tbuckley/cabot-search huggingface dataset:
Abstract 5279: LPS-TLR4 binding increases metastatic potential of colorectal cancer cells
Authors: Rich YC Hsu, Carlos HF Chan, Jonathan D. Spicer, Mathieu C. Rousseau, Rushika Perera, Betty Giannias, Simon Rousseau, Lorenzo E. Ferri
Journal: Cancer Research (2010)

Abstract Objective: Infectious complications in colorectal cancer patients undergoing curative resection are associated with cancer recurrence, but the exact mechanism is not well understood. Toll-like receptor 4 (TLR4) is the sole receptor for lipopolysaccharide (LPS), a gram-negative bacterial antigen involved in such infectious complication. TLR4 expression has been found on several cancer types. We hypothesize that LPS promotes cancer cell metastatic potential via TLR4 signaling in colorectal cancer cells. Methods: We compared the effects of LPS stimulation on two well-characterized colorectal cancer cell lines: Caco-2 (non-metastatic) and HT-29 (metastatic). Flow cytometry was performed to detect cell surface TLR4 and various integrin expression. Cancer cells were incubated with or without 0.1 µg/mL LPS for 4 hours. In vitro static adhesion assay was used to study the ability of cell adhesion to extracellular matrix proteins (fibronectin, collagen I and collagen IV). Intravital microscopy, a technique used to study microcirculation in vivo, was carried out to observe dynamic attachment of intra-splenic injected cancer cells to C57/BL6 mouse liver sinusoids. Results: Caco-2 cells lack TLR4 receptors and are unresponsive to LPS treatment. In contrast, HT-29 cells were shown to express TLR4 receptors and HT-29 responds to LPS by a 2-fold increase of β1, but not α5, integrin expression in LPS-treated HT-29 cells (Mean Fluorescence Intensity:1041 vs. 458(untreated)). LPS-treated HT-29 cells showed enhanced attachment to fibronectin (1.6-fold; p &amp;lt; 0.01), collagen I (3-fold; p &amp;lt; 0.01) and collagen IV (2-fold; P &amp;lt; 0.01) relative to controls in vitro. Similarly, adherence of HT-29 cells to hepatic sinusoids in vivo was increased by LPS treatment (2 fold; p &amp;lt; 0.05). Conclusion: These data suggest that LPS-TLR4 signaling in colorectal cancer cells increases the metastatic potential. LPS-TLR4 mediated signaling cascade may be a valuable therapeutic target for the prevention of cancer metastasis. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 5279.
THU0259 The levels of adiponectin are decreased in the skin and sera of diffuse cutaneous systemic sclerosis patients
Authors: Y. Kubo, S. Fukushima, M. Jinnin, T. Makino, I. Kajihara, A. Ichihara, K. Makino, H. Ihn
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Adiponectin is protein hormone produced by visceral and subcutaneous fat cells. In many past studies, adiponectin plays some roles in inflammation, angiogenesis and tissue remodeling, and induces the production of the anti-inflammatory mediators. Recently, adiponectin has also attracted attention for its involvement in the pathogenesis of collagen diseases. De Sanctis et al. <h3>Objectives</h3> In this study, we determined the adiponectin expression in the sera and lesional skin of patients with systemic sclerosis (SSc). <h3>Methods</h3> Serum adiponectin concentrations were measured in 32 patients with SSc, 10 patients with SLE, 12 patients with dermatomyositis and 13 healthy subjects with specific enzyme-linked immunosorbent assays. Adiponectin mRNA was determined in skin tissues of 5 patients with diffuse cutaneous SSc (dcSSc), 7 patients with limited cutaneous SSc (lcSSc) and 7 healthy subjects with real-time polymerase chain reaction. <h3>Results</h3> There was significant reduction in serum adiponectin levels in patients with dcSSc compared with controls (11.2±8.0 vs 139.7±54.2pg/ml, <i>P</i> &lt;0.001). SSc patients with decreased serum adiponectin levels had higher modified Rodnan total skin thickness score and higher incidence of pulmonary fibrosis, pitting scars, diffuse pigmentation or anti-topoisomerase I antibody. Adiponectin mRNA levels in skin tissues from patients with dcSSc were also reduced. <h3>Conclusions</h3> Serum adiponectin levels may be a useful biomarker for fibrotic condition in patients with SSc. Clarifying the role of adiponectin in collagen diseases may lead to further understanding of the pathogenesis and new therapeutic approach. <h3>References</h3> Motoshima H, Wu X, Sinha MK, et al. Differential regulation of adiponectin secretion from cultured human omental and subcutaneous adipocytes: effects of insulin and rosiglitazone. J Clin Endocrinol Metab 2002;87(12):5662-7. De Sanctis JB, Zabaleta M, Bianco NE, Garmendia JV, Rivas L. Serum adipokine levels in patients with systemic lupus erythematosus. Autoimmunity 2009;42(4):272-4. <h3>Disclosure of Interest</h3> None Declared
TCT-278 Two year Clinical Impact of Postprocedural Incomplete Stent Apposition and Late Acquired Incomplete Stent Apposition After Deployment of Zotarolimus Eluting Stent or Everolimus Eluting Stent
Authors: Sang-Rok Lee, Yi-Shik Kim, Shin Eun Lee, Kyeonh-Ho Yun, Seok-Kyu Oh, Jei-Keon Chae, Jae-Ki Ko
Journal: Journal of the American College of Cardiology (2012)
Iatrogenic biliary injury in a patient with Roux-en-Y hepaticojejunostomy: stenting repair with single-balloon enteroscopy-assisted ERCP
Authors: Teresa Pinto-Pais, Rolando Pinho, Luísa Proença, Carlos Fernandes, Iolanda Ribeiro, Tiago Pereira, José Fraga, João Carvalho
Journal: Endoscopy (2014)

A 64-year-old woman who had previously undergone a Roux-en-Y hepaticojejunostomy because of iatrogenic bile duct injury during cholecystectomy, presented recurrent episodes of cholangitis due to a stenosis of the hepaticojejunostomy. A percutaneous transhepatic cholangiography with biliary dilation and plastic stenting of the biliodigestive anastomosis was performed. After a successful left duct approach, accidental laceration of the right biliary duct occurred. Percutaneous stenting was impossible because the guidewire repeatedly looped through the laceration.
AB0606 Effects of 12-month etanercept or certolizumab pegol therapy on disease activity, bone turnover markers and peripheral qct bone mineral density in patients with rheumatoid arthritis
Authors: A. Váncsa, H. P. Bhattoa, E. Végh, K. Gulyás, Á. Horváth, Z. Pethö, B. Juhász, F. Balázs, L. Pogácsás, I. Pál, Z. Szekanecz
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Rheumatoid arthritis (RA) has been associated with secondary bone loss in the majority of patients. Biologics may have effects on generalized bone loss, however, less information has become available on etanercept (ETN) and certolizumab pegol (CZP). <h3>Objectives</h3> In this study, we assessed the effects of anti-TNF treatment on inflammatory parameters, disease activity, bone turnover markers, bone mineral density (BMD) and radius quantitative CT (qCT) parameters in RA patients. <h3>Methods</h3> Twenty-six RA patients (female:male=22:4) were treated with either ETN or CZP for 12 months. The mean disease duration was 9.7 years. Inflammatory parameters (ESR, CRP), disease activity (DAS28), autoantibodies, bone turnover markers (OC, CTX, P1NP), vitamin D3, lumbar spine and femoral DEXA, as well as radius qCT, a method capable of assessing total, trabecular and cortical density, were assessed at baseline and after 12 months of treatment with biologics. <h3>Results</h3> DAS28 values improved significantly during the anti-TNFα therapy (5.06, 3.71, 3.10 and 2.90 mean DAS28 at baseline and after 3, 6 and 12 months, respectively). DEXA and bone markers showed no significant changes in BMD at the lumbar spine or femur region. Similarly, radius qCT revealed no significant changes in total density. However, peripheral qCT showed increased trabecular density after 12 months of anti-TNF therapy (BMD: 220 mg/cm<sup>3</sup> and T-score: +0.4) in comparison to baseline values (BMD: 203 mg/cm<sup>3</sup>, T-score: -0.29). <h3>Conclusions</h3> One-year anti-TNFα therapy using ETN or CZP may prevent further bone loss in RA. Biologic treatment may have beneficial effects ont he trabecular bone. <h3>Disclosure of Interest</h3> None Declared
Abstract 2963: The Foxp3 transcription factor expression in human gynecologic cancer cell lines
Authors: Park Yu Ran, Kim Yong-Man, Lee Shin Wha, Kim Dae-Yeon, Kim Jong-Hyeok, Nam Joo-Hyun, Kim Young-Tak
Journal: Cancer Research (2010)

Abstract Objectives: The forkhead box protein 3 (Foxp3) transcription factor is considered as a master control gene for the function of regulatory T cells. However, recently some publications revealed that Foxp3 in cancer expressed higher than other tissues. A very recent publication describes the expression of Foxp3 in pancreatic carcinoma cells providing evidence that this could be an important tumor escape mechanism. As a result, some research considered that Foxp3 is associated with carcinogenesis, and cancer progression. To this end, This study was scheduled to investigate whether the expression of Foxp3 transcription factor can occur in gynecologic tumor types. Materials and methods: Ten tumor cell lines of cervical, ovarian, breast cancer origins were selected. The cell lines of cervical cancer were SiHa, HeLa, and Caski. Ovarian cancers were OV-CAR-3, SK-OV-3, SNU-8, and SNU-251. MDA-MB-231, MCF-7,and T47-D were selected as breast cancer cell lines. They were maintained in specific medium (RPM1640, DMEM (Dulbecco's modified Eagle's medium)). The cell lines were cultured for a period of 2 weeks. Detection of Foxp3 mRNA was performed using both conventional quantitative real-time PCR, the RT2 PCR Primer Set for Foxp3 (SuperArray, USA, forward 5’ GGCATCGTGATGGACTCCG 3’ and reverse 5’ GCTGGAAGGTGGACAGCGA 3′). β-Actin was used as a reference gene. All experiments were repeated three times. Results: The expression of Foxp3 mRNA was revealed in all tumor cell lines studied. This expression did not relate to the tissue of origin of each line. Relative expression values for tumor cells varied widely between 0.21 and 4.97 (1.71±0.09). Cervical cancer cell lines expressed highly Foxp3 mRNA in relative expression values for tumor cells. The highest expression level of Foxp3 in cervical cancer cell lines were with the SiHa cell lines. OV-CAR-3 cell lines expressed highly in ovarian cancer cell lines. In breast cancer cell lines, Foxp3 mRNA expression revealed the highest levels in T47-D cell lines. Conclusion: Foxp3 mRNA was detected in all tumor cell lines, albeit in variable levels, not related to the origins of tissue. We offer evidence that Foxp3 mRNA expression, characterizes tumor cells of various tissue origins. The biological significance of these findings warrants further investigation in the context of tumor immune escape, and especially under the light of current anti-cancer efforts interfering with Foxp3 expression. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 2963.
Abstract P1-17-01: Differences in Survival among Women with Stage III Inflammatory and Non-Inflammatory Locally Advanced Breast Cancer Appear Early: A Large Population Based Study
Authors: S Dawood, NT Ueno, V Valero, W Woodward, TA Buchholz, GN Hortobagyi, AM Gonzalez-Angulo, M. Cristofanilli
Journal: Cancer Research (2010)

Abstract Background Significant improvements in the survival of women with breast cancer have been observed and are attributed to a multidisciplinary approach and the introduction of polychemotherapy regimens. The objective of this population based study was to determine if differences, if any, in survival exist among women with inflammatory (IBC) and non-IBC locally advanced breast cancer (LABC) diagnosed in this era. Methods The Surveillance, Epidemiology and End Results Registry was searched to identify women with stage IIIB and C breast cancer who were diagnosed between 2004 and 2007 who had undergone surgery and radiation therapy. Patients were categorized as either having IBC or non-IBC LABC according the AJCC 6th edition criteria. Breast cancer specific survival (BCS) was estimated using the Kaplan-Meier product limit method and compared across groups using the log rank statistic. Cox models were then fitted to compare the association between breast cancer type and BCS after adjusting for patient and tumor characteristics. Results Eight hundred and twenty eight (19.2%) women and 3476 (80.8%) women had stage IIIB/C IBC and non-IBC LABC respectively. Median follow up was 19 months. 2-year BCS was 90% (95% CI 88-91%) for the whole cohort and 84% (95% CI 80%-87%) and 91% (95% CI 90%-91%) among women with IBC and non-IBC LABC respectively. In the multivariable model compared to women with non-IBC LABC women with IBC had a 43% increased risk of death from breast cancer that was statistically significant (HR=1.43, 95% CI 1.10-1.86, p=0.008). Conclusion In the era of multidisciplinary management and anthracycline and taxane based polychemotherapy regimens women with IBC continue to have inferior survival outcomes compared to women with non-IBC LABC with differences in survival appearing early. Citation Information: Cancer Res 2010;70(24 Suppl):Abstract nr P1-17-01.
Artifact of Cold Lesions on Skull SPECT of a Patient With Paget's Disease Secondary to Pixel Overflow
Authors: W J Shih, C Pulmano, J K Han
Journal: Clinical Nuclear Medicine (1999)

Various SPECT imaging artifacts have been described. One of them is pixel overflow caused by excessive radiotracer deposition in bone, resulting in areas of very low or absent activity on SPECT. Paget's disease of bone is characterized by intense and extensive radiotracer localization on bone imaging. A patient with Paget's disease is described whose planar bone scintigraphy and radiography showed osteoblastic and sclerotic areas of the skull, whereas SPECT showed photopenic and photon-deficient areas interposed with diffuse uptake in the skull. This indicates that bone SPECT might give artifacts of cold lesions secondary to pixel overflow as a result of excessive radiotracer deposition.
128 TOLL-LIKE RECEPTOR-ACTIVATED HUMAN HEPATOCYTES PRODUCE INFLAMMATORY CYTOKINES AND TYPE III INTERFERONS, RESULTING IN IFN-γ-MEDIATED SUPPRESSION OF HCV IN VITRO
Authors: R. Broring, M. Lutterbeck, K. Kleinehr, A. Paul, G. Gerken, J.F. Schlaak
Journal: Journal of Hepatology (2012)
Long-Term Maintenance Therapy with the TLR-9 Agonist MGN1703 in a Subgroup of Metastatic Colorectal Cancer Patients from the Impact Study
Authors: W. Scheithauer, J. Riera-Knorrenschild, H. Kopp, D. Nitsche, J. Kuhlmann, A. Zurlo, H.J. Schmoll
Journal: Annals of Oncology (2014)
Multiplexed Tumor Marker Profiling at Single-Cell Resolution: Quantifying Breast Cancer Molecular Signatures.
Authors: H. Liu, M. Huebschman, H. Garner, N. Lane, L. Cheng, D. Rana, A. Lin, G. Hughes, J. Uhr
Journal: Cancer Research (2009)

Abstract Excluding skin cancers, about 1.5 million new cases of cancer and about 450,000 cancer related deaths occur each year in the United States. The validation and molecular profiling of tumor markers are contributing to new paradigms in cancer research. In this presentation, we will discuss the information that can be obtained by using an Intelligent Single-Cell Optical Profiling Engine (I-SCOPE), consisting of hyperspectral imaging, multiplexed biomarker kits, and bioinformatics tools, to markedly expand the molecular profiling of tumor markers on individual carcinoma cells.Using biomarker antibodies conjugated to particular fluorochromes, we developed a multiplex of 10 different fluorochrome conjugates, one for each different tumor marker plus a nuclear dye. Staining and scanning using the I-SCOPE system showed that it can presently distinguish 10 different fluorochromes in a single pass, resulting in the identification of spatial location and relative intensity of each biomarker being interrogated. By using this system, we analyzed thousands of tumor cells from touch preparations of tumor tissue, circulating tumor cells (CTCs) in pleural fluid and blood, and disseminated tumor cells (DTCs) from bone marrow with 2 multiplex kits for a total of 17 different tumor markers. We have utilized clinically-accepted markers such as estrogen receptor (ER), progesterone receptor (PR), and HER2 in addition to biomarkers undergoing investigation such as B-cell lymphoma 2 (Bcl-2) and urokinase-type plasminogen receptor (uPAR). Furthermore, with the ability to simultaneously image 10 markers, each panel can also contain desired positive and negative controls such as CD45 (positive for white blood cells, negative for CTCs) and cytokeratin (positive for epithelial cells).The results of immunophenotyping of individual tumor cells with 17 different tumor markers indicated that the average expression of each tumor marker in 25 tumor cells was a reproducible representation of the tumor. However, comparison of individual CTCs' expression levels revealed remarkable heterogeneity in primary breast cancer cases.We conclude that hyperspectral microscope imaging together with individual tumor cell analysis represents a major step forward in developing a far more detailed and precise molecular signature of a patient's cancer. Further studies might demonstrate how it can facilitate treatment tailored to the individual patient's tumor, an important objective as new oncology drugs with specific molecular targets become more prevalent. Citation Information: Cancer Res 2009;69(24 Suppl):Abstract nr 6002.
Abstract 479: p53 mutations and Ink4a/Arf deletion cooperate to induce metastatic skin carcinomas
Authors: Zhongyou Li, Olga Mejia, Carlos Caulin
Journal: Cancer Research (2010)

Abstract Mutations in the p53 tumor suppressor gene are found in about half of the squamous cell carcinomas (SCC) that arise in the skin and oral cavity. Most of these mutations are missense mutations that result in the expression of altered forms of p53, some of which acquire oncogenic properties. We previously showed that the p53 gain-of-function mutation p53R172H cooperates with Ras activation during skin cancer initiation, progression to carcinoma and metastasis. However, it is unclear whether p53 gain- and loss-of-function mutations predispose differently to SCC formation when activated in the absence of additional oncogenic mutations. To address this question we generated mice in which deletion of p53 (loss-of-function) or activation of the p53R172H mutation (gain-of-function) were induced in mouse stratified epithelia. We found that over 70% of the mice developed skin or oral SCCs, with similar kinetics for mice with p53 gain- or loss-of-function mutations, suggesting that in the absence of Ras mutations the oncogenic role of p53R172H in SCC initiation is minimized. To identify mechanisms leading to SCC development in these mice we analyzed the status of pathways that are frequently involved in human SCCs. We observed that Erk1/2 activation was blocked in most of the SCCs. Consistently, oncogenic mutations in Ras genes were only found in &amp;lt;5% of the SCC analyzed. Notably, we found overexpression of cyclin D1 and activation of Akt in over 50% of the SCCs, suggesting an important contribution for these oncogenic alterations in SCC development in these mice. Importantly, p16INK4a and p19ARF were overexpressed in most of the SCCs, suggesting that in the absence of p53, alternative tumor suppressor mechanisms are activated to prevent tumor progression. To determine whether p53 mutations and p16/p19 cooperate in SCC formation we generated mice in which p53 mutations and deletion of the Ink4a/Arf locus were induced in the epidermis. These mice developed skin carcinomas significantly faster than mice with mutations in p53 only. In addition, in the presence of the Ink4a/Arf deletion, the p53R172H mutation induced accelerated SCC formation compared to deletion of p53, again suggesting that the oncogenic properties of mutant p53 are exposed in the presence of additional genetic alterations. The tumors that developed in these mice were classified as spindle cell carcinomas (SPCC) and generated metastasis in over 60% of the mice. Ongoing experiments are underway to identify molecular mechanisms involved in the generation of SPCCs and metastasis in this model. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 479.
Hodgkin's Disease, Lymphomatoid Papulosis, and Cutaneous T-Cell Lymphoma Derived from a Common T-Cell Clone
Authors: Thomas H. Davis, Cynthia C. Morton, Robert Miller-Cassman, Steven P. Balk, Marshall E. Kadin
Journal: New England Journal of Medicine (1992)

Lymphomatoid papulosis is a benign cutaneous eruption that in 10 to 20 percent of patients is associated with the development of lymphoma. The atypical cells of lymphomatoid papulosis histologically resemble the malignant cells of cutaneous T-cell lymphoma or the Reed-Sternberg cells of Hodgkin's disease. We studied a patient in whom lymphomatoid papulosis developed in 1971, Hodgkin's disease in 1975, and cutaneous T-cell lymphoma in 1985, to determine whether these diseases are clonally related.
AB0439 Clinical remission following treatment with tumour necrosis factor-alpha antagonists is not accompanied by changes in asymmetric dimethylarginine in patients with rheumatoid arthritis
Authors: T. Dimitroulas, A. Sandoo, T. Toms, J.J. Veldhuijzen van Zanten, J. Smith, G. Kitas
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Rheumatoid arthritis is characterised by impaired endothelial function which contributes to increased cardiovascular morbidity and mortality. Modern therapies such as tumour necrosis factor alpha antagonists appear to reduce cardiovascular risk in this population. Asymmetric dimethylarginine (ADMA) is an endogenous competitive inhibitor of nitric oxide synthase and contributes to endothelial dysfunction. <h3>Objectives</h3> The aim of the present longitudinal study was to investigate the effects anti-tumour necrosis factor alpha medications on serum concentrations of ADMA following 12 weeks of treatment in patients with rheumatoid arthritis. <h3>Methods</h3> Thirty-five patients (age (mean ± SD) 55±15 years, 21 women) who qualified for anti-TNFα therapy were included in the study. Disease activity score 28 and health assessment questionnaire were performed in all patients prior to starting anti-tumour necrosis factor alpha treatment, and 2 weeks and 3 months after initiation of treatment. ADMA was measured by ELISA at the same time points. Repeated measures ANOVA and LSD post hoc analyses were used to analyse changes in ADMA levels. <h3>Results</h3> Anti-tumour necrosis factor alpha therapy significantly reduced ESR (p&lt;0.03), CRP (p&lt;0.00), disease activity score 28 (p&lt;0.00) and health assessment questionnaire (p&lt;0.00). ADMA levels did not change significantly following 2 weeks or 3 months treatment with tumour necrosis factor alpha inhibitors. Changes in ADMA levels were not associated with changes in disease activity at 2 weeks and at 3 months. <h3>Conclusions</h3> Reduction in inflammation after treatment with tumor necrosis factor alpha antagonists does not affect ADMA levels in patients with rheumatoid arthritis. <h3>References</h3> Turiel M, Atzeni F, Tomasoni L, de Portu S, Delfino L, Bodini BD, Longhi M, Sitia S, Bianchi M, Ferrario P, Doria A, De Gennaro Colonna V, Sarzi-Puttini P. Non invasive assessment of coronary flow reserve and ADMA levels: a case-control study of early rheumatoid arthritis patients. Rheumatology 2009;48:834-839. A, Veldhuijzen van Zanten JJ, Metsios GS, Carroll D, Kitas GD. Vascular function and morphology in rheumatoid arthritis: a systematic review. Rheumatology (Oxford). 2011 Nov;50(11):2125-39. <h3>Disclosure of Interest</h3> None Declared