tbuckley/cabot-search huggingface dataset:
PWE-215 Numerical analysis of colour fluorescence ratio and contrast using video autofluoresence endoscopy accurately identifies high grade dysplasia or cancer in patients with Barrett's oesophagus
Authors: V Subramanian, J Mannath, D F Boerwinkel, L Alvarez-Herrero, W L Curvers, C J Hawkey, J J Bergman, K Ragunath
Journal: Gut (2012)

<h3>Introduction</h3> Autofluorescence endoscopy (AFE) is a novel technique that identifies early neoplasia in Barrett9s oesophagus (BE) by highlighting differences in tissue autofluoresence (AF). It has high sensitivity but is associated with false positive rates up to 80%. We aimed to develop numerical measures of AF to reduce the false positive rates of AFE. <h3>Methods</h3> Images of AFE lesions in patients with BE were prospectively collected. Blinded anonymised images were de-gamma corrected and average grayscale values in the red, green and blue channels of the abnormal and background normal area were quantified. The autofluoresence intensity (ratio of average red to green channel greyscale value of lesion compared to background), colour contrast index (between lesion and background), hue, saturation and lightness (of the lesion) were calculated. A decision tree based on the training set was developed with the J48 algorithm in WEKA3.2.4, using a 10-fold cross validation strategy. The performance of the model developed was assessed on an independently collected test dataset. <h3>Results</h3> There were 82 images (37 high grade dysplasia/cancer) in the training set and 164 images (51 high grade dysplasia/cancer) in the test set. The decision tree classifier developed utilised only autofluoresence intensity and colour contrast index and had a sensitivity of 97%, specificity of 77%, and negative predictive value of 98% in detecting high grade dysplasia/cancer in the independent test set. The false positive rate of AFE was reduced from 70% to 16%. <h3>Conclusion</h3> Numerical analysis of colour fluorescence and contrast is a reliable, objective and accurate method of reducing the false positive rate of AFE and can be easily incorporated into real time endoscopy. <h3>Competing interests</h3> V Subramanian: None declared, J Mannath: None declared, D Boerwinkel: None declared, L Alvarez-Herrero: None declared, W Curvers: None declared, C Hawkey: None declared, J Bergman Grant/Research Support from: Olympus Medical, K Ragunath Grant/Research Support from: Olympus Medical.
389 ENHANCING VIRUS-SPECIFIC IMMUNITY IN VIVO BY COMBINING THERAPEUTIC VACCINATION AND PD1/PD-L1 BLOCKADE IN CHRONIC HEPADNAVIRAL INFECTION
Authors: J. Liu, E. Zhang, Z. Ma, A. Kosinska, X. Zhang, I. Möller, P. Seiz, D. Glebe, B. Wang, D. Yang, M. Lu, M. Roggendorf
Journal: Journal of Hepatology (2013)
Abstract 3815: Murine tumors demonstrate variable responses to ischemia-reperfusion injury
Authors: Eric G. Sheu, Kohei Wakatsuki, Sean M. Oakes, Cyrus Ahmadi-Yazdi, Francis D. Moore
Journal: Cancer Research (2010)

Abstract Introduction: Acute ischemia/reperfusion (I/R) of normal tissues causes an inflammatory reaction initiated by binding of auto-reactive IgM antibody to an ischemia-induced self-antigen. Whether this inflammatory cascade also affects cancers - for example, after acute I/R during surgical resection or in conditions of chronic ischemia - is unclear. We examined the effect of I/R injury in three murine tumor models: B16F10 melanoma, Lewis lung carcinoma (LLC), and small intestinal adenomas of the APCmin/+ mouse. Methods: LLC and B16F10 cell lines were implanted into the hindlimbs of C57BL/6 mice. Ischemia was induced by external tourniquet ligation of the femoral vessels. Small intestinal tumors in APC min/+ mice were subjected to ischemia by vascular clip occlusion of the superior mesenteric artery. Control animals underwent hindlimb ischemia to the non-tumor bearing hindlimb or laparotomy alone. Following graded times of ischemia and reperfusion, tumors and surrounding normal tissue were harvested for histological examination. Immunohistochemistry was performed for IgM and activated caspase-3. For hindlimb injury, mice were recovered and followed for LLC and B16F10 tumor growth. Results: Ischemia-reperfusion causes injury of LLC and B16F10 tumors. In contrast, intestinal adenomas of APCmin/+ mice showed no signs of injury following ischemia, despite induction of necrosis and apoptosis of adjacent normal intestinal epithelium. Tumor susceptibility to ischemic injury correlated with immuno-histochemical deposition of IgM antibody. Ischemic injury of B16F10 significantly reduced tumor growth (36% volume reduction compared to control injury, p &amp;lt;0.05). In contrast, LLC tumor growth was significantly increased after ischemia (35% increased compared to control injury, p &amp;lt; 0.01) Conclusions: The three murine tumor models examined are each affected differently by an acute I/R injury, in contrast to the conserved inflammatory cascade induced in normal tissues following ischemia. APCmin/+ adenomas evade ischemia-induced IgM binding and injury. While both LLC and B16F10 are acutely injured, the long term effects on growth are divergent. Targeted manipulation of the host inflammatory response to ischemia-reperfusion may be a method to influence tumor progression and growth. 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 3815.
Abstract 4931: Inhibitor of DNA binding 4 (Id4) suppresses MMP2 mediated invasion of glioblastoma-derived cells by direct inactivation of twist-1 function.
Authors: Gilbert J. Rahme, Mark A. Israel
Journal: Cancer Research (2013)

Abstract Invasion of normal tissues by high grade glioma is a key aspect of increased morbidity and mortality associated with these tumors. Malignant glioma comprise over 70% of primary brain tumors with a median survival ranging from 12 to 15 months for patients with glioblastoma multiforme (GBM), the highest grade of glial tumors. Inhibitor of DNA binding (Id) genes are highly expressed in development and tumorigenesis and some members (Id1, Id2 and Id3) have been linked to increased tumor invasion. In sharp contrast to these members of the Id gene family, we found that Id4 expression in GBM-derived cells decreased invasion in in vitro assays. Results of gain-of-function and loss-of-function experiments indicated that Id4 expression decreased GBM invasion and suppressed a gene, matrix metallo-protease 2 (MMP-2), which encodes a proteolytic enzyme key for the destruction of glial tumor extracellular matrix. Western blot and zymography analysis demonstrated that conditioned media from Id4 expressing cells had low levels of pro-MMP2 and cleaved MMP2. An antibody that is known to inactivate MMP-2 was used to demonstrate that MMP2 accumulated in media conditioned by Id4 deficient cells was sufficient to rescue the invasive activity lost in cells expressing high levels of Id4. These findings confirmed that MMP2 suppression by Id4 is responsible for the decrease in invasion observed in Id4 expressing glioma cells. Twist-1 is a well described mediator of invasion. Co-IP and co-localization studies demonstrated an interaction suggesting a direct inhibition of Twist-1 by Id4. Other data indicate that Id4 also blocks Twist-1 induced transcription of MMP2. Importantly, Twist-1 overexpression can rescue the invasion defect induced by Id4 expression, providing further support that the Id4/Twist-1 interaction mediates the function of Id4 in suppressing GBM invasion. Analysis of The Cancer Genome Atlas (TCGA) data indicated a significantly better survival and prognosis for GBM patients with high Id4 expression (Z&amp;gt;1) suggesting that Id4 could have an important role in the survival of GBM patients. Our data provide strong evidence demonstrating that Id4 suppresses GBM invasion by inhibiting Twist-1 induced expression of MMP2. To our knowledge, this is the first report of an Id protein acting as an inhibitor of invasion rather than mediating the pro-invasive functions of the other Id-gene family members. Citation Format: Gilbert J. Rahme, Mark A. Israel. Inhibitor of DNA binding 4 (Id4) suppresses MMP2 mediated invasion of glioblastoma-derived cells by direct inactivation of twist-1 function. [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 4931. doi:10.1158/1538-7445.AM2013-4931
THU0188 Lymphoproliferative complications in the course of primary sjægren’s syndrome: Prevalence and common features in a large cohort of patients:
Authors: L. Quartuccio, C. Baldini, R. Priori, E. Bartoloni Bocci, F. Carubbi, M. Isola, M. Maset, S. Salvin, N. Luciano, G. Picarelli, A. Alunno, A. Marrelli, R. Gerli, G. Valesini, S. Bombardieri, S. De Vita
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Primary Sjögren’s syndrome (pSS) is the autoimmune disease most often associated with lymphoma. Mixed cryoglobulinemia as well as persistent parotid swelling are the well known pre-lymphomatous clinical conditions. <h3>Objectives</h3> To describe the prevalence of lymphoproliferative complications (defined as B-cell lymphoma or definite conditions predisposing to lymphoma, i.e, cryoglobulinemic vasculitis (CV) and major salivary gland swelling) in a cohort of pSS patients followed in five Rheumatologic Centres. <h3>Methods</h3> Demographic, clinical, laboratory and histopathologic data in 1170 pSS were retrospectively collected according to a standard protocol. Univariate analyses were performed. <h3>Results</h3> Prevalence of lymphoma in this SS cohort was 4.4% (51/1170), prevalence of CV (1) was 3.9% (33/850), and prevalence of salivary gland swelling and/or myoepithelial syaladenitis was 30.9% (362/1170). Salivary gland swelling and/or MESA, CV and lymphoma shared many laboratory features, i.e., positive rheumatoid factor (RF), hypocomplementemia and leucopenia, as well as a the presence of purpura as clinical hallmark of the circulating immune complexes (table 1). Interestingly, polyclonal hypergammaglobulinemia was strictly associated with salivary gland swelling, but it was not associated with CV or lymphoma; on the other hand, serum monoclonal component was significantly associated with CV or lymphoma, but not with salivary gland swelling and/or MESA. <h3>Conclusions</h3> Salivary gland swelling and CV are confirmed as red flags for lymphoma evolution in pSS and are strictly linked (2). Polyclonal hypergammaglobulinemia is not a red flag for lymphoma in pSS. B-cell clonal proliferation from polyclonal to monoclonal likely occurs in the target tissue of pSS (e.g. salivary gland MALT tissue), predisposing to CV and/or to lymphoma. Cryoglobulinemia marks the emergence of abnormal RF-positive B-cell clones, but MALT lymphoma may also occur in the absence of cryoglobulinemia. <h3>References</h3> De Vita S et al. Ann Rheum Dis 2011 De Vita S, et al. Rheumatology 2012 <h3>Disclosure of Interest</h3> None Declared
OP0115 Clinical and radiological outcome in outpatients with rheumatoid arthritis followed by medical, nursing or shared care – a two year randomised controlled trial
Authors: J. Primdahl, H.C. Horn, R. Petersen, K. Hørslev-Petersen
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Studies have indicated that follow-up by nursing consultations or different versions of shared care are not inferior to medical follow-up in controlling disease activity in patients with rheumatoid arthritis (RA) (1,2). <h3>Objectives</h3> To explore whether RA patients disease status, function and progression of erosions would differ depending on the type of follow-up care: 1) planned nursing consultations every three months, 2) shared care with no planned consultations but access to the General Practitioner and a nurse-led telephone help-line or 3) traditional rheumatologist initiated follow-up. <h3>Methods</h3> In a randomised controlled trial 287 adult outpatients in stable non-biological treatment, DAS-28&lt;3.2, HAQ&lt;2.5 and at least 18 months of disease duration were allocated to one of the three types of follow-up care for the following two years. DAS-28, HAQ, VAS-fatigue and pain were assessed at enrollment, one and two years follow-up. Clinical evaluation was performed yearly by a blinded investigator. Mixed effect models were used to examine the data. Progression of erosions in hands and feet from x-rays at baseline and two-years follow-up were explored in logistic regression analysis controlling for erosions and positive anti-CCP at baseline. <h3>Results</h3> Across all participants a significant increase was seen in DAS-28 (0.51, p&lt;0.001), HAQ (0.086, p=0.012) and pain (4.26, p=0.019) from baseline till two-years follow-up. VAS-fatigue remained stable during the two years. No significant differences were seen between the groups in these outcome measures or in the number of participants with DAS-28&gt;3.2 at two-year follow up (28 (29%), 19 (20%) and 17 (18%) of the participants in the medical, shared care and nursing group respectively). The odds ratio for progression on x-rays in the shared care and the nursing group did not differ from the medical group (shared care OR 0.56, p=0.264 (CI: 0.28-1.55), nursing group OR 1.03, p=0.945 (CI: 0.44-2.56)). There was no significant difference between the groups in the number of adverse events. <h3>Conclusions</h3> In patients with established RA and low disease activity it is considered to be safe to implement shared care and nursing consultations without differences in disease control compared to traditional medical follow-up. <h3>References</h3> [1]Hewlett S, Kirwan J, Pollock J, Mitchell K, Hehir M, Blair PS et al. Patient initiated outpatient follow up in rheumatoid arthritis: six year randomised controlled trial. BMJ 2005; 330(7484):171. [2]Hill J, Thorpe R, Bird H. Outcomes for patients with RA: A rheumatology nurse practitioner clinic compared to standard outpatient care. Musculoskeletal Care 2003; 1(1):5-20. <h3>Disclosure of Interest</h3> None Declared
Abstract 3127: Cigarette smoke condensate (CSC) induces differential expression and promoter methylation profiles of critical genes involved in lung cancer in NL-20 lung cells <i>in vitro</i>: Short-term and chronic exposure
Authors: Lascelles E. Lyn-Cook, Beverly Word, Bibi Mwamba, Beverly D. Lyn-Cook, George Hammons
Journal: Cancer Research (2012)

Abstract Lung cancer is the leading cause of cancer deaths in the United States. Smoking accounts for a large number of those deaths. Recently, the Food and Drug Administration has been given authority to regulate any new cigarette products coming to market and further demonstrate the harm caused by constituents in cigarettes or those chemicals created from smoking. Establishing early diagnostic markers are critical to effective prevention programs. This study examined the effects of cigarette smoke condensate on expression and promoter methylation profile of critical genes involved in various stages of lung cancer development, such as E-cadherin (ECAD), O6-mehyl-guanine-DNA methyltransferase (MGMT), and RASSF1A. NL-20 cells were treated with 0.1, 1, 10 or 100 µg/ml of CSC for 24, 48 and 72 hrs for short-term exposures. ECAD showed a significant decrease in expression after 72 hrs with both 10 and 100 µg/ml CSC. This decrease in expression correlated to hypermethylation of the ECAD promoter at both concentrations using MSP analysis. MGMT expression increased only with the concentration of 100 µg/ml CSC at all time points. This correlated to an unmethylated profile of the promoter at this concentration. RASSF1A promoter profile was methylated in the control samples. However, when treated with 10 or 100 µg/ml CSC, an unmethylated promoter profile was noted. This correlated to increased expression of RASSF1A at both the 10 and 100 µg/ml concentrations. No changes were noted at 0.1 or 1 µg/ml of CSC in NL-20 lung cells. For chronic studies, the cells were exposed for 30 days with 10 or 100 µg/ml CSC, with media changes every three days adding new CSC. After 30 days, cells showed morphological changes associated with transformation. Foci were noted. These cells were further analyzed for further changes in critical genes involved in lung cancer. This study provides critical data showing epigenetic regulation of critical genes involved in DNA repair, invasion and tumor suppressor with treatment of lung cells with CSC. 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 3127. doi:1538-7445.AM2012-3127
Prediction of PSA spikes by isotope and patient age following permanent prostate brachytherapy
Authors: C. Bostancic, G. S. Merrick, W. Butler, K. Wallner, Z. Allen, R. Galbreath, J. Lief, S. Gutman
Journal: Journal of Clinical Oncology (2007)

15535 Background: To evaluate prostate specific antigen (PSA) spikes (bounces) following permanent prostate brachytherapy in low-risk patients randomized to Pd-103 or I-125. Methods: The study population consisted of 164 prostate cancer patients who were part of a prospective randomized trial comparing Pd-103 with I-125 for low-risk disease. Sixty-one patients (37.2%) received short course cytoreductive androgen deprivation therapy (ADT). No patient received supplemental XRT. The median follow-up was 5.4 years. All patients were implanted at least 3 years prior to analysis. On average, 10.1 post-treatment PSA’s were obtained per patient. Biochemical disease-free survival was defined as a PSA = 0.40 ng/mL after nadir. A PSA spike was defined as a rise of = 0.2 ng/mL followed by a durable decline to pre- spike levels. Multiple clinical, treatment and dosimetric parameters were evaluated as predictors for a PSA spike. Results: Forty- four patients (26.9%) developed a PSA spike including 45.7% (21/46) of the hormone naïve I-125 patients and 14.0% (8/57) of the hormone naïve Pd-103 patients. In hormone naïve patients, the mean time between implant and spike was 22.6 months and 18.7 months for I-125 and Pd-103 patients, respectively. In patients receiving neoadjuvant ADT, the incidence of spikes was comparable between isotopes (28.1% for I- 125 and 20.7% for Pd-103). The incidence of spikes was substantially different in patients &lt; 65 vs = 65 years of age (16.3% vs. 38.5%). In multivariate Cox regression analysis, patient age at implant (p &lt; 0.001) and isotope (p = 0.002) were significant predictors for spike. Conclusions: In low-risk prostate cancer patients, PSA spikes are most common in patients implanted with I-125 and/or younger than 65 years of age. Differences in isotope-related spikes are most pronounced in hormone naïve patients. No significant financial relationships to disclose.
The Value of Early SPECT/CT and Hand-Held γ-Camera in Radio-Guided Surgery
Authors: Paloma García-Talavera, María Luisa González-Selma, María Ángeles Ruiz, Claudia Gamazo, Aurora Sainz-Esteban, Juan Gabriel Villanueva, Roberto Olmos
Journal: Clinical Nuclear Medicine (2014)

A patient with primary hyperparathyroidism underwent radio-guided surgery by means of a γ-probe and a hand-held γ-camera. Before surgery, a parathyroid double-phase planar scintigraphy and an early SPECT/CT with 99mTc-MIBI were performed and suggested an ectopic parathyroid adenoma with early washout. The hand-held γ-camera was very useful for the localization of a parathyroid adenoma, which could not be found with the probe probably due to its faint uptake and to a high blood pool activity because it was localized next to the great vessels. Besides, it demonstrated the complete extirpation of the parathyroid tissue.
AB0871 Effect of cigarette smoking in chinese patients with ankylosing spondylitis
Authors: C.T. Chou, C.H. Chen, H.A. Chen, H.T. Liao, C.H. Liu
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Accumulating evidence showed smoking has been associated with inflammation and play a pivotal role in the development of RA. <h3>Objectives</h3> To investigate whether the smoking has an association with ankylosing spondylitis (AS) on disease activity, functional ability and physical mobility in Chinese patients. <h3>Methods</h3> Seventy-five Chinese male AS patients in Taiwan were enrolled in the cross-sectional study. Patients completed the questionnaires, containing BASDAI, BASFI and BAS-G. Meanwhile, physical examinations were performed, including lumbar flexion (modified Schober index, MSI), intermalleolar distance (IMD), cervical rotation (CR), lateral lumbar flexion (LLF), fingertip-to-floor distance (FFD), chest expansion (CE) and occiput-to-wall distance (OWD). Smoking habit included smoking duration, and smoking intensity (pack-years of smoking) <h3>Results</h3> Among the physical mobility parameters, MSI (p&lt;0.001), CR (p=0.034), LLF (p=0.002) and CE (p=0.016) were significantly reduced in the AS patients with smoking as compared to those with non-smoking. OWD was significantly increased in the patients with smoking than those with non-smoking (p=0.003). ESR was significantly higher in the AS patients with smoking than those with non-smoking (p=0.03). Among the 35 smoking AS patients, smoking intensity significantly correlated with BASFI (r =0.481, p=0.005), CR (r = -0.401, p=0.031), FFD (r =0.485, p=0.004), and OWD (r =0.473, p=0.005). <h3>Conclusions</h3> The cigarette smoking is associated systemic inflammation, and poor physical mobility in Chinese AS patients, and quit smoking is an important recommendation for AS patients. <h3>Disclosure of Interest</h3> None Declared
Role of Hexamethylmelamine in the Treatment of Ovarian Cancer: Where is the Needle in the Haystack?
Authors: J. H. EDMONSON, H. S. WIEAND, G. W. MCCORMACK
Journal: JNCI Journal of the National Cancer Institute (1988)

Journal Article Role of Hexamethylmelamine in the Treatment of Ovarian Cancer: Where is the Needle in the Haystack? Get access JOHN H. EDMONSON, JOHN H. EDMONSON 1Mayo ClinicRochester, MN 55095 Search for other works by this author on: Oxford Academic PubMed Google Scholar HARRY S. WIEAND, HARRY S. WIEAND 1Mayo ClinicRochester, MN 55095 Search for other works by this author on: Oxford Academic PubMed Google Scholar GREG W. MCCORMACK GREG W. MCCORMACK 2Fargo Clinic737 Broadway, Fargo, ND 58123 Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 80, Issue 14, 21 September 1988, Pages 1172–1173, https://doi.org/10.1093/jnci/80.14.1172 Published: 21 September 1988