tbuckley/cabot-search huggingface dataset:
Elevated 68Ga Prostate-Specific Membrane Antigen Activity in Metastatic Non–Small Cell Lung Cancer
Authors: Deepa Shetty, Han Loh, Chuong Bui, Robert Mansberg, Amanda Stevanovic
Journal: Clinical Nuclear Medicine (2016)

A 71-year-old man with a background of treated stage IIIB non–small cell lung cancer was referred for 68Ga prostate-specific membrane antigen (PSMA) PET/CT for staging of prostate cancer. In addition to the PSMA uptake in the known prostate malignancy, the study also demonstrated increased PSMA uptake in an enlarging left lower lobe lung mass with diffusely increased PSMA uptake in an enlarged thyroid gland and bilateral enlarged supraclavicular lymph nodes. Fine-needle aspiration biopsy of the thyroid gland and a left supraclavicular lymph node demonstrated metastatic adenocarcinoma from a primary lung cancer.
Gastrinomas in the Duodenums of Patients with Multiple Endocrine Neoplasia Type 1 and the Zollinger-Ellison Syndrome
Authors: Miriam Pipeleers-Marichal, Guido Somers, Gerard Willems, Alan Foulis, Clem Imrie, Anne E. Bishop, Julia M. Polak, Walter H. Häcki, Bernhard Stamm, Philipp U. Heitz, Günter Klöppel
Journal: New England Journal of Medicine (1990)

In patients with multiple endocrine neoplasia type 1 (MEN-1), gastrinomas are common and thought to occur predominantly in the pancreas. We describe eight patients with MEN-1 and hypergastrinemia (seven with the Zollinger—Ellison syndrome) in whom we searched for neuroendocrine tumors in the pancreas and duodenum.
Tc-99m Pertechnetate Scintigraphy To Diagnose Rectal Duplication
Authors: SUPATPORN TEPMONGKOL, SYDNEY HEYMAN
Journal: Clinical Nuclear Medicine (1999)

An 8-year-old girl was hospitalized for repeated evaluation for recurrent painless rectal bleeding. Results of the first colonoscopy were normal up to the hepatic flexure. Laboratory evaluations revealed normal prothrombin time, partial prothrombin time, complete blood count, and erythrocyte sedimentation rate. On this admission, results of a Meckel's scan were negative for Meckel's diverticulum. Repeated colonoscopy revealed a rectal diverticulum 5 cm above the anal verge with mildly inflamed cobblestone mucosa. A review of the Meckel's scan showed abnormal uptake in the rectal area. The barium enema showed a duplication of the distal rectum. At surgery, the duplication was found to be 2 cm long and lined by gastric-type epithelium.
AB0740 The frequency of occult hepatitis b infection in rheumatic diseases and the role of anti-hbc test in routine practice
Authors: S. Yilmaz, K. Sener, I. Simsek, M. Cinar, R. Gumral, H. Erdem, A. Kubar, S. Pay
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Most of the drugs used in rheumatic diseases suppress the immune system, especially corticosteroids and anti-TNF agents, therefore may cause reactivation in patients with hepatitis B virus (HBV). Studies have shown that HBV reactivation due to immunosuppression is not a case only in patients with chronic HBV infection, but also in patients with occult diseases. The presence of HBV DNA in liver tissue and/or in serum in the absence of detectable hepatitis B surface antigen (HBsAg) is called occult HBV infection. Evidence is accumulating that HBV is present in patients who are HBsAg negative, but have antibody to hepatitis B core antigen (anti-HBc) Therefore, guidelines recommend that anti-HBc IgG tests should be added to HBsAg and anti-HBs tests before initiation of immunosuppressive therapy. <h3>Objectives</h3> In the present study we aimed to determine the prevalence of occult HBV infection in patients receiving immunosuppressive agents and examine the role of anti-HBc as a screening test for occult infection in Turkish patients with rheumatic diseases. <h3>Methods</h3> Consecutive patients using immunosuppressive agents for rheumatic diseases seen in rheumatology outpatient clinic and who are negative for HBsAg were included. The demographic features, received treatment in last 3 months and liver function tests of all patients were recorded. HBsAg, Anti-HBs and anti-HBc IgG tests were studied in all participants along with the quantification of HBV-DNA by real-time PCR. <h3>Results</h3> Total 116 patients included to the study (59 spondylarthritis, 39 romatoid arthritis, and 18 others). The demographic features and received treatment in last 3 months were presented in Table 1. In this HBsAg negative group, 27 patients (23%) were found to be positive for anti-HBc IgG. In this subgroup, 19 patients were anti-HBs Ab positive while isolated anti-HBc IgG positivity were detected in other 8 patients. None of the patients was found as HBV-DNA positive. <h3>Conclusions</h3> Since none of our patients with isolated anti-HBc positivity had detectable levels of HBV-DNA in their serum, using anti-HBc test for screening seems not to be justified. While our results suggest that prevalence of occult HBV infection is ignorable among patients with rheumatic diseases in Turkey, considering the preliminary feature of our results (target study population is 300) full results should be waited to reach such a definite conclusion. <h3>Disclosure of Interest</h3> None Declared
The conker tree
Authors: T. Greenhalgh
Journal: BMJ (1997)

I was more resentful than usual about being on call. Earlier, the children had waved me off to Saturday surgery and asked if I would be back for lunch. We'll go to Hampstead Heath and look for conkers, they had said, hopefully.

But it was now 1 30 pm and there seemed little chance of any daylight hours with the family. I had seen the usual stream of worried well and one genuine emergency. Sulkily, I chewed on a dry cheese sandwich in the car on my way to visit an 83 year old lady who had developed a dense paralysis the day before. …
OP0096 Tobacco smoking is associated with increased disease activity in HLA-B27 positive axial spondyloarthritis patients, but does not alter the course of disease activity
Authors: A. Ciurea, A. Scherer, U. Weber, M. Nissen, P. Exer, J. Bernhard, G. Tamborrini, R. Mueller, B. Weiss, R. Kissling, B.A. Michel, A. Finckh
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Smoking is associated with increased disease activity in patients with ankylosing spondylitis (AS) and early axial spondyloarthritis (SpA) in cross-sectional studies, however causation has not been established. <h3>Objectives</h3> To investigate the impact of smoking on disease activity in patients with axial SpA. <h3>Methods</h3> We included all patients from a Swiss population-based axial SpA cohort (SCQM) with available smoking and HLA-B27 status fulfilling the ASAS 2009 criteria for axial SpA. The primary and secondary outcomes for this analysis were the BASDAI and the AS disease activity score (ASDAS-CRP) respectively. The primary exposure of interest was smoking (ever/never) and a secondary analysis examined smoking as current/past/never. We compared clinical and demographic characteristics between smokers and non-smokers cross-sectionally. The course of BASDAI and ASDAS were analysed using random slope multivariate longitudinal regression models, adjusted for the following potential confounders: baseline levels of BASDAI or ASDAS, anti-TNF treatment, age at first symptoms, disease duration, gender, HLA-B27, BMI and education. <h3>Results</h3> Of the 1129 patients who fulfilled our inclusion criteria, 60% fulfilled the modified New York criteria, 62% were smokers (37% current smokers, 25% past smokers), 84% were HLA-B27 positive, 66% were male, mean age was 39.7 years and mean symptom duration at baseline was 13,5 years. As shown in previous reports, smoking was associated with a higher level of baseline disease activity. Mean BASDAI levels were +0.7 (95% CI: +0.4;+1.0) higher in smokers, with no difference between former and current smokers (wilcoxon test p=0.6). The association of smoking and BASDAI levels varied with regards to HLA-B27 status in the adjusted model (effect modification by HLA-B27, p=0.004). The adjusted mean BASDAI levels were 0.8 (95% CI: +0.3;+1.4) higher in HLA-B27 smokers compared to non-smokers, while no significant differences were observed in HLA-B27 negative smokers (-0.35 [95% CI: -0.9;+0.2]). The adjusted longitudinal evolution of BASDAI was similar between smokers and non-smokers (p=0.7). Similar results were found using ASDAS as the outcome. <h3>Conclusions</h3> In this large observational cohort of axial SpA, the cross-sectional associations between smoking and BASDAI or ASDAS levels depended on the HLA-B27 status; only HLA-B27 positive patients demonstrated increased disease activity with smoking. However, smoking did not alter the long-term evolution of BASDAI and ASDAS in axial SpA, challenging the notion of a causal effect of this environmental factor on disease activity. <h3>Disclosure of Interest</h3> None Declared
N-Myc Drives Neuroendocrine Prostate Cancer Initiated from Human Prostate Epithelial Cells
Authors: John K. Lee, John W. Phillips, Bryan A. Smith, Jung Wook Park, Tanya Stoyanova, Erin F. McCaffrey, Robert Baertsch, Artem Sokolov, Justin G. Meyerowitz, Colleen Mathis, Donghui Cheng, Joshua M. Stuart, Kevan M. Shokat, W. Clay Gustafson, Jiaoti Huang, Owen N. Witte
Journal: Cancer Cell (2016)
Paracoccidioidomycosis simulating cancer diagnosed by endoscopic ultrasound-guided fine needle aspiration
Authors: G. Silva Neto, R. Ganc, R. Colaiacovo, F. Bueno, F. Bernardi, L. Rossini
Journal: Endoscopy (2012)

A 57-year-old woman presented with abdominal pain, jaundice, and a 12-kg weight loss over the preceding 6 months. The abdominal computed tomography (CT) scan demonstrated a mass located in the head of pancreas (6.4 × 5.8 cm). Endoscopic retrograde cholangiopancreatography (ERCP) was performed for biliary drainage with the insertion of a single 10-Fr plastic stent in the common bile duct (CBD), which led to an improvement in her jaundice.
Abstract 5033: Relationship between microRNA expression and Gleason grading system in prostate cancer
Authors: Katsuki Tsuchiyama, Hideaki Ito, Minekatsu Taga, Konosuke Oshinoya, Kenichi Nagano, Osamu Yokoyama, Hiroshi Itoh
Journal: Cancer Research (2012)

Abstract Background: Recent studies have shown that some microRNA (miRNA) expression profiles are associated with clinicopathological findings, including “Gleason score (GS)” in human prostate cancer (PC). However, the direct relationship between “Gleason pattern (GP)” and miRNA expression remains unclear. In this study, we investigated the miRNA expression profile in each GP (GP 3, GP 4, and GP 5). Methods: Formalin-fixed, paraffin-embedded (FFPE) tissue samples obtained from radical prostatectomy (patient set 1, n = 43, including [GP 3] n = 22, [GP 4] n = 35, and [GP 5] n = 12) and prostate needle biopsy (patient set 2, n = 9, [GP 4] n = 9) were used. Cancer tissues and adjacent normal counterparts were collected separately using laser-captured microdissection with subsequent isolation of total RNA. Real time reverse transcription polymerase chain reaction (RT-PCR) was performed to determine the relative expression of miRNAs, including miR-31, -34c, -96, -182, -183, -205, -221, and miR-222, which are currently reported to be involved in the progression of PC. Results: In the radical prostatectomy samples (patient set 1), relative expression (mean ± SE) of miR-31, miR-34c, and miR-205 in every GP was significantly decreased (miR-31: [GP 3] 0.028 ± 0.007, [GP 4] 0.047 ± 0.017, and [GP 5] 0.071 ± 0.022; miR-34c: 0.208 ± 0.066, 0.419 ± 0.219, and 0.210 ± 0.054; and miR-205: 0.021 ± 0.008, 0.015 ± 0.003, and 0.050 ± 0.023, all p-values &amp;lt; 0.01) compared to normal counterparts. However, there was no significant difference between GP 3, GP 4, and GP 5. Meanwhile, in GP4, expression of miR-31, miR-182, and miR-205 in tissues obtained from high-grade cancer (GS 8 or GS 9) were significantly higher than those in tissues obtained from intermediate-grade cancer (GS 7) (miR-31: [high grade] 0.071 ± 0.027, [intermediate grade] 0.011 ± 0.003, p = 0.040; miR-182: 1.745 ± 0.278, 0.864 ± 0.136, p = 0.021; and miR-205: 0.022 ± 0.005, 0.005 ± 0.002, p = 0.002, respectively). Validation testing of biopsy samples (patient set 2) revealed that the relative expression of miR-182 was similarly and significantly higher in high-grade cancer tissue (high grade: 1.863 ± 0.381, intermediate grade: 0.717 ± 0.196, p = 0.043). Conclusion: The expression of miR-182 differed by cancer grade even in the same GP 4, and this difference was detected in both biopsy and radical prostatectomy samples. Our findings suggest that evaluations of miRNA expression with respect to Gleason grading in biopsy samples may contribute to more accurate preoperative cancer risk evaluation. 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 5033. doi:1538-7445.AM2012-5033
THU0184 Predictive Marker for the Long-Term Discontinuation of Infliximab in Rheumatoid Arthritis with Clinical Remission
Authors: M. Yamasaki
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> Patients who achieved disease remission continuously, biologic DMARDs are able to start tapering. But the predictive markers to stop biologic DMARDs were not well known. <h3>Objectives</h3> To assess the clinical characteristics of rheumatoid arthritis (RA) patients treated with infliximab (IFX) and achieved long-term discontinuation of infliximab with clinical remission. <h3>Methods</h3> Efficacy was evaluated by DAS28CRP. Analyze the clinical parameters between patients with more than 2 year discontinuation of IFX and the others. <h3>Results</h3> 52 (7 men, 45 women, average age 52.4 years old) of RA patients were treated with IFX and enrolled in this study. Overall remission rate was 51.9%. However there were no significant differences between patients with remission and without remission in combination therapy with or without MTX, duration of disease before using IFX and initial DAS28 score, MMP-3 ratio (MMP-3 at initial/MMP-3 at 5th IFX) was the only predictive marker at the start of IFX therapy for the discontinuation of IFX with clinical remission (4.71±5.18 vs1.15±0.57, p=0.0279). Assessing the clinical parameters at the final treatment with IFX, there were significant differences between patients with remission and without remission in DAS28CRP (1.30 vs. 2.54, p=0.016). ROC analysis was performed and the cut off point was DAS28CRP=2.08 (AUC0.94) to detect patient with long-term discontinuation of IFX. <h3>Conclusions</h3> MMP-3 ratio was the predictive marker to achieve clinical remission with IFX. DAS28CRP less than 2.08 was also as predictive marker to achieve long-term discontinuation of IFX in RA with clinical remission. <h3>Disclosure of Interest</h3> : None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.4147
Abstract 5331: A novel function of p21 in inhibition of epithelial-mesenchymal transition through microRNAs.
Authors: Xiao L. Li, Toshifumi Hara, Youngeun Choi, Murugan Subramanian, Princy Francis, Sven Bilke, Robert L. Walker, Marbin Pineda, Yu-an Yang, Ji Luo, Lalage M. Wakefield, Ben H. Park, Thomas Brabletz, Dipanjan Chowdhury, Paul S. Meltzer, Ashish Lal
Journal: Cancer Research (2013)

Abstract The tumor suppressor p21 inhibits cell proliferation during the stress response. However, p21 can also directly regulate gene expression by repressing specific transcription factors. Here, we identified p21-regulated miRNAs by sequencing small RNAs from HCT116-p21+/+ and HCT116-p21-/- cells. Three abundant clusters, miR-200b-200a-429, miR-200c-141 and miR-183-96-182 were down-regulated in p21-depleted HCT116 and MCF10A cells. Loss of p21 induced epithelial-mesenchymal transition (EMT) and enhanced migration and invasion in multiple model systems. Identification of genome-wide targets of the miR-183-96-182 cluster indicated that miR-183 and miR-96 repressed common targets, including SLUG, ZEB1, ITGB1 and KLF4, to inhibit EMT, migration and invasion. In turn, elevated ZEB1 levels in HCT116-p21-/- cells directly repressed miR-183-96-182 cluster transcription, revealing a feedback loop. Re-introduction of miR-200, miR-183 or miR-96 in HCT116-p21-/- cells inhibited migration and invasion. These novel findings suggest that coordinated down-regulation of three miRNA clusters upon loss of p21 in unstressed cells promotes EMT, migration and invasion. Citation Format: Xiao L. Li, Toshifumi Hara, Youngeun Choi, Murugan Subramanian, Princy Francis, Sven Bilke, Robert L. Walker, Marbin Pineda, Yu-an Yang, Ji Luo, Lalage M. Wakefield, Ben H. Park, Thomas Brabletz, Dipanjan Chowdhury, Paul S. Meltzer, Ashish Lal. A novel function of p21 in inhibition of epithelial-mesenchymal transition through microRNAs. [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 5331. doi:10.1158/1538-7445.AM2013-5331
Reversible Changes of Brain Perfusion SPECT for Carbon Monoxide Poisoning–Induced Severe Akinetic Mutism
Authors: Shao-Yuan Chen, Chun-Chieh Lin, Yi-Te Lin, Chung-Ping Lo, Chen-Hsu Wang, Yu-Ming Fan
Journal: Clinical Nuclear Medicine (2016)

Purpose This study aimed to characterize changes in regional cerebral blood flow (rCBF) in patients who experienced carbon monoxide (CO) poisoning and subsequently developed severe delayed neuropsychiatric sequelae (DNS) with akinetic mutism. We determined whether these changes were reversible in parallel with improvements in neuropsychological function in response to treatment, including hyperbaric oxygen therapy. Methods Patients who developed severe DNS with akinetic mutism after acute CO intoxication between 2007 and 2011 were enrolled. 99mTc-ECD brain SPECT findings were compared between the patients with severe akinetic mutism and age-matched control subjects to characterize the pattern of rCBF. Perfusion SPECT was correlated with clinical outcomes after treatment with statistical parametric mapping (SPM8); the height threshold was P < 0.01 at peak level, and the corrected false discovery rate was P < 0.05 at the cluster level. Results Seven patients with akinetic mutism were analyzed. All patients had neurological symptoms caused by acute CO exposure, and all recovered to nearly normal daily function after initial treatments. In all cases, after a "lucid interval," DNS progressed to akinetic mutism. The SPECT images acquired at the onset of akinetic mutism demonstrated variable hypoperfusion in frontal-temporal-parietal regions, with the greatest severity in the left temporal-parietal regions. In parallel, we performed functional neuropsychiatric tests. After treatment, the brain SPECT showed significantly fewer hypoperfusion regions, and neuropsychiatric tests showed dramatically improved function. Conclusions Our findings demonstrated both cerebral cortical and subcortical injuries in patients with CO-induced akinetic mutism. Improvement in rCBF correlated well with functional recovery after treatment.
Abstract 3221: Analysis of the relationship between autophagy and senescence in response to Adriamycin in breast tumor cells
Authors: Xu Di, Scott C. Henderson, David A. Gewirtz
Journal: Cancer Research (2010)

Abstract Autophagy is a conservative biological process, which involves the degradation of intracellular components (proteins or organelles) via the fusion of autophagosomes with lysosomes. Autophagy has been reported to have both cytoprotective and cytotoxic actions in response to either chemotherapy or radiation in different tumor model systems. In previous studies (Elmore LW et al., J Biol Chem. 2002 Sep 20; 277(38): 35509-15.), Adriamycin (doxorubicin), one of the primary chemotherapeutic drugs utilized in the treatment of breast cancer, was shown to induce a pronounced senescence response within 72hrs in MCF-7 breast tumor cells (at a clinically relevant concentration of 1μM, with a 2 hr exposure). Interestingly, Adriamycin was also observed to cause a time-dependent increase of autophagy within 72hrs (by acridine orange, Monodansylcadaverine) staining and electron microscopy). The current study was designed to evaluate the relationship between Adriamycin-induced autophagy and senescence in MCF-7 breast tumor cells. The antioxidants, GSH (glutathione) and NAC (N-acetyl cysteine), were previously shown to effectively block Adriamycin-induced senescence (Di X. et al., Biochem Pharmacol. 2009 Apr 1; 77(7):1139-50.). We now demonstrate that both GSH and NAC also effectively abolish Adriamycin-induced autophagy in MCF-7cells (as confirmed by the disappearance of punctuated red fluorescence staining (RFP-LC3) induced by Adriamycin. Unexpectedly, however, the autophagy inhibitors, 3-MA or wortmannin, failed to block Adriamycin-induced senescence (based on β-Gal staining). Another autophagy inhibitor, chloroquine, showed a significant blockade to β-Gal staining, although typical senescence morphology phenotypes, such as cell enlargement and flattening were still observed by phase contrast microscopy. Silencing of the autophagic protein, ATG5, failed to completely block Adriamycin-induced senescence, although the MCF-7/ATG5 knockdown cells showed decreased and delayed β-Gal staining. Taken together, our studies suggest that that autophagy proceeds and may contribute to the development of Adriamycin-induced senescence. The fact that blockade of senescence (by reactive oxygen scavengers) abrogates Adriamycin-induced autophagy further suggests that senescence and autophagy may be collaterally regulated in response to Adriamycin in MCF-7 cells. Both autophagy and senescence may be related to tumor dormancy (Gewirtz DA, Autophagy. 2009 Nov 24; 5(8).). Further studies are in progress to delineate the roles (cytoprotective or cytotoxic) of autophagy and the relationship of autophagy to senescence, tumor dormancy and sensitivity to chemotherapy and radiation. 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 3221.
Functional and genetic screening of acute myeloid leukemia associated with mediastinal germ cell tumor identifies MEK inhibitor as an active clinical agent
Authors: Jessica T. Leonard, Philipp W. Raess, Jennifer Dunlap, Brandon Hayes-Lattin, Jeffrey W. Tyner, Elie Traer
Journal: Journal of Hematology & Oncology (2016)

Hematologic malignancies arising in the setting of established germ cell tumors have been previously described and have a dismal prognosis. Identification of targetable mutations and pathway dysregulation through massively parallel sequencing and functional assays provides new approaches to disease management. Herein, we report the case of a 23-year-old male who was diagnosed with a mediastinal germ cell tumor and subsequent acute myeloid leukemia. A shared clonal origin was demonstrated through identification of identical NRAS and TP53 somatic mutations in both malignancies. The patient's leukemia was refractory to standard therapies with short interval relapse. Functional assays demonstrated the patient's blasts to be sensitive to the mitogen-activated protein kinase kinase (MEK) inhibitor trametinib, correlating with the activating NRAS mutation. The patient experienced a sustained partial remission while on trametinib therapy but ultimately suffered relapse of the germ cell tumor. The leukemic clone remained stable and sensitive to trametinib at that time. This case highlights the potential power of combining genetic sequencing and in vitro functional assays with targeted therapies in the treatment of rare diseases.
395 COX-2 DRIVES THE SELECTIVE INDUCTION OF APOPTOSIS BY THE ENDOCANNABINOID 2-ARACHIDONOYL GLYCEROL IN HEPATIC STELLATE CELLS
Authors: S.V. Siegmund, A. Wojtalla, M. Schlosser, T. Sauerbruch, M.V. Singer
Journal: Journal of Hepatology (2012)