tbuckley/cabot-search huggingface dataset:
Abstract 1190: Gene expression profiling identified FYN as an important gene in tamoxifen resistance and a predictor of early recurrence in patients treated with endocrine therapy .
Authors: Daniel Elias Roro, Henriette Vever, Henrik Ditzel
Journal: Cancer Research (2013)

Abstract To elucidate the molecular mechanisms of tamoxifen resistance in breast cancer we performed microarray profiling and identified 366 genes with altered expression in 4 tamoxifen-resistant (TamRs) vs. the parental tamoxifen-sensitive MCF-7/S0.5 cell lines. Most of these genes were functionally linked to cell growth, proliferation, death and control of gene expression and included FYN, PRKCα, ITPR1, DPYD, DACH1, GBP1 and PRLR. Increased expression of FYN was observed in TamR cells and treatment with FYN-specific interfering RNA or a specific Src family kinase (SFK) inhibitor restored the anti-proliferative effect of tamoxifen in these cells. TamR cells also expressed increased levels of phosphorylated breast cancer antiestrogen resistance protein 1 (pBCAR1), an important downstream SFK substrate in the MAPK pathway. Evaluation of the association of subcellular localization of FYN in cancer tissue and clinical endpoints was made in 2 cohorts of ER+ breast cancer patients, one with advanced disease (N=47) and the other with early breast cancer (N=76). The result showed that plasma membrane-associated FYN expression in the cancer cells strongly correlated with longer progression-free survival compared to FYN expression not associated with the plasma membrane (p&amp;lt;0.0002) in the advanced disease cohort. Similarly, in the early breast cancer patients, plasma membrane associated FYN expression was associated with longer metastasis-free survival (p&amp;lt;0.003) and overall survival (p&amp;lt;0.0005) independent of tumor size, grade and node status. Our results indicate that FYN plays an important role in tamoxifen resistance, and its subcellular location in breast tumor cells may be an important novel biomarker of response to endocrine therapy in breast cancer. Citation Format: Daniel Elias Roro, Henriette Vever, Henrik Ditzel. Gene expression profiling identified FYN as an important gene in tamoxifen resistance and a predictor of early recurrence in patients treated with endocrine therapy . [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 1190. doi:10.1158/1538-7445.AM2013-1190
To twist or not to twist: a case of ERCP in situs inversus totalis
Authors: Kumkum Patel, Jay Patel, Siddharth Mathur, Yitzchak Moshenyat
Journal: Endoscopy (2014)

A 57-year-old woman with history of hypercholesterolemia and situs inversus totalis presented with a chief complaint of epigastric pain and poor appetite for 2 days. The epigastric pain was 7/10 in intensity with no radiation. On physical examination, she had no abdominal scars but there was evidence of hepatosplenomegaly and epigastric tenderness on palpation, although Murphy's sign was negative; bowel sounds were normal on auscultation. The results of laboratory testing revealed normal aspartate transaminase (AST) and alanine transaminase (ALT) levels, but an elevated total bilirubin of 1.3 mg/dL. The alkaline phosphatase (ALP) level was 112 IU/L (normal 45 – 115 IU/L) and the γ-glutamyltransferase (GGT) was 195 IU/L (normal 0 – 42 IU/L). Biliary ultrasound revealed a moderately dilated common bile duct and multiple gall stones. A computed tomography (CT) scan of the abdomen and pelvis confirmed the diagnosis of situs inversus totalis with hepatosplenomegaly ([Fig. 1]).
Abstract 1428: Upregulation of IKBKE promotes glioma cell migration and invasion by phosphorylation of Snail
Authors: Jianping Guo, Qiang Huang, Shaokun Shu, Donghwa Kim, Steven S. Brem, Jin Q. Cheng
Journal: Cancer Research (2011)

Abstract IKBKE is a member of IκB kinase (IKK) family. Previous studies have shown that IKBKE is an oncogene in breast and ovarian cancer. In this study, we demonstrate that IKBKE is frequently upregulated in human glioma and regulates cell invasion, a process that causes incurable surgery for glioma. Increase expression of IKBKE was detected in 7 of 11 glioma cell lines and 41 of 57 primary tumors examined, which closely correlates with high grade tumors and patient poor overall survival. Further, ectopic expression of IKBKE induces and knockdown of IKBKE decreases cell migration and invasion. Notably, E-cadherin protein and mRNA levels were inversely regulated by IKBKE. Moreover, we demonstrated that IKBKE directly binds and phosphorylates Snail at Ser-165. The phosphorylation of Snail induces its stability and nuclear translocation and represses E-cadherin expression. Taken together, these findings indicate that IKBKE could play a pivotal role in gliomagenesis and invasion. 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 1428. doi:10.1158/1538-7445.AM2011-1428
OP0040 Patients from Wealthier Countries Perform Better on Clinical Disease Activity Measures, but Show Worse Person Reported Outcomes: Table 1.
Authors: P. Putrik, S. Ramiro, A.P. Keszei, I. Hmamouchi, M. Dougados, M. Hifinger, L. Gossec, A. Boonen
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> Inequalities in health between low and high income countries are often reported, but it is not known whether clinical disease activity measures ("objective") and person reported outcomes ("subjective") follow the same patterns in patients with RA. <h3>Objectives</h3> To investigate the patterns in RA health outcomes across countries with different level of socio-economic development. <h3>Methods</h3> Data from a cross-sectional multinational (17 countries) study COMORA was used. Contribution of gross domestic product (GDP) to clinical disease activity measures (DAS28, total joint count (TJC), swollen joint count (SJC), and erythrocyte sedimentation rate (ESR)) and person reported outcomes (Patient global assessment (PatGA), fatigue, Physician global assessment (PhysGA) and function assessed with health assessment questionnaire (HAQ)) was explored. All models were adjusted for potentially relevant confounders, including age, gender, education and comorbidities (Wolfe-Michaud index). Models were computed with and without adjustment for current RA medication (steroids, NSAIDs and DMARDs). Additionally, models with person reported outcomes were adjusted for the presence of erosive disease, TJC, SJC, and ESR. GDP was dichotomized in low and high GDP countries (with a cut-off of 21500 international dollars per capita (adjusted to purchasing power parity), which by data inspection was the one that discriminated best both groups). <h3>Results</h3> A total of 3920 RA patients from 17 countries (range 30-411) were included in COMORA (mean age 56 y.o. (SD13), 82% females). In models adjusted for medication, low GDP countries had on average 0.8 higher DAS28, 2.24 and 1.71 higher scores on TJC and SJC, respectively, and 8.92 higher ESR compared to high GDP countries. At the same time, patients from low GDP societies had a 0.44 and 0.14 lower score on patient and physician global assessment, respectively and 0.9 lower score on fatigue compared to high GDP countries. HAQ was not associated with GDP (Table). <h3>Conclusions</h3> Patients from countries with lower socio-economic welfare score worse on clinical measures of disease activity (DAS28 and its components), however, score systematically better on person reported outcomes (patient global assessment and fatigue). Cultural factors that may play a role in reporting of more subjective outcomes should be further explored. <h3>Disclosure of Interest</h3> P. Putrik: None declared, S. Ramiro: None declared, A. Keszei: None declared, I. Hmamouchi: None declared, M. Dougados: None declared, M. Hifinger Employee of: Hexal AG, Germany (inactive employment, maternity leave), L. Gossec: None declared, A. Boonen: None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.2035
Marked Uptake of Tl-201 in Intracranial Extracerebral Cavernous Hemangioma
Authors: XIAO-MING WANG, KOTARO HIGASHI, KOICHIRO AYABE, YUKIKO MOTOMURA, MANABU OGUCHI, ITARU YAMAMOTO, TAKAAKI IIDA, HIDEAKI IIZUKA, TAKAYUKI NOJIMA
Journal: Clinical Nuclear Medicine (1999)

A case of intracranial extracerebral cavernous hemangioma in the middle fossa is presented. A 78-year-old woman was hospitalized because of progressive gait disturbance and left eyelid ptosis. Enhanced CT images showed a markedly enhanced tumor in the middle fossa. The diagnosis based on CT scans was a parasellar meningioma. Tl-201 SPECT scans showed a prominent ring-like accumulation in the tumor on early imaging. Tl-201 uptake became reduced and remained scant on delayed images. After surgery, the pathologic diagnosis was intracranial extracerebral cavernous hemangioma. The described Tl-201 uptake pattern may be specific for intracranial extracerebral cavernous hemangioma.
ASSESSING LEFT VENTRICULAR FILLING PRESSURE USING FINGER PHOTOPLETHYSMOGRAPHY DURING THE VALSALVA MANEUVER PREDICTS 30-DAY HEART FAILURE OUTCOMES
Authors: Nisha A. Gilotra, Brett Wanamaker, Hussein Rahim, Katherine Kunkel, Saadia Rizvi, Steven Schulman, Ryan Tedford, Stuart Russell, Harry A. Silber
Journal: Journal of the American College of Cardiology (2016)
Abstract 4793: Aberrant methylation of CDH1 correlates with poor prognosis in patients with head and neck squamous cell carcinoma
Authors: Bianca L. Rivera-Peña, Adriana Baez
Journal: Cancer Research (2011)

Abstract Objective: CDH1 codes for E-cadherin, a key adhesion molecule of epithelial cells, whose loss of expression has been associated with carcinogenesis in several types of cancer. Promoter hypermethylation of CDH1 results in loss of expression of E-cadherin and may be involved in the development of metastasis and a poorer prognosis. The purpose of this study was to determine the methylation profile of CDH1 in a cohort of HNSCC patients and evaluated its association with clinicopathological parameters. Methods: CDH1 methylation status was determined using the Methylight assay in a cohort of 59 patients that had CDKNA (p16) methylation status assessed previously. Correlations between clinical parameters and methylation profiles were statistically analyzed using Fisher's exact test and chi-square test when appropriate. Results: Aberrant methylation of CDH1 was detected in 78% of the cases analyzed. In 33% of the patients had also CDKN2A aberrantly methylated. Most patients (69%) with CDH1 aberrantly methylated were in advanced stages of the disease (III/IV). They also had a poorer survival rate. No statistically significant association was found between CDH1 hypermethylation and gender, age, risk factors and staging. Conclusion: CDH1 aberrantly methylated was detected at early and late stages of the disease. These results suggest that CDH1 hypermethylation may have a role in the initiation and in progression of HNSCC and potentially reduce the survival of HNSCC patients. 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 4793. doi:10.1158/1538-7445.AM2011-4793
FRI0394 Subclinical heart involvement in patients with systemic sclerosis: a controlled study
Authors: C. Papagoras, N. Tsifetaki, K. Achenbach, A. Georgiou, S. Tsiouris, A. Fotopoulos, A. A. Drosos
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> The pathophysiological hallmarks of systemic sclerosis (SSc), i.e. functional and morphological vascular alterations, systemic inflammation and aberrant collagen deposition may affect the cardiovascular system and produce an array of clinical manifestations, e.g. pulmonary arterial hypertension, restrictive cardiomyopathy, conduction heart disturbances or premature atherosclerosis. <h3>Objectives</h3> To investigate cardiac structural and functional parameters in SSc patients without clinically evident heart disease. <h3>Methods</h3> SSc patients and age- and sex-matched healthy controls underwent transthoracic echocardiography for the evaluation of left ventricular (LV) morphology and function, of cardiac valves and for the estimation of pulmonary systolic arterial pressure (PASP). Additionally, patients underwent stress-rest myocardial perfusion imaging (MPI) scintigraphy by single-photon emission computed tomography (SPECT) for the detection of reversible myocardial perfusion defects. <h3>Results</h3> Thirty-three female and 4 male SSc patients with a mean age of 54.4 years and 37 matched controls were studied. Nineteen patients had diffuse and 18 limited SSc, with a mean disease duration of 18.6 years. Echocardiography revealed LV hypertrophy in 9 patients (24.3%), but in none of the controls (p=0.001) and LV diastolic dysfunction in 17 (45.9%) patients and 15 (40.5%) controls (p=0.639). After exclusion of patients with arterial hypertension, LV hypertrophy was still found in 23.1% (p=0.002 vs controls) and LV diastolic dysfunction in 38.5% (p=0.868 vs controls). Median LV ejection fraction (EF) was 67% (range 50-80) and 66% (range 54-78) in patients and controls respectively (p=0.436). SSc patients had median PASP 30 (range 20-51) mmHg, while controls had median PASP 20 (14-28) mmHg (p&lt;0.001). Of the 35 SSc patients who underwent scintigraphic MPI, 21 patients (60%) exhibited reversible LV perfusion defects. Their mean age was 51.8 years. In all cases ischemia was graded as mild or moderate and in only one case as significant. There were no statistically significant differences regarding demographics, echocardiography or autoantibody profile between patients with and without ischemia. <h3>Conclusions</h3> Left ventricular hypertrophy and raised PASP were more common in SSc patients than healthy controls. Moreover diastolic dysfunction and reversible ischemia were found in a significant proportion in this group of mostly female middle-aged SSc patients. A high level of awareness for subclinical heart involvement is warranted when treating patients with SSc. <b>Disclosure of Interest</b>: None Declared
Some Characteristics of a Human Cell Line (AICHI-4) Established From Tumorous Lymphatic Tissue of Hodgkin's Disease&lt;xref ref-type="fn" rid="FN2"&gt;2&lt;/xref&gt;
Authors: Yohei Ito, Osamu Shiratori, Soji Kurita, Toshitada Takahashi, Yoshinori Kurita, Kazuo Ota
Journal: JNCI Journal of the National Cancer Institute (1968)

A human cell line (AICHI-4) was established from the lymphatic tissue of a patient with typical Hodgkin's disease. Morphologically the culture appeared to have three types of cells, small, medium-sized, and giant, which could possibly be interpreted as lymphocytes, reticulum cells, and Hodgkin's cells, respectively. Some additional findings on the growth pattern and chromosome analysis of the cell line are also described.
Abstract 2293: MicroRNA-1826 targets VEGFC, beta-catenin (CTNNB1) and MEK1 (MAP2K1) in human bladder cancer.
Authors: Hiroshi Hirata, Yuji Hinoda, Koji Ueno, Varahram Shahryari, Z. Laura Tabatabai, Rajvir Dahiya
Journal: Cancer Research (2012)

Abstract Introduction and Objective: The Wnt/beta-catenin (CTNNB1) and Ras-Raf-MEK-ERK signaling pathway play an important role in bladder cancer progression. Tumor suppressive miRNAs targeting these cancer pathways may provide a new therapeutic approach for bladder cancer. Methods: We initially identified miRNA-1826 potentially targeting CTNNB1, VEGFC, MEK1 using several target scan algorithms. The expression of miR-1826 was confirmed in bladder cancer tissues and bladder cancer cell lines. Then we performed several functional analyses of miR-1826. Finally 3′UTR luciferase assay and Western blot were performed to look at relationship between miR-1826 and target genes. Results: MiR-1826 expression was significantly lower in bladder cancer tissues and bladder cancer cell lines (J82, T24, TCC-SUP) compared to normal bladder tissues and normal bladder cell lines (SV-HUC-1). The expression of miR-1826 was lower in bladder cancer tissues and inverse correlation of miR-1826 with several clinical parameters (pT, grade) was observed. The functional analyses showed that miR-1826 inhibited bladder cancer cell viability, invasion and migration. Also we also found increased apoptosis and G1 cell cycle arrest in miR-1826 transfected bladder cancer cells. 3′UTR luciferase activity and protein expression of these target genes (CTNNB1, MEK1, VEGFC) were significantly down-regulated in miR-1826 transfected bladder cancer cells (J82, T24). To examine whether the effect of miR-1826 was through CTNNB1 (beta-catenin) or MEK1 knock down, we knocked down CTNNB1/MEK1 mRNA using a si-RNA technique. We observed that CTNNB1 or MEK1 siRNA knockdown resulted in effects similar to those with miR-1826 in bladder cancer cells. Conclusions: Our data suggests that the miR-1826 plays an important role as tumor suppressor via CTNNB1/MEK1/VEGFC down-regulation in bladder cancer. 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 2293. doi:1538-7445.AM2012-2293
Adventures among Viruses
Authors: Christopher Howard Andrewes
Journal: New England Journal of Medicine (1950)

DURING the past sixteen years influenza has been, I imagine, the virus that has received most study and attention in the laboratory, though poliomyelitis must run it very close. It has been studied by workers trained in very different disciplines and approaching it from many angles. Perhaps most novel and exciting is the work based on Hirst's1 discovery of the power of the virus to agglutinate red cells of fowls. Directly deriving from this finding is the demonstration that influenza virus, or a part of it, has an enzyme-like action upon a carbohydrate-containing protein; this protein is present in serum . . .
Abstract 1899: Induction of phase 2 antioxidant genes by the aqueous extract of Matricaria chamomilla (Chamomile) through Keap1-Nrf2 signaling pathway
Authors: Natarajan Bhaskaran, Sanjeev Shukla, Sanjay Gupta
Journal: Cancer Research (2010)

Abstract Induction of phase 2 detoxifying enzymes in response to naturally occurring agents provides an effective means of protection against oxidative stress. Increasing lines of evidence show that the Keap1-Nrf2 complex is a key molecular target of phase 2 enzyme inducers. The transcription factor Nrf2 is a member of basic leucine-zipper NF-E2 family and interacts with the antioxidant response element (ARE) in the promoter region of phase 2 detoxifying enzymes. A cytoplasmic actin-binding protein, Keap1, is an inhibitor of Nrf2 and sequesters it in the cytoplasm. Various extracellular stimuli and inducers dissociate this complex, allowing Nrf2 to translocate into the nucleus, binding with ARE and induce the expression of various antioxidant genes. Recently natural compounds have been established as activators of phase 2 antioxidant enzymes through Nrf2 signaling pathway. We used aqueous chamomile extract obtained from dried flowers to investigate its effect on Nrf2 activation and induction of phase 2 enzymes in human prostate cancer PC-3 and LNCaP cells. Treatment of these cells with chamomile at 1-40μM concentration equivalent to aglycone apigenin caused significant dissociation of Keap1 from the Keap1-Nrf2 complex with significant decrease of Keap1 in the cytoplasm in dose- and time- dependent fashion. Similarly, a marked decrease in Nrf2 was observed in the cytoplasm after chamomile treatment. Chamomile treatment further led to increase in phase 2 enzymes including superoxide dismutase, NAD(P)H dehydrogenase [quinone] 1 and catalase in these cells which correlated with nuclear Nrf2 expression in dose- and time- dependent manner. Taken together, these molecular evidences provide an insight into the mechanism underlying the induction of phase 2 enzymes through Keap1- Nrf2 signaling pathway by chamomile, endorsing its antioxidant function. 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 1899.
Tl-201 and Ga-67 Scintigraphy in Non-Hodgkin's Lymphoma
Authors: ROBERT MANSBERG, SURJIT S. WADHWA, VICTOR MANSBERG
Journal: Clinical Nuclear Medicine (1999)

Ga-67 scintigraphy is routinely used to stage and monitor non-Hodgkin's lymphoma (NHL). It is highly sensitive in high-grade NHL but less so in intermediate- and low-grade NHL. Several studies have reported the use of Tl-201 in the low and intermediate grades of NHL and found it superior in low-grade NHL. In this study, the authors evaluated the utility of combined Ga-67 and Tl-201 scintigraphy in low, intermediate, and unusual types of NHL. Combined Tl-201 and Ga-67 scintigraphy were done in 33 patients (18 women, 15 men; age range, 21-91 years; mean age, 56 years). Tl-201 and Ga-67 had similar overall patient sensitivity in the 33 patients studied. However, the use of both agents increased the over-all patient sensitivity from 67% (for Ga-67 only) to 82% and improved the overall site detection from 59 positive sites with Ga-67 to 81 abnormal sites with both Tl-201 and Ga-67. The combined use of Tl-201 and Ga-67 scintigraphy in low- and intermediate-grade NHL resulted in increased disease and site detection and is beneficial for clinical follow-up.
CLINICAL IMPACT OF BRADYCARDIA ON THE INCIDENCE OF ATRIAL FIBRILLATION IN A POPULATION-BASED COHORT STUDY
Authors: Takashi Kobayashi, Yoshihiro Kokubo, Makoto Watanabe, Aya Higashiyama, Yoko M. Nakao, Takuya Watanabe, Kunihiro Nishimura, Misa Takegami, Michikazu Nakai, Shiro Kamakura, Kengo Kusano, Yoshihiro Miyamoto
Journal: Journal of the American College of Cardiology (2015)