tbuckley/cabot-search huggingface dataset:
Abstract 2435: Assessment of vascular disrupting properties of sodium meta-arsenite treatment using Dynamic contrast-enhanced MRI in colon cancer allograft model
Authors: Young Joo Min, Hee-Soon Lee, Wha Ja Cho, Ho Yong Lee, Jong Cheol Lee, Sungchan Park, Hee-jung Cha, Hyun Jin Park, Jin Seo, Young Han Lee, Ho Taek Song, Chang Hoon Moon
Journal: Cancer Research (2012)

Abstract PURPOSE: Sodium meta-arsenite is an orally bioavailable arsenic compound that currently undergoing clinical evaluation. The sodium meta-arsenite leads to blood vessel congestion, the selective destruction of the vasculature, and extensive necrosis in experimental tumors. The aim of this study is to assess the ability of dynamic contrast enhanced magnetic resonance imaging (DCE-MRI) to measure the antivascular effects of sodium meta-arsenite in colon cancer allograft model. MATERIALS AND METHODS: Mice CT26 colon cell carcinoma allografts were treated with sodium meta-arsenite or saline. Changes in tumor vascularity were assessed by DCE-MRI. DCE-MRI data were analyzed calculating the k(ep). For histologic analysis, liver, spleen and tumor tissues were taken at 8, 24 and 48 hours after sodium meta-arsenite injection from CT26 tumor allograft models. RESULTS: DCE-MRI results showed comparison between pre-treatment and 24 hr post-treatment Gd-DTPA contrast enhancement T1-weighted MR image. Enhancement has been significantly decreased in sodium meta-arsenite treated group than sham injection group. We also showed extensive central necrosis of tumor by 24 h after treated with sodium meta-arsenite (10 mg/kg, i.p.). CONCLUSION: These results suggest that DCE-MRI could quantitatively visualized the perfusion efficacy of the sodium meta-arsenite acting as a VDA in colon caner allograft model 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 2435. doi:1538-7445.AM2012-2435
PTU-144 When Are Gastric Ulcers Malignant? Predictors Of Benign Disease
Authors: S Thanaraj, A Sainsbury, R Cochrane, C Selinger
Journal: Gut (2014)

<h3>Introduction</h3> Gastric ulcers can harbour malignancy and the National Institute for Health and Care Excellence (NICE) therefore recommends follow-up gastrocopy (FU-OGD). Predictors of benign gastric ulcers can potentially reduce the burden of FU-OGD. <h3>Methods</h3> All patients with a first endoscopic diagnosis of gastric ulcer between January 2012 and September 2013 at this large teaching hospital were included. Patients with known gastric ulcers prior to study period or those referred for tertiary assessment were excluded. We defined neoplastic disease as histological evidence of gastric dysplasia or malignancy. Benign disease was defined as patients with complete ulcer healing, those with 2 sets of benign biopsies and no endoscopic suspicion of malignant disease, or in cases without FU-OGD one set of negative biopsies and at least 360 days cancer free survival. Patients with insufficient follow-up were excluded. We analysed the influence of demographic, endoscopic and histological factors on the likelihood of benign disease using chi-square test for categorical and t-test for continuous variables. Independence of variables was analysed using linear regression analysis. <h3>Results</h3> Of 377 patients included 350 (92%) had benign disease. 19 patients were diagnosed with adenocarcinomas, 2 with dysplasia, 5 with lymphomas, and 1 with melanoma. Patient sex, indication for gastroscopy and helicobacter pylori status did not influence the likelihood of benign disease. Benign disease was significantly associated with ulcer location in the antrum (p = 0.001), endoscopic benign appearance (p &lt; 0.001), non-cratered ulcer morphology (p &lt; 0.001), benign histology on 1st biopsy (p &lt; 0.001), younger age (64 vs 73 years, p = 0.02), lower number of ulcers (1.4 vs 2, p &lt; 0.001) and smaller ulcer size (10 vs 28 mm, p &lt; 0.001). After linear regression analysis only endoscopic benign appearance (p = 0.03), benign histology on 1st biopsy (p &lt; 0.001), lower number of ulcers (p &lt; 0.001) and smaller ulcer size (p = 0.004) were independent predictors of benign disease. <h3>Conclusion</h3> We have demonstrated that several simple factors collected during index endoscopy and ulcer biopsy can predict benign disease. Risk stratification according to those factors could be used to re-examine the need for FU-OGD for all patients with gastric ulceration. If prospectively verified the described predictive factors could be used to identify low risk patients who do not require endoscopy. This may be a strategy to reduce the burden of FU-OGD. <h3>Disclosure of Interest</h3> S. Thanaraj: None Declared, A. Sainsbury: None Declared, R. Cochrane: None Declared, C. Selinger Grant/research support from: Ferring, Shire, Nycomed, Warner Chilcott.
Robert J Doig
Authors: H. P. Doig
Journal: BMJ (2012)

Robert J Doig was born in Lennoxtown, Stirlingshire, the second son of Dr R S Doig (MBE, MD, MOH) and Lucienne, his French mother. When he was yet an infant the family moved to Stornoway on the Isle of Lewis, where he grew up and received a first class education at the Nicolson Institute.

Robert enjoyed swimming and running. His ability …
Incarcerated Inguinal Hernia From Metastatic Pleural Mesothelioma
Authors: Vien X. Nguyen, Ba D. Nguyen, Panol C. Ram, Michael C. Roarke
Journal: Clinical Nuclear Medicine (2012)

PET/CT provides a comprehensive staging, post-therapeutic surveillance, and outcome prognosis of malignant pleural mesothelioma based on its hypermetabolic behavior. This ability of PET may allow the monitoring, prediction, and detection of uncommon distant gastrointestinal clinical manifestations of this disease. The authors present a case of PET/CT imaging of pleural mesothelioma disseminating to the abdomen and pelvis, inducing an incarcerated inguinal hernia.
Diet and Smoking: Intervention Works Among Children
Authors: Philippe Chemaly
Journal: JNCI Journal of the National Cancer Institute (1989)

Diet and Smoking: Intervention Works Among Children Get access Philippe Chemaly Philippe Chemaly Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 81, Issue 13, 5 July 1989, Pages 978–979, https://doi.org/10.1093/jnci/81.13.978 Published: 05 July 1989
Abstract 985: Design of a model for the development of cisplatin resistance in H526 human small cell lung cancer xenografts.
Authors: Paula B. Caffrey, Gerald D. Frenkel
Journal: Cancer Research (2013)

Abstract Treatment of Small Cell Lung Cancer (SCLC) often fails due to the rapid development of resistance to chemotherapy drugs. Reversal of resistance has proven to be difficult to achieve; thus, we have suggested an alternative strategy - prevention of its development [Frenkel &amp; Caffrey, Current Pharmaceutical Design, (2001) 7: 1595-1614]. In order to investigate this possibility we previously designed a model of the development of cisplatin resistance in ovarian cancer xenografts, which mimics the development of clinical resistance in ovarian cancer patients [Caffrey &amp; Frenkel, Cancer Chemotherapy Pharmacology (2000) 46: 74-78]. We used this model to identify compounds which are able to prevent resistance; these are being further investigated in a Phase I clinical trial. We have now designed an analogous model of the development of resistance in SCLC xenografts. Mice were injected sc with H526 SCLCL cells. Those bearing visible tumors were injected i.p. with a single “pretreatment” dose of cisplatin ranging from 0.75 - 3.0 mg/kg. On the 3rd, 5th or 7th day after this pretreatment, mice were injected i.p. with a single “high” dose of cisplatin (3.0 mg/kg). This high dose decreased the growth rate of control (PBS pretreated) tumors by 40%. Tumors whose growth curve was decreased by less than 40% were considered resistant. Our results indicated that several potential models resulted in a low incidence of resistance. However, pretreatment with 1.5 mg/kg followed seven days later by high dose treatment of 3.0 mg/kg consistently resulted in the development of cisplatin-resistant tumors. This model can be used to screen a variety of agents for their ability to prevent the induction of platinum resistance in SCLC tumors. Supported by a grant from the PA State System of Higher Education. Citation Format: Paula B. Caffrey, Gerald D. Frenkel. Design of a model for the development of cisplatin resistance in H526 human small cell lung cancer xenografts. [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 985. doi:10.1158/1538-7445.AM2013-985
361 ENGRAFTMENT AND PROLIFERATION OF TRANSPLANTED HUMAN HEPATIC STELLATE CELLS IN THE LIVER OF IMMUNODEFICIENT MICE
Authors: D. Benten, J. Kluwe, J. Wirth, V. Kumaran, B. Joseph, T. Volz, M. Lütgehethmann, K.K. Bhargava, K. Cheng, A. Follenzi, S. Gupta
Journal: Journal of Hepatology (2012)
THE CAROTID SINUS IN NEUROPSYCHIATRIC CASES
Authors: MILTON GREENBLATT, MAX RINKEL, HARRY C. SOLOMON
Journal: American Journal of Psychiatry (1949)

The electroencephalographic, electrocardiographic, and clinical effects of carotid sinus stimulation, unilaterally and bilaterally, were studied in 122 individuals. In every case in whom satisfactory carotid sinus compression was performed cardiac slowing or asystole was obtained immediately. One-fourth of the cases showed asystoles, usually 3-5 seconds in duration but varying up to 9 seconds. In 66% of the cases high voltage 3 per second slow waves appeared abruptly in the EEG diffusely and symmetrically, after 10 seconds of sustained forceful compression of the carotid sinuses. In 6o% of the cases unconsciousness with a short tonic-clonic seizure occurred immediately after the appearance of the slow-wave discharge. The seizure lasted 5-15 seconds, with recovery immediate and complete. These effects of compression could be repeated many times with remarkable consistency without any cumulative or permanent effects upon the EEG or EKG. Compression of the common carotid arteries below the bifurcation produced immediate acceleration of the heart. The central effects were obtained after approximately 10 seconds of sustained compression and were similar to those obtained by carotid sinus compression. Elevation of blood pressure reduces the central effect of carotid sinus compression. Electric shock and prefrontal lobotomy facilitate the central effect of carotid sinus compression. The central effects of carotid sinus compression described above are thought to be due largely to interference with the carotid circulation to the brain.
A1.84 Switching off B cells by Fc-engineered anti-CD19 antibody (XmAb5871)
Authors: Daniel Szili, Marcell Cserhalmi, Zsuzsanna Bankó, Gyorgy Nagy, David E Szymkowski, Gabriella Sármay
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background and Objectives</h3> CD19 is a B cell-specific marker present on pre-B cells, immature and mature B cells but lacking on plasma cells. CD19 is a positive co-receptor of B cell receptors (BCR) and a target of the tyrosine kinase Lyn in activated B cells. Phosphorylated CD19 recruits Lyn, PI3K and Vav, enhancing B cell activation. In contrast, FcgRIIb is also a target of Lyn, but when co-engaged with BCR is phosphorylated, recruits SHP2 and SHIP phosphatases, and inhibits B cell activation. XmAb5871 is an Fc engineered anti-CD19 that binds to FcgRIIb with approximately 400 higher affinity as compared to its native IgG1 Fc counterpart (Horton HM et al. J. Immunol. 2011, 186:4223-4233). Our aim was to clarify if Fc-engineered CD19 antibody amplifying the FcgRIIb-mediated inhibitory pathway in activated B cells is able to inhibit not only BCR-mediated but also TLR9-stimulated signals. The innate receptor TLR9 plays a role in the etiology of systemic autoimmune diseases by lowering the signalling threshold of B cells. An agent that could inhibit both BCR- and TLR9-mediated signals may block autoantibody production without B cell depletion, and have therapeutic potential in systemic autoimmune diseases. <h3>Materials and Methods</h3> We studied early and late signalling events in B cells purified from human blood or tonsils by negative selection. The cells were stimulated by single, double or triple combined signals via BCR, TLR9 and CD19. We monitored the phosphorylation of FcgRIIb and ERK, induction of the activation marker CD38, cell proliferation, cytokine and antibody production of B cells. <h3>Results</h3> We show that XmAb5871 decreases BCR-induced ERK and AKT activation in B cells. In functional assays, we found that cell proliferation, plasma cell differentiation and cytokine production induced by the combined BCR and TLR9-mediated signals were inhibited by XmAb5871. The synergistically enhanced secretion of IL-6, IL-10 and TNFα induced by the BCR and TLR9 double signals was almost completely blocked by XmAb5871. Moreover, the Fc-engineered anti-CD19 inhibited the differentiation of citrullinated filaggrin peptide-specific antibody-forming cells from rheumatoid arthritis patients. <h3>Conclusion</h3> These data indicate that an Fc-engineered anti-CD19 antibody amplifying FcgRIIb inhibits activated B cells including autoantibody as well as cytokine production, and thus might be a useful new therapeutic strategy to suppress pathogenic B cells in autoimmune disease. <h3>Acknowledgement</h3> The work was supported by the National Development Agency OTKA 80689 fund.
Abstract LB-68: Mouse mammary tumor virus suppress apoptosis through Src signaling in the mammary epithelial cells
Authors: Hyoung H. Kim
Journal: Cancer Research (2012)

Abstract Many receptors in the hematopoietic immune cells use common signaling pathway that relies on immunoreceptor tyrosine-based activation motif (ITAM). ITAMs are highly conserved sequence. Signal transduction by these motifs is mediated by Src family tyrosine kinases including Lyn, Fyn, Lck. ITAM bearing proteins are found in many oncogenic viruses and associated with transformation and tumorigenesis in epithelial and endothelial cells. These proteins include Epstein Barr Virus LMP2A, Kaposi's sarcoma virus K1, and bovine leukemia virus gp30. MMTV envelope protein is another viral ITAM bearing protein implicated in mammary tumor development. We previously have shown that MMTV envelope protein expression transform mouse mammary epithelial cells and Src kinases are important mediators in this transformation. To study how ITAM signaling affects transformation and progression of mammary tumor we developed mammary cell lines that express MMTV provirus and have a mutated ITAM counterpart. Using PCR based expression profiling we found that MMTV-ITAM turns on the embryonic transcription factors and induce epithelial-mesenchymal transition which is important in malignant tumor progression. Many genes related to cell adhesion and invasion was changed. Anti-apoptotic regulator bcl-2 level was significantly increased. Importantly MMTV expressing cells became resistant to apoptosis induced by serum starvation. Cells transduced with ITAM mutated MMTV were indistinguishable from wild type cells. We also found Src kinase, a downstream signal transducer of ITAM signaling is activated in the MMTV expressing cells, and MMTV induced apoptosis resistance was completely restored by Src inhibitor PP2. Our results show that MMTV suppress apoptosis through ITAM mediated Src tyrosin kinase signaling. The studies in signaling pathways and apoptosis resistance induced by ITAM containing proteins in nonhematopoietic cells could lead to the development of effective treatment of cancers in which ITAM-mediated signaling plays a role. 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 LB-68. doi:1538-7445.AM2012-LB-68
Abstract 269: A novel mechanism of p21 induction by oxaliplatin in p53 deficient cancer cells
Authors: Weiguo Xu, Dawei Li
Journal: Cancer Research (2012)

Abstract p21(CDKN1A) is a well known cyclin-dependent kinase (cdk) inhibitor. As a critical cell cycle checkpoint of p53 mediated DNA damage response, p21 interferes with cyclin-CDK2 complex, blocking cell cycle at the G1/S interface, thus reducing the risk of DNA damaged cells transforming to cancer cells. Activation of p21 checkpoint by therapeutic agent is often associated with cancer cell cycle arrest and effective tumor suppression. However, many cancer lost wild type p53 while p21 in these cells maintains at a low level. In these cells p21 transcription is mainly controlled by p53-independent mechanisms through various cis-acting elements and these type of cancer are often more likely to resist chemo treatment. In search of effective therapeutic agents against p53 negative and drug resistant cancers we used SKOV3, a p53 deficient cancer cell line, to assess the ability of common therapeutic drugs to induce p21 expression. Promoter-reporter assays suggest p21 promoter is significantly stimulated by Oxaliplatin in SKOV3 cells compared with most common drugs used in chemotherapy. Through the promoter deletion analysis we identified a previously unreported Oxaliplatin responsive cis-acting element located between −237 to −220bp in the p21 promoter. Genomic DNA functional element analysis using ENCODE (Encyclopedia of DNA Elements) Consortium suggests that a vertebrate-conserved element overlaps well with the newly discovered Oxaliplatin responsive element. This conserved promoter element is required for the effective induction of p21 promoter activity by Oxaliplatin and such induction is positively related to drug induced S-phase cell cycle arrest. Finally, the ability of p21 induction of chemotherapy drugs is well correlated with their effectiveness of reducing SKOV3 xenograft tumors in nude mice. 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 269. doi:1538-7445.AM2012-269
Hypophysectomy in the Treatment of Breast Cancer
Authors: A. G. Jessiman, D. D. Matson, F. D. Moore
Journal: New England Journal of Medicine (1959)

AS part of an over-all program at the Peter Bent Brigham Hospital, Boston, to investigate and improve the management of patients with advanced cancer of the breast, the possible role of hypophysectomy has been explored. The purpose of this paper is to report a series of 53 patients with advanced carcinoma of the breast treated by surgical hypophysectomy. Each case has been carefully studied, and alterations in the rate of progress of the disease and in the endocrinologic background of the host have been documented.No attempt will be made here to review the large literature on hypophysectomy in cancer. . . .
SAT0400 Ultrasound assessment of the enthesopaty in patients with ankylosing spondylitis without history of entheseal involvement
Authors: F.A. Vreju, P. Ciurea, A. Rosu, A. Barbulescu, A. Musetescu, I. Gofita-Cojocaru, C. Hoanca, M. Florea, B.A. Chisalau
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Enthesitis is one of the most common and specific manifestations of spondyloarthropathy (SpA). Ultrasonography has demonstrated to be a highly sensitive tool in the evaluation of entheses in patients with spondyloarthropathy (SpA). <h3>Objectives</h3> The objectives of the study were to determine the prevalence of subclinical entheseal involvement in spondyloarthropathy patients in lower limbs. <h3>Methods</h3> The study was included 25 patients with spondylarthritis – 15 with ankylosing spondylitis and 10 with psoriatic arthritis, without known history of entheseal involvement. Besides, 20 healthy sex- and age-matched controls were included. All patients with no clinical evidence of arthritis or enthesitis underwent an US examination. All US findings were identified according to GUESS. Clinical examination and ultrasound were consecutively performed at each of the entheses to detect signs indicative of enthesopathy. <h3>Results</h3> A total of 246 enthesis in patients with ankylosing spondylitis and psoriatic arthritis (due to the psoriatic lesions on the knee) were evaluated by US. In 88 of 246 (35.77%) entheses, grayscale US found signs indicative of enthesopathy and in 17/246 (6.9%) entheses PD signal was detected. In the healthy population, US found signs of enthesopathy in 12 of 200 (6.0%) entheses and no PD signal was detected. The GUESS score was higher in patients with ankylosing spondylitis than in the psoriasis group, and both scores were significantly higher than in healthy controls (P&lt;0.0001). <h3>Conclusions</h3> Our results indicate that both grayscale US and PD findings demonstrate a higher sensitivity for enthesopathy of ultrasonography, with respect to physical examination indicative. Due to the US ability to detect signs of subclinical enthesopathy, further study is needed about the prognostic value of the ultrasound findings for predicting clinical onset of entheseal involvement. <h3>Disclosure of Interest</h3> None Declared
U.S. Will Not Reach Tobacco Goal for Year 2000
Authors: H. McIntosh
Journal: JNCI Journal of the National Cancer Institute (1995)

Journal Article U.S. Will Not Reach Tobacco Goal for Year 2000 Get access Hugh McIntosh Hugh McIntosh Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 87, Issue 8, 19 April 1995, Pages 563–564, https://doi.org/10.1093/jnci/87.8.563 Published: 19 April 1995