tbuckley/cabot-search huggingface dataset:
Abstract 5546: UVC irradiation inhibits superficial tumor growth in the brain of nude mice
Authors: Masashi Momiyama, Yukihiko Hiroshima, Atsushi Suetsugu, Yasunori Tome, Sumiyuki Mii, Shuya Yano, Takashi Chishima, Michael Bouvet, Itaru Endo, Robert M. Hoffman
Journal: Cancer Research (2012)

Abstract Temozolomide and UVC light were used for induction of cancer cell apoptosis of cancer cells which was imaged in real time at the subcellular level in the brain. Temozolomide inhibited brain tumor growth (p &amp;lt; 0.001). UVC irradiation inhibited superficial brain tumor growth (4.7-fold) (p &amp;lt; 0.0001) and improved survival (39.0%) (p = 0.002). This model can be used to evaluate new treatment modalities of brain metastasis or brain cancer at the subcellular level. In order to visualize single cancer cell nuclear-cytoplasmic dynamics of cancer cells in the brain in real time, including mitosis and apoptosis, Lewis lung cancer cells or human U87 glioma cells were injected into the brain either stereotactically or via the carotid artery of nude mice. The cancer cells were labeled with GFP in the nucleus and RFP in the cytoplasm, such that mitosis and apoptosis could be clearly imaged. A craniotomy open window was made for real-time fluorescence imaging of the cancer cells growing in the brain. Mitosis as well as treatment-induced apoptosis of the individual cancer cells were imaged in real time. UVC irradiation was initiated 1 day after the cancer cell inoculation and tumors were irradiated for 120 seconds on days 1, 4, 7, and 10. The tumor volume and survival were compared with untreated mice. UVC irradiation inhibited 4.7-fold changes in the brain tumor growth (p &amp;lt; 0.0001) and improved 39% higher survival (p = 0.002). 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 5546. doi:1538-7445.AM2012-5546
Pathologic Uptake in F-18 FDG Positron Emission Tomography of the Residuals of a Surgically Removed Needle Abscess
Authors: GERALD WOLF, REINGARD MARIA AIGNER, THOMAS SCHWARZ
Journal: Clinical Nuclear Medicine (2002)

WOLF, GERALD M.D.; MARIA AIGNER, REINGARD M.D.; SCHWARZ, THOMAS M.D. Author Information
S69 Transcriptional Mechanisms Regulating Expression of the Avb6 Integrin in IPF
Authors: AL Tatler, G Saini, A Goodwin, O Gbolohan, RL Clifford, M Al’Hourani, J Porte, S Violette, P Weinreb, A Knox, G Laurent, P Wolters, J Gauldie, M Kolb, G Jenkins
Journal: Thorax (2012)

TGF-β is fibrogenic cytokine implicated in the pathogenesis of idiopathic pulmonary fibrosis (IPF). The integrin αVβ6 can activate TGF-β, and dysregulation of this pathway is thought to play a role in the pathogenesis of pulmonary fibrosis. TGF-β induces αVβ6 integrin expression and aVb6 integrins are upregulated in fibrotic regions of lungs from patients with IPF. This raises the possibility that dysregulation of a self-regulating feedback loop may promote IPF. This study aims to investigate the mechanisms involved TGF-β-induced β6 expression and how this may be dysregulated in IPF. Using QPCR and flow cytometry we assessed expression of the integrin β6 (ITGB6) in lung epithelial cells. An ITGB6 promoter-luciferase construct and truncated mutants were used to identify the regulatory region of the promoter. Dominant negative (dn) constructs were used to assess the role of Smad proteins. Binding of transcription factors to the promoter was assessed by chromatin immunoprecipitation (ChIP). TGF-β caused concentration- and time-dependent increases in αVβ6 and ITGB6 mRNA, and increased activity of the ITGB6 promoter. Truncated mutants of the promoter showed that loss of 2 Smad binding sites resulted in loss of promoter activity. Co-transfection of dnSmad3 with the ITGB6 promoter reporter inhibited basal and TGF-β-induced promoter activity whereas dnSmad2 had little effect. dnSmad3 reduced TGF-β-induced αvβ6 cell surface expression. ChIP demonstrated binding of Smad3 and Smad4 to the promoter in response to TGF-β. Binding of Smad3 to the ITGB6 promoter was higher in lung tissue derived from IPF patients compared with controls. Finally, we identified a region of the ITGB6 promoter responsible for repressing transcription of the gene and demonstrate that siRNA targeting the transcription factor ELK1 increases αvβ6 expression. In conclusion, TGF-β increases expression of αVβ6 by transcriptional regulation involving Smad3. Furthermore, enhanced binding of Smad3 to the ITGB6 promoter in patients with IPF suggests dysregulated synthesis of αvβ6 integrins may promote IPF. Finally, we identified ELK1 as a potentially important negative regulator of αvβ6 expression. This highlights a positive feedback loop which could be dysregulated through hyperstimulation and impaired repression leading to amplification of αvβ6 mediated TGF-β activation that could be fundamental to IPF pathogenesis.
GENDER RELATED DIFFERENCES IN THE OBSERVED REGIONAL MYOCARDIAL DISTRIBUTION OF 99M-TECHNETIUM SESTAMIBI : IMPROVEMENT WITH NONUNIFORM ATTENUATION CORRECTION
Authors: J. Viggiano, J. McClellan, J. Maffei, A. Alavi, L. I. Araujo
Journal: Clinical Nuclear Medicine (1996)

Viggiano, J.; McClellan, J.; Maffei, J.; Alavi, A.; Araujo, L. I.Editor(s): Blend, Michael; Haseman, Michael Author Information
Abstract 298: Tumor-associated lymphatic vessels: Hijacking mechanisms of peripheral tolerance
Authors: Melody A. Swartz, Amanda W. Lund, Jacqueline D. Shields, Iraklis C. Kourtis, Sachiko Hirosue
Journal: Cancer Research (2012)

Abstract Lymphatic vessels drain fluid, antigens, and immune cells from the periphery to the lymph nodes (LNs). In addition to transporting activated dendritic cells to mount adaptive immune responses in the LN, lymphatic drainage is brings soluble antigens from the periphery to LN-resident immature dendritic cells and B cells. It is also the most common site for cancer metastasis. Despite its importance, the role of tumor-associated lymphatic vessels and their drainage to the LN in regulating host immune responses to the tumor is poorly understood. We show that tumor expression of VEGF-C, the most potent lymphatic growth factor, promotes pro-tumor immune tolerance by several mechanisms. For one, it enhances drainage to the draining LN, where tumor antigens along with suppressive cytokines bathe the LN and could affect B and T cell education there. Second, tumor VEGF-C upregulates CCL21 in the tumor stroma and surrounding lymphatic vessels, which itself promotes T cell infiltration and suppression. Third, VEGF-C drives peritumoral and LN lymphangiogenesis, which can modulate the myeloid cell repertoire towards more suppressive phenotypes. These changes resulted in increased infiltrations of regulatory T cells and myeloid-derived suppressor cells, and increased levels of regulatory cytokines. Interestingly, VEGF-C-expressing tumors were impervious to prior immunization against tumor antigen, unlike control-transfected tumors, which were hindered by the vaccine-induced immune response. Together, these findings suggest that lymphatic drainage serves to maintain peripheral tolerance and that tumors may hijack such mechanisms to escape host immunity. 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 298. doi:1538-7445.AM2012-298
P05.02 * KIAA1549:BRAF FUSION GENE IN PEDIATRIC BRAIN TUMORS OF VARIOUS HISTOGENESIS
Authors: C. Baldi, M. Antonelli, M. Badiali, F. R. Buttarelli, L. Moi, P. Nozza, A. Arcella, M. Massimino, M. Sanson, F. Giangaspero
Journal: Neuro-Oncology (2014)

INTRODUCTION: Pediatric GBMs (pGBM) are histologically indistinguishable from adult GBM (aGBM) however they are molecularly distinct. Few molecular data exists on the mechanism underlying development and progression of pGBM, whereas a number of gene expression profiling analyses performed in aGBM helped to identify molecular events leading to oncogenesis and provided more accurate means for classification of subtypes, outcomes and even response to treatments. The KIAA1549:BRAF fusion (K-B) gene has been considered a driver of genetic events and a useful diagnostic marker in adult pilocytic astrocytoma (PA). The K-B fusion, on the other hand, is an unusual finding in pediatric diffuse astrocytomas and oligoastocytoma and not reported in pHGG On the other hand, it has been reported a low frequency of B_F fusion gene in adult diffuse gliomas in association with IDH1 mutations. METHODS: To further elucidate the possible occurrence of the K-B fusion gene in non-PA tumors, we investigated its presence in a series of 69 pediatric brain neoplasms of different histogenesis and grade (34 non PA and 35 PA). Fusion has been investigated through the analysis of messenger RNA by reverse-transcription polymerase chain reaction (RT-PCR) followed by sequencing. Selected cases were screened for mutational analysis for IDH1, BRAFv600 and H3F3A. Positive cases have undergone to confirmation by the interphase Fluorescence in situ Hybridization (FISH) analysis and quantitative PCR (Taqman). RESULTS: We detected the KIAA1549:BRAF fusion (K-B) gene in 5 out of 34 (14.7%) non-PA primary tumors, i.e. 1 glioblastoma, 1 anaplastic astrocytoma, 1 anaplastic PXA, 1 ependymoma and 1 AT/RT. The fusion gene was also found in 21 out of 35 PAs (63.6%) and in 1/3 (33%) WHO grade I gangliogliomas. Quantitative PCR and FISH analysis confirmed the presence of the K-B fusion gene. The frequency of fusion harboring nuclei in non-PA neoplasms was lower than in PAs. Screening for IDH1, BRAFv600, and H3F3A mutations disclosed one case with the IDH1 and one with the K27M-H3.3 mutation, both unassociated with the K-B gene. CONCLUSION: Our study indicates that: 1) the K-B fusion gene can occasionally be detected in non-PA tumors of various histogenesis; 2) its occurrence in these neoplasms is probably due rather to a random alteration related to genomic instability than to a driving molecular event, as in PAs; and 3) the K-B fusion gene's role as a diagnostic marker outside the histological spectrum of pediatric low-grade gliomas should be carefully considered.
Carrier Detection in X-Linked Agammaglobulinemia by Analysis of X-Chromosome Inactivation
Authors: Eric R. Fearon, Jerry A. Winkelstein, Curt I. Civin, Drew M. Pardoll, Bert Vogelstein
Journal: New England Journal of Medicine (1987)

We used a recently developed strategy to analyze patterns of X-chromosome inactivation in human cell populations in order to study female members of families with X-linked agammaglobulinemia — i.e., to detect the carrier state and to test the hypothesis that the disorder results from a defect intrinsic in the development of B cells. According to this strategy, recombinant-DNA probes simultaneously detect restriction-fragment–length polymorphisms and patterns of methylation of X-chromosome genes. Random X-inactivation patterns were observed in isolated peripheral-blood granulocytes, T lymphocytes, and B lymphocytes of women who were not carriers. In contrast, one of the two X chromosomes was preferentially active in the peripheral B cells, but not the T cells or granulocytes, of three carriers of the disorder. This observation strongly supports the hypothesis that X-linked agammaglobulinemia results from an intrinsic defect in B-cell development. Moreover, the analysis described here can be used for direct identification of carriers in families with this disease. (N Engl J Med 1987; 316:427–31.)
<i>Campylobacter jejuni</i>Infections Associated with Raw Milk Consumption — Utah, 2014
Authors: Kenneth R. Davis, Angela C. Dunn, Cindy Burnett, Laine McCullough, Melissa Dimond, Jenni Wagner, Lori Smith, Amy Carter, Sarah Willardson, Allyn K. Nakashima
Journal: MMWR Morbidity and Mortality Weekly Report (2016)

In May 2014, the Utah Public Health Laboratory (UPHL) notified the Utah Department of Health (UDOH) of specimens from three patients infected with Campylobacter jejuni yielding indistinguishable pulsed-field gel electrophoresis (PFGE) patterns. All three patients had consumed raw (unpasteurized and nonhomogenized) milk from dairy A. In Utah, raw milk sales are legal from farm to consumer with a sales permit from the Utah Department of Agriculture and Food (UDAF). Raw milk dairies are required to submit monthly milk samples to UDAF for somatic cell and coliform counts, both of which are indicators of raw milk contamination. Before this cluster's identification, dairy A's routine test results were within acceptable levels (<400,000 somatic cells/mL and <10 coliform colony forming units/mL). Subsequent enhanced testing procedures recovered C. jejuni, a fastidious organism, in dairy A raw milk; the isolate matched the cluster pattern. UDAF suspended dairy A's raw milk permit during August 4-October 1, and reinstated the permit when follow-up cultures were negative. Additional cases of C. jejuni infection were identified in October, and UDAF permanently revoked dairy A's permit to sell raw milk on December 1. During May 9-November 6, 2014, a total of 99 cases of C. jejuni infection were identified. Routine somatic cell and coliform counts of raw milk do not ensure its safety. Consumers should be educated that raw milk might be unsafe even if it meets routine testing standards.
AB0843 Evaluation of endothelial function in patients with limited systemic sclerosis through echo doppler of the brachial artery and hand fingers capillaroscopy
Authors: T.M. Fernandes, M.N.L. Azevedo, E.F. Salles, N.V. Ribeiro, A.S. Papi, B.R. Bica
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Systemic sclerosis is a chronic disease of the connective tissue, featured by excessive collagen deposition in the skin and internal organs associated to vascular damage. Its limited form (lSSc) is characterized by cutaneous fibrosis restricted to face, neck and extremities. <h3>Objectives</h3> The aim of this study was to evaluate the reactivity of the brachial artery, endothelium-dependent and endothelium-independent, in patients with lSSc comparing with healthy subjects of the same sex, age and race and also compare these findings with the structural abnormalities found in capillaroscopy of the scleroderma group. <h3>Methods</h3> Twenty women, adults, non-obese, non-smokers, non-diabetics, non- dyslipidemics or hypertensive who fulfill criteria to lSSc according to American College of Rheumatology were submitted to Doppler exam of the right brachial artery. The dilatators response was analyzed; endothelium-dependent, after ischemia for 5 minutes in the right low arm and the dilatator response, endothelium-independent, after administering 300 micrograms of sublingual nitroglycerin (NTG). Such results were compared with the response obtained in healthy subjects. Controls were comparable to the study group according to age, sex and race. Only the scleroderma group was submitted to capillaroscopy after Doppler exam. <h3>Results</h3> The brachial artery longitudinal diameter (BAD) was significantly lower in the basal moment 1, 3.57±0.52mm and 3.93±0.39mm, respectively on patient group(P) and control group(C), p=0.005. The vascular reactivity after ischemia/reactive hyperaemia (RH) and NTG showed no significant difference between the groups (8.60±5.45mm vs. 9.26±5.91mm and 25.01±12.55mm vs. 19.59±7.94 mm, respectively in group P and group C). Furthermore, no statistically significant difference was found between erythrocyte velocity (EV) after RH and NTG (110.2±43.86cm/s vs. 102.0±25.89cm/s and 63.80±17.69cm/s vs. 65.4±12.90cm/s, respectively in group P and group C). <h3>Conclusions</h3> Although group P has shown lower BAD, the endothelium-dependent and independent dilatation was preserved in both groups. Scleroderma subjects who have more anatomical abnormalities in microcirculation demonstrated by capillaroscopy were the same individuals who presented less reaction to ischemic stimulus during echo Doppler. The authors concluded that in the scleroderma group, although advanced structural disease in microcirculation was identified by capillaroscopy it did not correlate with a dysfunctional endothelium. These findings reinforce the benefit of treating these patients in attempt to reduce the morbid-mortality in the evolution of this severe disease. <h3>Disclosure of Interest</h3> None Declared
Population based screening in Scotland reduces bowel cancer deaths
Authors: J. Wise
Journal: BMJ (2011)

Faecal occult blood testing can cut the number of colorectal cancer deaths by 27%, says the first study to show the impact of a population based screening programme.

The study, funded by the Scottish government Health Department, found a 10% reduction in bowel cancer deaths among all those invited for screening compared with those not invited. This rose to 27% among participants who actually completed the test. The research was presented at the National Cancer Research Institute Cancer Conference in Liverpool on 9 November.

Previous randomised controlled trials of faecal occult blood testing have shown a combined overall reduction in colorectal mortality of 16% in those invited for screening and 23% in participants.

Study author, Robert Steele, professor of surgery at the University of Dundee, said: “For the first …
Abstract 4958: Analysis of the AKT signaling pathway in prostate cancer using a streamlined Western blot workflow
Authors: Kelli Feather-Henigan, Rachael Berry, Greg Kilmer, Brian Webb
Journal: Cancer Research (2010)

Abstract Relative protein levels in the Akt pathway were analyzed in metastasized and normal prostate cancer cell lines using a new streamlined Western blot workflow and compared to a traditional Western blot method. Protein expression levels in the Akt pathway are commonly studied using Western blotting; however, current Western blot techniques involve multiple time-consuming steps taking more than 5 hours or even days. We used a streamlined Western blot workflow that combines a rapid 10-minute protein transfer and a one-hour immunoblotting protocol. When using an overnight primary antibody incubation, the protocol requires less than 30 minutes. Importantly, this method does not require the use of additional equipment or consumables and does not limit throughput. These data illustrate that current Western blot techniques involving multiple time-consuming steps can be streamlined to yield comparable results for phospho-specific and total protein targets. Results obtained in the analysis of the Akt pathway yielded comparable sensitivity to traditional Western blotting methods for both low- and high-abundance target proteins. Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend. 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 4958.
AB0854 Effect of tumour necrosis factor alpha inhibitor on serum level of DICKKOPF-1 protein and bone morphogenetic proteins in patients with active ankylosing spondylitis
Authors: M. Korkosz, J. Gasowski, P. Leszczynski, K. Pawlak-Bus, S. Jeka, J. Zalewska, B. Kwasny-Krochin, T. Grodzicki
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Ankylosing spondylitis (AS) is a remodeling arthritis involving axial skeleton, characterized by chronic inflammation and new bone formation (1). The link between inflammation and new bone formation in AS is complex and has not been entirely explained. Current understanding of relationship between inflammation and osteoproliferation is largely based on biomarkers studies which may lead to identification and application of biomarkers specific for bone formation and ankylosis (2). <h3>Objectives</h3> To examine changes of serum level of bone remodeling molecules: Dickkopf-1 (Dkk-1), sclerostin, wingless protein-3a and bone morphogenetic protein-7 (BMP-7) during 6 months of anti-TNF treatment in active ankylosing spondylitis (AS) to assess whether inflammation and osteogenesis are coupled. <h3>Methods</h3> Forty patients with axial AS were included; 20 with active disease for TNF inhibitor treatment and 20 non-active for non steroidal anti-inflammatory drug treatment. Markers of bone remodeling and inflammation were assessed at baseline and after 6 months. <h3>Results</h3> In the TNF inhibitor treated group Dkk-1 significantly decreased from 196.8 pg/ml (95% CI 94.1-399.0) to 116.3 pg/ml (95% CI 38.0-301.6); and BMP-7 significantly increased from 1.4 pg/ml (95% CI 0-23.0) to 20.3 pg/ml (95% CI 4.9-41.3). There was a significant negative correlation between Dkk-1 and BMP-7 at month 6 (r=-0.64; P 0.004) in this group. Non-parametric regression analysis including disease duration, age, sex and baseline CRP confirmed statistically significant effect of treatment on time related changes of Dkk-1 and BMP-7. Erythrocyte sedimentation rate and C-reactive protein as well as Bath Ankylosing Spondylitis Disease Activity Index decreased significantly in anti-TNF treated group. <h3>Conclusions</h3> Inflammation and osteoproliferation in active AS with mean disease duration 8,8 years are coupled. New bone formation in AS occurred if inflammation was successfully depressed. Among the potential biomarkers of bone remodeling Dkk-1 and BMP-7 showed significant time alterations and correlative interactions. <h3>References</h3> Braun J, Sieper J. Ankylosing spondylitis. Lancet 2007 Apr 21;369(9570):1379-1390 Maksymowych WP. Biomarkers in spondyloarthritis: From pathophysiology to disease assessment. Joint Bone Spine 2011 Nov 25.doi:10.1016/j.jbspin.2011.09.018 <h3>Disclosure of Interest</h3> None Declared