tbuckley/cabot-search huggingface dataset:
Abstract LB-440: Global DNA hypomethylation is independently associated with clinical diagnosis of gastric cancer, inflammation severity, and metaplasia
Authors: Rafael E. Guerrero-Preston, Martha Jahuira-Arias, Robert Gilman, Ethan Soudry, Jimena Perez, Andrea Mancinelli, Helen Unger, Carmen Ili-Gangas, Priscilla Brebi-Mieville, David Sidransky
Journal: Cancer Research (2011)

Abstract Background: DNA hypomethylation of repetitive elements has been shown to play a significant role in gastric carcinogenesis. However, Biomarker Development Trials on gastric mucosa that quantify global 5-methyl cytosine (5mC) content across repetitive and non-repetitive regions of the genome are lacking. Methods: We utilized an ELISA-based approach to quantify the global DNA Methylation Index (GMI) in a gastric cancer case-control study. Quantification of global DNA methylation was obtained by differential methylation calculation of 5mC relative to global cytidine (5mC +C) in samples compared to a hypermethylated human genomic DNA control. Results: A cohort of 209 patients, a slight majority of which were women (52%) with a mean age of 63 years, were diagnosed by endoscopy at three outpatient clinics in Perú. Utilizing the updated Sydney, 50 adenocarcinoma cases and 159 non-tumor controls were subsequently confirmed by pathologists. The GMI mean was significantly lower (p-value &amp;lt; 0.0001) for clinically defined cases, mean = 3.6 (95% CI, 3.03, 4.07) compared to controls, mean = 6.2 (95% CI, 5.37,7.03). The GMI mean was also significantly lower (p-value = 0.0001) for cases defined by pathologists, mean = 3.7 (95% CI, 2.99, 4.39) compared to controls, mean = 5.6 (95% CI, 4.94, 6.34). In stratified analyses, we found the GMI mean to decrease as the severity of inflammation increased. The GMI mean was significantly lower (p-value =0.02) for moderate inflammation, mean = 4.7 (95% CI, 3.66, 5.72) compared to mild inflammation, mean = 6.4 (95% CI, 5.34,7.5). The GMI was also non-significantly reduced in patients with intestinal metaplasia, mean =4.81 (95% CI, 3.5,6.10) when compared to patients without metaplasia, mean = 5.96 (95% CI 5.09, 6.83). Discussion: We have shown significant differential global DNA hypomethylation in the progression of gastric lesions through the multistep carcinogenesis stages leading to gastric cancer in a case-control study. In patients diagnosed as controls, global hypomethylation was shown to decrease as the levels of inflammation increased. Patients with intestinal metaplasia also had a lower GMI than those without metaplasia. GMI may be a potentially useful biomarker for clinical detection, inflammation severity, and disease progression in gastric cancer. These results should be replicated in a larger study. 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 LB-440. doi:10.1158/1538-7445.AM2011-LB-440
The Value of EUS in Diagnosis and Treatment for Gastric MALT Lymphoma
Authors: Jian Chen, Liang Zhong, Jie Liu
Journal: Endoscopy (2011)

Aims: Most primary gastric lymphomas are classified as mucosa-associated lymphoid tissue (MALT) lymphoma, which is low-grade malignant and caused by long-term Helicobacter pylori infection. The present study was to review the clinical significance of endoscopic ultrasongraphy in 13 suspected gastric MALT lymphoma cases.
EXPERIENCIA SOBRE LA UTILIZACIÓN DE LAS PRÓTESIS AUTOEXPANDIBLES EN CCR
Authors: M Bocanegra, E Morcillo, L Vázquez, J Mostazo, C Gonzalez, I Pinazo, E Omonte, R Manteca, F García-Consuegra, JR Perea
Journal: Endoscopy (2014)

Introducción: Las prótesis autoexpandibles metálicas (PAM) han supuesto una alternativa válida en el tratamiento de urgencia de la obstrucción maligna colorrectal. Su empleo permite tanto la posibilidad de una cirugía diferida con menores tasas de morbilidad y mortalidad (prótesis puente) como su colocación definitiva paliativa en los casos no candidatos a cirugía.
Abstract 4011: Why does this <i>APC</i> exon 9 mutation causes severe and not attenuated familial adenomatous polyposis (FAP)
Authors: Peh Yean Cheah, Yu Hui Wong, Carol Loi, Poh Koon Koh, Choong Leong Tang
Journal: Cancer Research (2012)

Abstract Familial adenomatous polyposis (FAP), an autosomal dominantly inherited form of colorectal cancer (CRC), is characterized by up to thousands of adenomatous polyps in the colon and rectum of an affected individual by the second or third decade of life. The risk of cancer is virtually 100% if the polyps are not removed in time. Germline mutation in the tumor suppressor, adenomatous polyposis coli (APC) gene causes the majority (80%) of FAP. Point mutation in 5′end of exon 9 of APC usually results in an attenuated form of FAP (aFAP), characterized by later age of onset (forth or fifth decade of life) and much less (&amp;lt;100) polyps. The presence of a physiological in-frame isoform with exon 8 spliced to 3′end of exon 9 (exon 9a) dilutes any deleterious effect of the mutation. We report here an interesting case of a proband with an APC mutation in 5′end of exon 9 that presented with 6 synchronous advanced CRC at age 37. The novel insertion-deletion (indel) mutation at codon 409 removes an exonic splice enhancer site that causes skipping of the whole of exon 9 in the mature transcript, resulting in a premature stop codon at exon 10 and a truncated protein that removes all of the β-catenin (CTNNB1) binding motifs, thus activating the downstream T-cell transcription factor (Tcf) pathway. This surprising consequence of the indel would not have been identified if the mutation screening has not begun with the protein truncation test and the APC transcript. The finding indicates the necessity of examining any point mutation in the 5′end of exon 9 for exonic splice enhancer or repressor site to avoid clinical mismanagement and counseling based on just the mutation site. 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 4011. doi:1538-7445.AM2012-4011
Abstract 4688: Met receptor tyrosine kinase cross-talk in tumorigenesis
Authors: Andrea Lai, Morag Park
Journal: Cancer Research (2011)

Abstract The Met receptor tyrosine kinase (RTK) is a cell surface, transmembrane protein that is activated in response to the growth factor Hepatocyte Growth Factor (HGF) and initiates multiple downstream signaling pathways that predominantly promote cell migration and invasive cell growth. These processes are essential for Met-dependent signals during development. Dysregulated signaling of Met has been characterized in cancers, and include mechanisms such as point mutations, gene amplification, overexpression, and loss of negative regulation and more recently evidence of Met cross talk with other RTKs has been established. However, the role of Met cross-talk with other cell surface receptors in tumorigenesis, is still poorly understood. Recent studies in non-small cell lung cancer cell lines have established that amplification of MET contributes to acquired resistance to the EGFR inhibitor gefitinib through phosphorylation of HER3, a member of the EGF receptor family of RTKs. As HER3 phosphorylation was demonstrated to occur under conditions of MET amplification, we have investigated whether HER3 phosphorylation and signaling is a common event in other cell lines where MET is amplified. In gastric cancer cell lines with MET amplification where Met is overexpressed and constitutively active, HER3 is phosphorylated. Met and HER3 are also found in a complex, as established through co-immunoprecipitation. Interestingly, upon treatment with a small molecule kinase inhibitor targeting Met, HER3 phosphorylation and association between the two receptors decreases. Thus, in cells that express high levels of constitutively active Met, cross-talk with other receptors, such as HER3, may be another mechanism through which Met promotes tumorigenesis. The interaction of Met with HER3 will be addressed at the mechanistic level and these data will be presented. Kinase inhibitors that target single RTKs have proven susceptible to resistance. Inhibition of one RTK often results in upregulation of signaling through another receptor, and in this way, re-establish pathways essential for tumorigenesis. Determining how and under what conditions RTKs cross-talk with one another may allow identification of potential resistance mechanisms, as well as other targets for multi-targeted therapies. 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 4688. doi:10.1158/1538-7445.AM2011-4688
Computer-Vision-Guided Human Pulse Rate Estimation: A Review
Authors: Arindam Sikdar, Santosh Kumar Behera, Debi Prosad Dogra
Journal: IEEE Reviews in Biomedical Engineering (2016)

Human pulse rate (PR) can be estimated in several ways, including measurement instruments that directly count the PR through contact- and noncontact-based approaches. Over the last decade, computer-vision-assisted noncontact-based PR estimation has evolved significantly. Such techniques can be adopted for clinical purposes to mitigate some of the limitations of contact-based techniques. However, existing vision-guided noncontact-based techniques have not been benchmarked with respect to a challenging dataset. In view of this, we present a systematic review of such techniques implemented over a uniform computing platform. We have simultaneously recorded the PR and video of 14 volunteers. Five sets of data have been recorded for every volunteer using five different experimental conditions by varying the distance from the camera and illumination condition. Pros and cons of the existing noncontact image- and video-based PR techniques have been discussed with respect to our dataset. Experimental evaluation suggests that image- or video-based PR estimation can be highly effective for nonclinical purposes, and some of these approaches are very promising toward developing clinical applications. The present review is the first in this field of contactless vision-guided PR estimation research.
AB0354 Adult onset still’s disease (AOSD):A report of 30 cases
Authors: B. Tejera, D. Grados, M. Martinez-Morillo, A. Riveros, S. Rodriguez, L. Mateo, S. Holgado, A. Olivé, X. Tena
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Adult Onset Still’s disease (AOSD) is a rare systemic disease of unknown etiology,characterized by fever peaks with a evanescent rash, arthritis and/or arthralgia that is associated with odynophagia, lymphadenopathy and hepatosplenomegaly. Laboratory test usually present with leukocytosis, neutrophilia, anemia and an increased in acute phase reactants. There is no pathognomonic laboratory test. Diagnosis is difficult and exclusion of other diseases is requered. <h3>Objectives</h3> To describe the clinical characteristics, treatment and outcome of a series of patients diagnosed with adult Still’s disease. <h3>Methods</h3> Retrospective (1978-2011). UniversityHospital with a referal area of 800,000 inhabitants.We reviewed the medical records of patients from the database service of Rheumatology. Inclusion criteria: Yamaguchi criteria. <h3>Results</h3> Thirty one patients were diagnosed: 9 men (30%) and 21 women (70%). The mean age at diagnosis was 39.9 years (16-68). All had fever associated with rash, except for 3 patients who were enrolled without a rash. The odynophagia was presented in all cases except 1. Polyarticular pattern predominated (22 patients, 73.3%) compared to oligoarticular (3 patients, 9.7%); in 5 patients was not found arthritis, however, arthralgia were seen in 96.7% of cases. Twelve patients had lymphadenopathies and eleven, splenomegaly. Seven patients had both clinical signs. Serositis was uncommon, affecting only 3 patients. Laboratory findings were as followed: leukocytosis with neutrophilia (22 patients, 73.3%), anemia with hemoglobin ≤12 g/dl (15 patients, 50%), with mean hemoglobin of 11.5g/dl, transaminitis (9 patients, 1%), high ferritin with an average of 6614 ng/ml in 19 patients (63.3%). The ESR was determined in 29 patients and was founded elevated in 24 (80%), with a mean of 77.4±39.8 mm in the first hour. C Reactive Protein was determinedin 26 cases, being elevated in 21 patients (70%).Joint radiographswere performed according to articular involvement and remained normal in 23 patients (76.7%). The treatment was: aspirin and/or NSAIDs (90%), corticosteroids (76%), other disease-modifying drugs, 15 patients (76.7%); biological drugs, 6 patients (20%). Mean follow-up: 88 months. The form of evolution of the disease was polycyclic in 15 patients (50%) and monocyclic on the other half of patients. Remission during follow-up was presented in 27 patients (93.1%). <h3>Conclusions</h3> The clinical and laboratory characteristicsof this series, did not differ from those reported by other authors. All in all Adult Onset Still’s disease responded to treatment. Biological drugs was required in one third of patients. <h3>Disclosure of Interest</h3> None Declared
Xanthogranulomatous Osteomyelitis of Rib Mimicking Malignant Lesions in 18F-FDG PET/CT Imaging
Authors: Yan-Li Wang, Hua Yu, Hua Zhang, Xin-Jian Cui, Jian-Kui Han
Journal: Clinical Nuclear Medicine (2013)

Xanthogranulomatous osteomyelitis is a rare inflammatory process characterized histologically by collection of foamy macrophages admixed with mononuclear cells. We describe 2 cases with chest and back pain; radiography and CT scan identified expansile osteolytic rib destructive lesions with soft tissue mass. F-FDG PET/CT revealed accumulation of F-FDG similar to malignancy. Xanthogranulomatous osteomyelitis was histologically confirmed with numerous foamy histiocytes admixed with inflammatory infiltrate.
THU0371 Increased expression of inflammatory cytokines and chemokines in an autoinflammatory disorder, nakajo-nishimura syndrome
Authors: K. Arima, N. Kanazawa, F. Furukawa, H. Ida, K. Yoshiura
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> The ubiquitin-proteasome pathway is responsible for selective degradation of short-lived, misfolded and toxic proteins. It plays an important rule in transcriptional regulation. Nakajo-Nishimura syndrome (NNS) (MIM 256040) is an autosomal recessive autoinflammatory disorder characterized by periodic fever, partial lipodystrophy, contracture of joints, skin rash and calcification of basal ganglia. Homozygous mutation in the PSMB8 gene and decreased chymotrypsin-like activity indicated that dysfunction of the proteasome can result in the autoinflammatory condition. <h3>Objectives</h3> To analyze the expression of inflammatory cytokines and chemokines in cells of proteasome impairment. <h3>Methods</h3> Skin fibroblasts obtained from NNS patients (n=3) and healthy controls were cultured in the presence or absence of proteasome inhibitor. Gene expression of 84 inflammatory cytokines and receptors were analyzed by SYBR Green-based quantitative reverse transcription-PCR. Serum samples were obtained from healthy controls (n=16), rheumatoid arthritis patients (n=5), and NNS patients (n=4). Concentrations of 48 different cytokines and chemokines were determined using a multiplex bead-based enzyme linked immunosorbent assay on a suspension array. Data were analyzed the Bio-Plex Manager 6.0 software. <h3>Results</h3> 26 up-regulated genes and 3 down-regulated genes were identified in cultured cells under the condition of proteasome inhibition. Among these candidate genes CXCL-10 was significantly increased by the inhibition of proteasome (4.10-fold, p=0.008). This was compatible with the higher concentration of in sera of patient with NNS. IL-8 was significantly up-regulated both in cells treated with proteasome inhibitor (151.38 fold p&lt;0.0001) and in cells obtained from patient with NNS (19.36 fold P&lt;0.0001). <h3>Conclusions</h3> These findings suggest that decrease of proteasome activity is associated with an increased expression of inflammatory cytokines. The ubiquitin-proteasome pathway would play an important rule against inflammation. This may provide a new insight into the pathogenesis of other persistent inflammatory diseases. <h3>References</h3> Arima K, Kinoshita A, Mishima H et al. Proteasome assembly defect due to a proteasome subunit beta type 8 (PSMB8) mutation causes the autoinflammatory disorder, Nakajo-Nishimura syndrome. Proc Natl Acad Sci U S A. 2011;108:14914-9. Liu Y, Ramot Y, Torrelo A et al. Mutations in PSMB8 cause CANDLE syndrome with evidence of genetic and phenotypic heterogeneity. Arthritis Rheum. in press <h3>Disclosure of Interest</h3> None Declared
Abstract 4947: Inhibition of Rapamycin induced AKT activation elicits differential anti-tumor response in head and neck cancers.
Authors: Padhma Radhakrishnan, Ulaganathan Baraneedharan, Muthu Dhandapani, Allen Thyakumar, Dency Pinto, Arun Prasath, Ayyappan Velu, A Kamal, Nilesh Brijwani, Rohini Nair, R Basavaraja, Misti Jain, Saravanan Thiyagarajan, Biswanath Majumder, Mallik Sundaram, Prasad Narayanan, Vikram D. Kekatpure, Pradip K. Majumder
Journal: Cancer Research (2013)

Abstract The PI3K/AKT/mTOR pathway is an important signaling axis that is perturbed in majority of cancers. Biomarkers such as pS6RP, GLUT1 and tumor FDG uptake are being evaluated in patient stratification for mTOR pathway inhibitors. In the absence of a clear understanding of the underlying mechanisms in tumor signaling, the biomarker strategy for patient stratification is of limited use. Here, we show that no discernible correlation exists between FDG uptake and the corresponding Ki67, GLUT1, pS6RP expression in tumor biopsies from Head and Neck Cancer (HNC) patients. Correlation between GLUT1 and pS6RP levels in tumors was observed but elevated pS6RP was noticed even in the absence of concomitant AKT activation, suggesting other downstream molecules of PI3K/AKT and/or other pathways upstream of mTOR, are active in these tumors. Using an ex-vivo platform, we identified putative responders to Rapamycin, an mTOR inhibitor in these tumors. However, Rapamycin did not induce anti-tumor effect in the majority of tumors with activated mTOR, potentially attributable to the observation that Rapamycin induces feedback activation of AKT. Accordingly, treatment of these tumors with an AKT inhibitor and Rapamycin uniformly resulted in abrogation of mTOR inhibition induced AKT activation in all tumors but failed to induce anti-tumor response in a subset. Phosphoproteomic profiling of tumors resistant to dual AKT/mTOR inhibitors revealed differential activation of multiple pathways involved in proliferation and survival. Collectively, our data suggest that in addition to biomarker based segregation, functional assessment of patient tumor prior to treatment with mTOR/AKT inhibitors might be useful for patient stratification. Citation Format: Padhma Radhakrishnan, Ulaganathan Baraneedharan, Muthu Dhandapani, Allen Thyakumar, Dency Pinto, Arun Prasath, Ayyappan Velu, A Kamal, Nilesh Brijwani, Rohini Nair, R Basavaraja, Misti Jain, Saravanan Thiyagarajan, Biswanath Majumder, Mallik Sundaram, Prasad Narayanan, Vikram D. Kekatpure, Pradip K. Majumder. Inhibition of Rapamycin induced AKT activation elicits differential anti-tumor response in head and neck cancers. [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 4947. doi:10.1158/1538-7445.AM2013-4947
Tumor and Infection Localization in AIDS Patients: Ga-67 and Tl-201 Findings
Authors: H. TURGUT TUROGLU, MUSTAFA F. AKISIK, SLEIMAN Y. NADDAF, WALID S. OMAR, JEFFREY S. KEMPF, HUSSEIN M. ABDEL-DAYEM
Journal: Clinical Nuclear Medicine (1998)

Examples of Ga-67 and Tl-201 scans in AIDS patients performed at St. Vincent's Hospital and Medical Center of New York are presented. Use of these methods is the adopted approach at this institution in AIDS patients for localizing sites of tumor or infection involvement. A Ga-67 scan is the most common nuclear medicine examination performed on AIDS patients. Sequential TI-201 and Ga-67 scans have a role in differentiating Kaposi's sarcoma from malignant lymphoma and opportunistic infections. For intracranial lesions, Tc-99m MIBI or Tl-201-201-201-201 chloride can differentiate malignant from benign inflammatory lesions.
Abstract 3350: Inhibition of breast cancer and cancer stem cells via a novel micheliolide analogue CY-9
Authors: Bryan W. Newman, Quan Zhang, Yaxin Lu, Jiadai Zhai, Yahui Ding, Weiwei Ma, Hongxia Fan, Jing Long, Haoliang Zhang, Miao Wang, Yue Chen, Duxin Sun
Journal: Cancer Research (2011)

Abstract Natural products that target cancer stem cells (CSCs) have the potential to treat cancers and reduce the occurrence of relapse. The sesquiterpene lactone parthenolide has received much attention for its ability to preferentially target CSCs over their normal equivalents. However, poor pharmacokinetics have severely limited the clinical use of parthenolide, and prompted synthesis of a water soluble analogue, LC-1. Although currently in Phase I trials for disseminated cancers, LC-1 suffers from a short half-life, which could potentially limit its efficacy. In order to identify new sesquiterpene lactones which function similarly to parthenolide and LC-1 but with improved pharmacokinetics, we tested a new micheliolide analogue CY-9 for activity against both breast cancer and CSCs. Using the MTS assay, SUM159 breast cancer cells displayed sensitivity to CY-9 with an IC50 of 5 μM, which is similar to reported inhibitory concentrations of parthenolide. SUM159 cells assayed for Aldefluor expression after a three day treatment with CY-9 (1, 2.5, 5 μM) showed a 27%, 64%, and 83% reduction in their CSC populations, respectively. This CSC depletion was largely reversed in SUM159 cells that were pre-treated with the antioxidant N-Acetyl-Cysteine (NAC) before exposure to CY-9. Inhibition of SUM159 CSC self-renewal after CY-9 treatment was assayed using tumorsphere formation of single SUM159 Aldefluor-positive cells. A seven day treatment of 5 μM CY-9 reduced SUM159 Aldefluor-positive cell tumorsphere formation by 74%. Under drug-free conditions, tumorsphere formation was reduced by 26% in the second passage, but returned to control levels by the third passage. Western blotting also showed that 5 μM CY-9 reduced the levels of nuclear NF-κB. These results demonstrate the effectiveness of our new micheliolide analogue CY-9 at targeting populations of both bulk breast tumor cells and CSCs. The slight reduction in tumorsphere formation under drug-free conditions suggests that inhibition of self-renewal plays a minor role in CY-9's activity against CSCs. Loss of CY-9 activity with cells pre-treated with NAC suggests that the inhibitory effect of CY-9 is partially mediated by its interaction with biologically relevant cysteines and/or ROS generation. Additionally, as NF-κB is vital for defense against cellular stressors such as ROS, depletion of nuclear NF-κB might also explain the observed inhibition with CY-9. Together, these results warrant further study of CY-9 as a potential therapy for breast cancer and CSCs. 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 3350. doi:10.1158/1538-7445.AM2011-3350