects more circulating epithelial cells than techniques using enrichment. Also cells with a low EPCAM expression are detected and not only the typical cells with bright expression found after immunomagnetic enrichment. The relative cheapness and reproducibility allows frequent monitoring during and after therapy Using 3 colour detection (EPCAMfitc, DAPI, Vimentin PE) living and dead circulating epithelial cells in EMT, or cells in EMT with stemcell markers (EPCAMfitc, Vimentin-PE, CD44PacBlue) can be detected. In early breast cancer (n = 135) cells can be found in 60% of patients and in 40% higher cell counts (&amp;gt;100 ml are detectable. A control population(n = 100) showed low numbers in 98% (e.g (&amp;lt;100 CECin 1 ml blood). Expression of the mesenchymal marker (vimentin) ranges between 10 and 40% with different expression. CD44 shows also a wide range of expression. Two main cell types can be distinguished: type 1 shows generalized but weaker expression patterns and a second type with very bright dotted expression. The clinical relevance of these subsets is not known and their behavior under therapy has not been analysed in depth yet. In advanced breast cancers high cell counts were detectable in most patients with a less agressive disease course. In the rapidly progressing unfavorable subtypes (TN and Her2+. HRneg) less or none cells were found. During crossvalidation in non cancer patients we found high cell numbers in several forms of liver affections (n = 108). The expression patterns of markers on these cells were not differing from those in cancer patients. So this same cell type merging EMT, stemcell an hypoxic stress markers is detectable in advanced and early breast cancer (n = 40) and in benign disease. These cells disappear or decrease after response to chemo or anti-hormonal therapy in cancer or antioxidant therapy in NAFLD. We believe that the evasion of these cells is driven by the same force in cancer as in non cancer conditions. We suggest that this are the wellknown hypoxic and hyperacidic conditions causing epithelial mesenchymal transition. Cancer cell hijack this functions occurring normally under these conditions to survive and to facilitate evasion. More comprehensive analysis (four colour analysis on the AMNIS Flowsight) is needed and should show differences in expression patterns of liver derived epithelial cells (LDEC) and real tumor derived epithelial cells (TDEC). Further clarification of these phenomena should give new insights of the biological events in early disease and the possibilities and reliability of “fluid biopsy”. Citation Information: Cancer Res 2012;72(24 Suppl):Abstract nr P1-07-16.
Abstract 3991: Protein phosphatase 2A (PP2A) downregulation is associated with androgen-independent and aggressive phenotypes in prostate cancer
Authors: Arun Bhardwaj, Sanjeev K. Srivastava, Seema Singh, Sumit Arora, Richard E. Honkanen, William E. Grizzle, Eddie Reed, Ajay P. Singh
Journal: Cancer Research (2012)

Abstract First line of therapy for advanced prostate cancer (PCa) is androgen-deprivation through surgical or chemical castration; however, in majority of cases, tumors relapse in an androgen-independent (AI) form. Once the PCa has recurred in AI form, it progresses to a highly aggressive disease with frequent metastasis and poses an increased risk of morbidity and death. Previously, we demonstrated that PPP2CA, which encodes for alpha-isoform of the protein phosphatase 2A (PP2A) catalytic subunit, is downregulated in prostate cancer. Furthermore, we showed that PP2A activity is inversely associated with AI growth of PCa cells through a novel mechanism, whereby loss of PP2A-mediated checkpoints leads to the activation of Akt and ERK and partially sustains androgen receptor (AR) signaling under steroid-deprived condition. Since AI phenotype of PCa is associated with enhanced metastatic potential, we have investigated, in this study, a role of PPP2CA in the aggressive behavior of the PCa cells. For this, we overexpressed PPP2CA in AI (C4-2 and PC-3) PCa cells, while silenced its expression in AD (LNCaP) PCa cells. We observed that overexpression of PPP2CA in C4-2 and PC-3 cells not only decreased their AI growth and clonogenic ability, but also led to reduced motility and invasion and enhanced cell-cell interaction. Conversely, we observed increased cell motility and invasion and decreased cell-cell interaction upon PPP2CA silencing in LNCaP cells. Immunoblot analyses demonstrated gain of epithelial and loss of mesenchymal markers in PPP2CA-overexpressing PCa cells or vice versa indicating a role of PP2A in opposing epithelial to mesenchymal transition (EMT). Altogether, these studies provide evidence for a functional role of PPP2CA in aggressive behavior of AI PCa cells. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 3991. doi:1538-7445.AM2012-3991
Will Your Cheese Taste Like a Hockey Puck With Stricter Food Labels?
Authors: S. Jenks
Journal: JNCI Journal of the National Cancer Institute (1992)

Journal Article Will Your Cheese Taste Like a Hockey Puck With Stricter Food Labels? Get access Susan Jenks Susan Jenks Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 84, Issue 5, 4 March 1992, Pages 292–293, https://doi.org/10.1093/jnci/84.5.292 Published: 04 March 1992
927 ROLE OF TUMOR NECROSIS FACTOR ALPHA, INTERLEUKIN-18 AND HLA-G GENE POLYMORPHISMS IN THE PROGRESSION OF LIVER FIBROSIS IN CHRONIC HEPATITIS C PATIENTS
Authors: F. Souza, M.V. Carneiro, A.C. Teixiera, S.C. Ferreira, L.A. Marano, M.G. Villanova, C.T. Mendes-Junior, S. Zucoloto, E.A. Donadi, A.D.L.C. Martinelli
Journal: Journal of Hepatology (2012)
Ligation of the Inferior Vena Cava in the Prevention and Treatment of Pulmonary Embolism
Authors: E. Everett O'Neil
Journal: New England Journal of Medicine (1945)

THE interruption of deep venous pathways in the treatment and prevention of pulmonary embolism has come to be a generally accepted surgical procedure. The preferred sites for division when deep venous thrombosis is present, or when pulmonary infarction has taken place without evident thrombosis but the latter is suspected, have been the superficial femoral veins, the common femoral veins and, in a few cases, the external and common iliac veins. In the majority of cases, section of the above-named vessels has been adequate to prevent further extension of thrombosis, with its possible detachment of a fatal or near-fatal embolus. It . . .
A Defect in Disaccharide Metabolism after Gastrojejunostomy
Authors: Joyce D. Gryboski, Walter R. Thayer, William A. Gryboski, Ira W. Gabrielson, Howard M. Spiro
Journal: New England Journal of Medicine (1963)

THE surgical procedure of partial gastrectomy with gastrojejunostomy often creates an aftermath of problems. Two of those most frequently encountered are chronic diarrhea and failure to gain weight. Weijers et al.1 have shown that a deficiency of sugar-splitting enzymes may cause chronic diarrhea and malnutrition in children. It is the purpose of this study to relate these problems that follow gastrojejunostomy to an inability of the patients to hydrolyze the disaccharides, lactose and sucrose.SubjectsControl subjects were divided into three groups. Ten healthy adult volunteers served as normal controls. The second group consisted of 6 patients with active duodenal . . .
ALDH isozymes downregulation effects on cell growth and gene expression in lung cancer cell lines
Authors: Jan Moreb, Maria Amaya, Blanca Ostmark, Lung-Ji Chang, Henry Baker, M Lopez, Wayne Chue
Journal: Clinical Cancer Research (2007)

B18   Using immunohistochemistry on patient pathological specimens, our group has recently reported high expression of these isozymes in non small cell lung cancer. Considering the biological activity of these enzymes and their role in drug resistance, we hypothesize that the down-regulation of ALDH may affect multiple biological pathways critical for cell proliferation. The A549 and H522 non small cell lung cancer cell lines were used in these experiments. ALDH3A1, ALDH1A1 or both were knocked-down using lentiviral-mediated expression of specific siRNAs. Cells expressing siRNA against green fluorescent protein (GFP) as well as the parent cell line (WT) were used as controls. Cells from the different experimental groups (5 in total for each cell line) were cultured for 48 or 72 hr, then harvested and manually counted. Cell proliferation assays (MTT) and colony forming assay were also performed to determine the effects of siRNA expression on cell growth. Furthermore, incubations of cells with ALDH inhibitors DEAB and disulfiram, were used in similar experiments for comparison. In order to investigate the effect of these isozymes on gene profiles, we performed microarray analysis using RNA obtained from A549 cell line in which ALDH activity was reduced by 95% using lentiviral mediated expression of siRNA against both isozymes (Lenti1+3). Results show that the cell lines in which the ALDH activity was down-regulated grew at significantly slower rates than the controls. The cell proliferation assay and the colony assay confirmed that the down-regulation of ALDH results in slower proliferation rate and lower colony formation. Both ALDH inhibitors resulted in a dose dependent inhibition of cell growth as well. Stringent microarray analysis methods were used to identify gene expression patterns that are specific to the knock down of ALDH activity and significantly different in comparison to the control groups: WT and GFP.  Validation of selected genes expression was done using real-time RT PCR. Detailed functional analysis was performed on 101 genes that were significantly different (P  7 fold in the Lenti 1+3 cells. The change in three of those genes was > 10 fold including GPR37, ID4, and EIF1AY genes which have been described before in association with different cancers.We conclude that the down-regulation of ALDH3A1 and ALDH1A1 is critical to the cellular homeostasis affecting multiple biochemical and biological pathways and results in the inhibition of cell proliferation and colony formation of lung cancer cells. These results imply that the down-regulation of these enzymes may affect not only the known sensitivity of lung cancer cells to certain chemotherapeutic drugs but it may also have a direct beneficial effect by altering certain biological processes important to the survival of these malignant cells.
Tc-99m HMPAO-Labeled Leukocytes in the Diagnosis of Mycotic Aneurysm
Authors: Julia Cortes, Juan I Alonso, Francisco Ruiz-Oliva, Soledad Alvarez, Jose Rodero, Pilar Alcorta
Journal: Clinical Nuclear Medicine (2002)

CORTES, JULIA M.D.*; ALONSO, JUAN I. M.D.*; RUIZ-OLIVA, FRANCISCO M.D.†; ALVAREZ, SOLEDAD M.D.*; RODERO, JOSE M.D.‡; ALCORTA, PILAR M.D.* Author Information
AB0320 Biologics Treatment Makes Poor Regression of Renal Amyloid Deposition despite Almost Removal from Gastric Mucosa in Amyloid A Amyloidosis Patients with Rheumatoid Arthritis
Authors: H. Uda, T. Harada, K. Shigematsu, A. Matsumoto, A. Mizumoto, T. Takama, O. Saiki
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> Reactive amyloid A (AA) amyloidosis is a serious and life-threatening systemic complication of rheumatoid arthritis (RA). Several biologics therapy reportedly regress gastric amyloid deposition in amyloid A (AA) amyloidosis patients with rheumatoid arthritis (RA), but it is uncertain whether the biologics therapy can also reduce renal amyloid deposition or not, because it is difficult to repeat a histological study in these patients. In patients with vascular type disease, renal involvements are limited (1), so that we can perform a follow-up renal biopsy. <h3>Objectives</h3> The purpose of the study is to compare the mass of amyloid deposition in kidney and gastric tract by biologics treatment in AA amyloidosis patients to whom serial histologically study were performed. <h3>Methods</h3> The diagnosis of AA amyloidosis was determined by Congo-red stain and anti-AA antibody of gastric biopsy specimen. RA patients who diagnosed AA amyloidosis and had given informed consent were enrolled in the study. The patients were received renal biopsy, and subsequently they were treated with tocilizumab or etanercept for more than three years. Gastric and renal biopsies were performed after biologics treatment at least three years9 interval. Renal biopsies were examined only in patients with AA amyloidosis of vascular type disease because renal function does not significantly deteriorate [1]. <h3>Results</h3> The vascular type of AA amyloid patients with RA received either etanercept or tocilizumab. The RA activity and laboratory data were significantly improved and sustained for more than 3 years during treating with the biologics. Before biologics treatment, renal biopsy specimens showed amyloid deposition around the blood vessels selectively (Fig. 1A). After biologics treatment, the regression of amyloid deposition was poor and similar to those observed in the initial study (Fig. 1B). Renal function of the patients was not also changed significantly. The results of AA deposition in kidney were also confirmed by anti-AA antibody. In the gastrointestinal tract, after treatment with etanercept or tocilizumab, amyloid mass was markedly regressed (Fig. 1D) compared to the initial study (Fig. 1C) as reported previously. <h3>Conclusions</h3> Amyloid deposition of the kidney, in contrast to the gastric tract, regress poorly in AA amyloidosis patients with RA even by biologics therapy, suggesting that regression of amyloid deposition is differently regulated between the kidney and the gastric tract. <h3>References</h3> Two distinct clinical courses of renal involvement in rheumatoid patients with AA amyloidosis. J Rheumatol. 2006;33:1482-7. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.5510
THU0201 Cognitive impairment in behçet’s disease is not associated to systemic disease activity, cumulative prednisone dose or white-matter lesions
Authors: L.A. Dutra, A.W.S. De Souza, H. Alessi, P. Braga Neto, B.D.V.S. Guedes, C.R. Gonçalves, A.J. da Rocha, P.H. Bertolucci, O.G.P. Barsottini
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Neuro-Behçet's disease (NBD) may present cognitive and behavioral symptoms, such as pseudobulbar affect, personality disorders and memory impairment. Because of its predilection for brainstem and basal ganglia, explanations for cognitive/behavioral deficits were related to a secondary dysfunction of frontal and temporal cortices due to damage of subcortical structures. Nontheless, patients without overt neurological manifestation may present cognitive impairment. <h3>Objectives</h3> Cognitive functioning in Brazilian NBD and Behçet's disease (BD) patients, and its relation with cumulative prednisone dose, systemic disease activity and white matter lesions were evaluated. <h3>Methods</h3> Brain MRI white-matter lesions and neuropsychological battery scores of NBD patients (NBDG), BD patients without overt neurological manifestation (BDG) and control (CON) groups, each one with 24 subjects, were compared. Hamilton Anxiety Scale (HAM), Beck Depression Inventory (BDI) was applied to all subjects. White-matter lesions were evaluated according to the age-related white matter changes scale. <h3>Results</h3> BDG and NBDG patients were impaired in language and executive function. Visual memory was impaired only in NBDG patients. Neuropsychological scores did not differ between active and non-active patients and did not correlate with cumulative prednisone dose. Also, multiple logistic regressions disclosed that neuropsychological scores were not related to age, gender, white-matter lesions, HAM or BDI. However higher educational level was associated to inferior risk of cognitive impairment (OR 0.77, 95% CI 0.62-0.96, p=0.021). <h3>Conclusions</h3> Patients with BD without overt neurological manifestation may present cognitive impairment, which does not relate to disease activity, white-matter lesions or cumulative prednisone dose. Low educational level is a risk factor for cognitive impairment in BD. <h3>Disclosure of Interest</h3> None Declared
BALANCING THE ROLE OF CARDIAC OUTPUT VERSUSS O2 EXTRACTION DURING MAXIMAL EXERCISE IN HEART FAILURE WITH REDUCED EJECTION FRACTION: PATHOPHYSIOLOGICAL INSIGHTS
Authors: Greta Generati, Francesco Bandera, Marta Pellegrino, Valentina Labate, Vincenzo Tufaro, Valeria Donghi, Eleonora Alfonzetti, Marco Guazzi
Journal: Journal of the American College of Cardiology (2016)
Insulin Receptor Assays Used in Human Studies: Merits and Limitations
Authors: Oluf Pedersen
Journal: Diabetes Care (1983)

The establishment of insulin receptor assays about 10 yr ago made it possible to study the regulatory role of the insulin receptor in a variety of physiologic and pathophysiologic conditions in man. Although it would be desirable to examine insulin receptors on muscle and liver cells, due to the ethical and technical limitations most clinical research in insulin receptor binding in man has been confined to accessible cell models, that is, fat and blood cells. The two major components of the receptor assay are (125I)-labeled insulin and isolated cells. Most iodoinsulin preparations used have differed with respect to purity, homogeneity, and distribution of (125I) within the molecule. This makes comparison of insulin binding data between laboratories difficult. Comparing monocytes, erythrocytes, and adipocytes as cell models each cell type possesses several limitations. The human adipocyte, however, has the advantage in that it allows simultaneous measurements of insulin receptor binding and biologic insulin effects under similar conditions of physiologic pH and temperature. Scatchard analysis has been widely used in the interpretation of insulin binding data. The assumptions and prerequisites required for the application of this mathematical approach are, however, not fulfilled. Furthermore, whether the nonlinear Scatchard plot is caused by multiple receptor classes or negative cooperativity in one homogeneous receptor class is an unsolved problem. In general there is a tendency to give values of total receptor concentration and affinity constants based on the negative cooperativity model. The informative value of these binding quantities is questionable, however, due to bias and lack of precision in data generation. Finally, generalization of insulin receptor results from one cell type to other insulin-binding tissues within the same individual should be avoided since the available literature suggests that the insulin receptor status and its changes seem to be tissue specific.
Abstract 4666: Genetic polymorphisms in the pre-microRNA flanking region and non-small cell lung cancer survival
Authors: Hongbing Shen, Zhibin Zhibin Hu, Jiaping Chen
Journal: Cancer Research (2011)

Abstract Rationale: Previously, we reported that common variants in pre-miRNA sequences played a role in the prediction of non-small-cell lung cancer (NSCLC) survival. Objectives: To assess whether variants in the pre-miRNA flanking region can influence the clinical behavior of NSCLC. Methods: we conducted a two-stage study to examine the impact of a panel of 85 SNPs on the overall survival of 923 NSCLC patients (568 in the screening set and 355 in the validation set) in China. Measurements and Main Results: Eleven single nucleotide polymorphisms (SNPs) were primarily associated with the NSCLC survival in the univariate analysis. However, in the validation set, only miR-30c-1 rs928508 was consistently a NSCLC survival predictor and the protective role of rs928508 AG/GG genotypes were more pronounced among early stage (stage I/II) patients and patients treated with surgery. The area under curve (AUC) at year 5 was significantly increased from 0.658 to 0.741 after adding the miR-30c-1 rs928508 risk score to the traditional clinical risk score (stage and surgery). Furthermore, in the genotype-phenotype correlation analysis, rs928508 AG/GG genotypes were associated with a significantly decreased expression of precursor and mature miR-30c (P=0.009 and 0.011), but not with that of its primary miRNA. The expression of the host nuclear transcription factor Y (NFYC) gene was correlated with pri-mir-30c-1, but not with rs928508 genotypes, implicating the co-regulation of the transcription of NFYC and pri-mir-30c-1. Conclusions: Our data indicated, for the first time, that genetic polymorphisms in the pre-miRNA flanking region may be prognostic biomarkers of NSCLC, and rs928508 is such a potential candidate. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 4666. doi:10.1158/1538-7445.AM2011-4666
Abstract 413: Overexpression of Snail is associated with lymph node metastasis and poor prognosis in patients with gastric cancer.
Authors: Chae Hwa Kwon, Na Ri Shin, Eun Hui Jeong, Chang In Choi, Hyun Jung Moon, In Sun Chu, Gwang Ha Kim, Tae Yong Jeon, Jae Hyuk Lee, Do Youn Park
Journal: Cancer Research (2013)

Abstract Background: Epithelial-mesenchymal transition (EMT) plays a significant role in tumor progression and invasion. Snail is a known regulator of EMT in various malignant tumors. This study investigated the role of Snail in gastric cancer. Methods: We examined the effects of silenced or overexpressed Snail using lenti-viral constructs in gastric cancer cells. Immunohistochemical analysis of tissue microarrays from 314 patients with gastric adenocarcinoma (GC) was used to determine Snail's clinicopathological and prognostic significance. Differential gene expression in 45 GC specimens with Snail overexpression was investigated using cDNA microarray analysis. Results: Silencing of Snail by shRNA decreased invasion and migration in GC cell lines. Conversely, Snail overexpression increased invasion and migration of gastric cancer cells, in line with increased VEGF and MMP11. Snail overexpression (≥75% positive nuclear staining) was also significantly associated with tumor progression (P &amp;lt; 0.001), lymph node metastases (P = 0.002), lymphovascular invasion (P = 0.002), and perineural invasion (P = 0.002) in the 314 GC patients, and with shorter survival (P = 0.023). cDNA microarray analysis revealed 213 differentially expressed genes in GC tissues with Snail overexpression, including genes related to metastasis and invasion. Conclusion: Snail significantly affects invasiveness/migratory ability of GCs, and may also be used as a predictive biomarker for prognosis or aggressiveness of GCs. Citation Format: Chae Hwa Kwon, Na Ri Shin, Eun Hui Jeong, Chang In Choi, Hyun Jung Moon, In Sun Chu, Gwang Ha Kim, Tae Yong Jeon, Jae Hyuk Lee, Do Youn Park. Overexpression of Snail is associated with lymph node metastasis and poor prognosis in patients with gastric cancer. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 413. doi:10.1158/1538-7445.AM2013-413
DETECTION OF ACUTE LOWER LIMB DEEP VEIN THROMBOSIS (DVT) USING Tc-99m DMP-444 SCINTIGRAPHY.
Authors: S. M. Salisbury, J. E. Seabold, S. L. Edell, J. A. Ponto, J. S. Murguia, S. Roth, J. A. Bricker
Journal: Clinical Nuclear Medicine (1999)

Salisbury, S.; Seabold, J. E.; Edell, S. L.*; Ponto, J. A.; Murguia, J. S.; Roth, S.*; Bricker, J. A. Author Information