tbuckley/cabot-search huggingface dataset:
Abstract P2-10-06: Identification and Referral of Appropriate Patients for Genetic Services in the Community Setting: An innovative Approach
Authors: R Sutphen, K Steenblock, E Carmany, A Trivedi, K. Lewis
Journal: Cancer Research (2010)

Abstract Although the U.S. Preventative Services Task Force, the HHS's Healthy People 2020 draft objectives and multiple professional medical societies recommend genetic counseling as the standard of care for women with family history suggesting increased risk for breast cancer, there is clear evidence that this standard is not being achieved. On the one hand, many women who are appropriate for genetic counseling are not receiving it, while on the other, many individuals are inappropriately undergoing BRCA testing. A number of factors have been identified as contributors to these poor public health outcomes, including lack of physician proficiency in genetics and lack of availability of genetic counseling services due to limited number of trained genetics professionals and their limited geographic distribution. We report a novel systematic approach implemented through a large regional health plan (approximately 500,000 members, 14,000 network providers, 112 commercial hospitals, and 58 medicare hospitals) to address these issues, and present data regarding its performance. Components of the program include: 1) implementation of a model BRCA coverage policy that follows USPSTF guidelines recommending genetic counseling, 2) increased access to genetic counseling via telephone delivery and 3) removal of financial, language, convenience and other barriers to genetic counseling services. The program was implemented in January, 2010 and data will be presented for January through September. Specific results include 1) changes in volume of BRCA testing (including by provider specialty), 2) decrease in rates of inappropriate BRCA test requests (i.e., requests not meeting national guidelines/clinical criteria for testing), 3) discrepancies in reported family history based on methods of data collection, 4) increased awareness and dissemination of genetic services in the community setting, and 5) cost-effectiveness estimates. This program may serve as a model for appropriate translation of genetic testing into public health benefit. Citation Information: Cancer Res 2010;70(24 Suppl):Abstract nr P2-10-06.
Abstract 3008: Shared gene expression alterations in prostate cancer and histologically benign prostate from patients with prostate cancer
Authors: Farhad Kosari, John C. Cheville, Cristiane M. Ida, R Jeffrey Karnes, Alexey A. Leontovich, Thomas J. Sebo, Sibel Erdogan, Stephen J. Murphy, George Vasmatzis
Journal: Cancer Research (2012)

Abstract The frequent observations of heterogeneous tumor foci in prostate cancers indicate that the molecular changes induced by carcinogenic insult take place over wide areas within the diseased prostate. These ‘field effect’ alterations provide important clues regarding the initiation of prostate cancer (PCa) and suggest targets for cancer prevention or biomarkers for early detection. However, PCa field effect biomarkers that have passed independent validation are lacking largely because these alterations are subtle and difficult to distinguish from unrelated small changes in gene expression in the benign prostate. We postulated that shared expression alterations in PCa and in benign prostate tissue in prostate glands that contain prostate cancer (BPC) would have a higher potential for independent validation than alterations identified in BPC alone. Expression analyses was performed on PCa (n = 37) and unmatched BPC (n = 36) and contrasted with benign prostate glands (BP) from patients free of prostate cancer (n =28). These analyses identified gene alterations that were concomitantly present in both PCa and BPC. The majority of the selected markers were validated by quantitative RT-PCR in an independent set of BPC (n = 33) and BP (n =18). Validated markers included genes and non-exonic sequences not previously associated with PCa field effect. A statistical model based on CCNB1 and non-exonic NACA locus discriminated between BPC and BP in the RT-PCR set and in an external microarray dataset with accuracies of 0.84 and 0.90, respectively. Genes with predominant expression in prostate stroma were identified by expression profiling of stroma and epithelial cells collected by laser captured microdissection. Pathway analysis identified enriched GO categories in BPC stroma including PDGFR signaling. These results validate our approach for finding PCa field effect alterations and demonstrate a prostate cancer transcriptome fingerprint in the adjacent non-neoplastic cells. 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 3008. doi:1538-7445.AM2012-3008
A case of propofol dependence after repeated use for endoscopy
Authors: S. Roh, J. Park, D. Kim
Journal: Endoscopy (2011)

A 27-year-old man with a history of diazepam and midazolam abuse was admitted to the Department of Psychiatry at Seoul National Hospital with propofol (2,6-diisopropylphenol) dependence as a result of repeated endoscopic procedures with propofol sedation. After first receiving propofol for endoscopy at the age of 24, the patient began visiting endoscopists with growing frequency with the sole aim of receiving propofol. He underwent endoscopy once a week in June 2007. In December 2007, he visited seven clinics over a ten-day period. In July 2008, he underwent endoscopy for 15 consecutive days. The patient’s propofol abuse continued until he was admitted to the closed psychiatric wards. He has since been hospitalized seven times for propofol dependence. The increased seeking behavior that led to the patient’s uncontrollable desire for propofol is a common pattern in substance dependence.
BT-02 * FUNCTIONALLY-DEFINED THERAPEUTIC TARGETS IN DIFFUSE INTRINSIC PONTINE GLIOMA
Authors: C. S. Grasso, Y. Tang, N. Truffaux, N. E. Berlow, L. Liu, M.-A. Debily, M. J. Quist, L. Davis, E. C. Huang, P. J. Woo, A. Ponnuswami, S. Chen, T. Johung, W. Sun, M. Kogiso, Y. Du, Q. Lin, Y. Huang, M. Hutt-Cabezas, K. E. Warren, L. Le Dret, P. S. Meltzer, H. Mao, M. Quezado, D. G. van Vuurden, J. Abraham, M. Fouladi, M. N. Svalina, N. Wang, C. Hawkins, E. Raabe, E. Hulleman, P. T. Spellman, X.-N. Li, C. Keller, R. Pal, J. Grill, M. Monje
Journal: Neuro-Oncology (2015)

Diffuse Intrinsic Pontine Glioma (DIPG) is a universally fatal childhood cancer. Here, we performed a chemical screen in patient-derived DIPG cell cultures along with RNAseq expression analysis and integrated computational modeling to identify potentially effective therapeutic strategies. Panobinostat, among the more promising agents identified, demonstrated efficacy in pontine orthotopic xenograft models of both H3K27M and histone WT DIPG. These data suggest the potential utility of specific drug combinations and provides evidence of in vivo treatment efficacy of the multi-histone deacetylase inhibitor panobinostat.
Cisplatin Prodrug-Conjugated Gold Nanocluster for Fluorescence Imaging and Targeted Therapy of the Breast Cancer
Authors: Fangyuan Zhou, Bing Feng, Haijun Yu, Dangge Wang, Tingting Wang, Jianping Liu, Qingshuo Meng, Siling Wang, Pengcheng Zhang, Zhiwen Zhang, Yaping Li
Journal: Theranostics (2016)

Theranostic nanomedicine has emerged as a promising modality for cancer diagnosis and treatment.In this study, we report the fabrication of fluorescence gold nanoclusters (GNC) conjugated with a cisplatin prodrug and folic acid (FA) (FA-GNC-Pt) for fluorescence imaging and targeted chemotherapy of breast cancer.The physio-chemical properties of FA-GNC-Pt nanoparticles are thoroughly characterized by fluorescence/UV-Vis spectroscopic measurement, particle size and zeta-potential examination.We find that FA-modification significantly accelerated the cellular uptake and increased the cytotoxicity of GNC-Pt nanoparticles in murine 4T1 breast cancer cells.Fluorescence imaging in vivo using 4T1 tumor bearing nude mouse model shows that FA-GNC-Pt nanoparticles selectively accumulate in the orthotopic 4T1 tumor and generate strong fluorescence signal due to the tumor targeting effect of FA.Moreover, we demonstrate that FA-GNC-Pt nanoparticles significantly inhibit the growth and lung metastasis of the orthotopically implanted 4T1 breast tumors.All these data imply a good potential of the GNC-based theranostic nanoplatform for fluorescence tumor imaging and cancer therapy.
Abstract C41: Heme oxygenase-1 and carbon monoxide modulate responses to DNA damage in prostate cancer
Authors: Barbara Wegiel, Anders Bjartell, Clair Harris, John Belcher, Gregory Vercellotti, Dave Gallo, Eva Csizmadia, Leszek Helczynski, Jenny Liao Persson, Leo E. Otterbein
Journal: Cancer Research (2009)

Abstract Heme oxygenase (HO) and carbon monoxide (CO), a product of HO activity generated during heme catalysis, exert differential effects on the apoptotic response dependently on the environmental milieu and cell types involved. The role of HO-1 and CO in modulating chemotherapeutic treatment in prostate cancer has not been tested. Our focus in this work explored the role of HO-1 and CO in modulating PCa cell death via DNA damage mechanisms. We examined HO-1 expression in PCa samples from 482 patients and found strong nuclear staining in moderately differentiated tumors (Gleason grade 3). Treatment of PCa cells with the chemotherapeutic agents, camptothecin or doxorubicin increased HO-1 activity in the cytosol, which correlated with increased cell death. Nuclear translocation of HO-1 resulted in decreased enzymatic activity. Low activity of HO-1 in the nucleus may confer resistance to chemotherapy due to the antiapoptotic effects of HO-1. Overexpression of cytosolic and active HO-1 or exogenous delivery of CO at low non-toxic concentrations (250 parts per million) in combination with a chemotherapeutic led to enhanced tumor cell death via caspase-3 activation. CO exposure of mice with established PC3 xenografts delayed tumor growth via accelerated apoptosis (TUNEL staining) and mitotic catastrophe of cancer cells as well as strong inhibition of angiogenesis (CD31 staining). Further, CO sensitized tumors to doxorubicin treatment with enhanced apoptosis and blockage of mitosis. In contrast, CO blocked chemotherapeutic-induced cell death in normal cells supporting a new function for HO-1/CO as cellular sensors of DNA damage. Taken together, our data demonstrate the importance of cellular localization of HO-1 in PCa progression and importantly that CO, in part regulates cellular sensitivity to DNA damaging agents. We propose a novel strategy to overcome resistance to chemotherapy as well as reducing the chemotherapeutic burden by employing CO at safe, non-toxic concentrations that permits preservation of normal cells and tissue. Citation Information: Cancer Res 2009;69(23 Suppl):C41.
SP0170 Descending Modulation of Pain
Authors: T. Dickenson
Journal: Annals of the Rheumatic Diseases (2013)

<h3></h3> There is clear evidence from both preclinical and clinical studies that both peripheral and central hyperexcitability play important roles in determining the level of pain perceived. Rightly, much emphasis has been put on spinal cord mechanisms in central excitability but it now becoming clear that spinal excitability can be regulated by descending pathways from the brain. These originate from predominantly monoamine systems (noradrenaline and 5HT) which are additionally implicated in control of emotions, fear, anxiety, thermoregulation and the sleep cycle and so may mediate these pain induced co-morbidities. Much of the early work in this area concentrated on descending inhibitions, now known to be predominantly noradrenergic, and failure of descending inhibitions has been reported in patients as has their recruitment in placebo analgesia as well as the actions of anti-depressant drugs in pain. However, pain could equally be increased by enhanced descending facilitations and data is accumulating on exactly this. These excitatory influences are likely to contribute to the development and maintenance of central sensitisation in the spinal cord. Recent work shows altered descending excitatory controls in patients with severe pain from osteoarthritis. These pathways form a link between emotional states and levels of pain, and may be one route by which coping and catastrophizing can alter the sensory components of pain at the level of the first relays. The levels of midbrain generated modulation, both positive and negative, may be a key factor in individual variations in pain and contribute to some "dysfunctional" pain states such as fibromyalgia. Preclinical and early clinical investigations related to monoaminergic pain modulation. Bannister K, Bee LA, Dickenson AH. Neurotherapeutics. 2009 Oct;6(4):703-12. <h3>Disclosure of Interest</h3> None Declared
P30 What difference does bedside ultrasound guidance make to pleural fluid aspiration and drainage in a district general hospital setting?
Authors: O. J. Bintcliffe, H. Al-Najjar, R. K. Sinha
Journal: Thorax (2011)

<h3>Background</h3> British Thoracic Society guidelines strongly recommend thoracic ultrasound prior to all pleural procedures for pleural fluid. Previous studies have shown lower rates of failure and pneumothorax following the use of chest ultrasonography prior to pleural procedures. <h3>Aim</h3> We have set out to identify, in a district general hospital environment, the effect of pleural ultrasound on selection of sites for pleural procedures, the change in operator9s confidence associated with those procedures and the reasons for changes in site selection. <h3>Methods</h3> 47 patients with suspected pleural effusions had an aspiration or drainage site marked based on clinical findings, chest radiography and CT scan. Sites were then marked after bedside thoracic ultrasound examination by a member of the respiratory team (Level 1 competence). The level of confidence associated with obtaining fluid safely was assessed both before and after ultrasound on a visual analogue scale. The distance between sites marked before and after ultrasound and whether the procedure performed was the same as originally planned were also recorded. <h3>Results</h3> Following thoracic ultrasound no procedure was considered safe in 13% (6/47). A procedure was carried out in 87% (41/47). In 78% of these (32/41), the preferred site was changed after ultrasound. The reasons were greater fluid depth in 69% (22/32), an anticipated greater yield during therapeutic aspiration in 16% (5/32) and the initial site not being safe in 16% (5/32). Sites marked prior to ultrasound were considered unsafe in 23% (11/47) due to risk of pneumothorax in 15% (7/47) or the clinically marked site being below the diaphragm in 9% (4/47). Bedside chest ultrasound increased the confidence associated with pleural procedures. The confidence after ultrasound of the performed procedure was increased by 1.09 (95% CI 0.85–1.34) on the 5-point visual analogue scale. <h3>Conclusions</h3> Bedside chest ultrasound prior to pleural procedures in this cohort resulted in a change in the preferred site in a considerable number of patients. Ultrasound increased the level of confidence with the selected pleural procedures and resulted in a change to the intended procedure in 23% (11/47) of cases which included completely abandoning the procedure in 12.7% of cases (6/47).
Tubercular lymph nodal mass mimicking pancreatic malignancy with extrahepatic biliary obstruction in a young woman
Authors: Narendra Choudhary, Mridula Guleria, Rajesh Puri, Randhir Sud
Journal: Endoscopy (2015)

A 20-year-old woman presented with a complaint of weight loss over the previous 2 months. There was no history of cough, expectoration, abdominal pain or altered bowel habits. She had no significant past history. An abdominal ultrasound scan showed an ill-defined mass lesion causing a biliary obstruction and dilatation of the intrahepatic biliary radicles. An abdominal computed tomography (CT) scan was also performed and this showed a 3 × 2.9-cm lesion probably arising from the head of the pancreas; however, the type and exact origin could not be determined.
Effect of Age at the Start of Iron Chelation Therapy on Gonadal Function in β-Thalassemia Major
Authors: Naomi Bronspiegel-Weintrob, Nancy F. Olivieri, Beverley Tyler, David F. Andrews, Melvin H. Freedman, F. John Holland
Journal: New England Journal of Medicine (1990)

Patients with transfusion-dependent thalassemia major tend to have abnormal growth and sexual maturation at puberty, presumably as a result of pituitary iron overload. This study was designed to determine whether chelation therapy with deferoxamine before the age of puberty would ameliorate this problem.
Thomas Alfred Plumley
Authors: T. A. Plumley
Journal: BMJ (2013)

The aim of this study was to determine the plasma levels and the tissue distribution of otilonium bromide, measured as total radioactivity, after oral administration of 2 mg/kg of<sup>14</sup>C-labeled drug to rats. Radioactivity levels were very low in the plasma (ranging from 2.7 ng Eq/ml at 1.5 h to 0.6 ng Eq/ml at 24 h) as compared with those found in the gastrointestinal (GI) tract, indicating negligible systemic otilonium bromide absorption. Results from both quantitative radioluminography of whole body tissue distribution and radioassay of dissected parts of the GI tract carried out with liquid scintillation counting clearly demonstrate the presence of radioactive compounds in the walls of the GI tract at all sacrifice times. In the other tissues and organs examined, radioactivity was only found in trace amounts in the liver. The presence of radioactivity in the GI walls reflected the transit kinetics of drug-enriched contents. The radioactivity in large intestine walls was measurable at otilonium bromide concentrations in the range of micromole equivalents/kg, from 4 to 8 h after drug administration. Total body radioactivity recovery was 95, 101, 24, and 9% at 1.5, 4, 8, and 24 h, respectively. In conclusion, orally administered <sup>14</sup>C-otilonium bromide is poorly absorbed systemically, as indicated by the very low plasma radioactivity levels, but it is able to effectively penetrate into the large intestine walls, a recognized target for drugs oriented toward irritable bowel syndrome therapy.
Eruptive Reddish-Yellow Coalescing Papules in the Axillae of a Middle-Aged Man
Authors: Lance W. Chapman, Kristen R. Elkins, Janellen Smith
Journal: JAMA Dermatology (2016)

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Aortoenteric Fistula Complicating an Infected Aortic Graft
Authors: RAKESH H. GANATRA, M. A. HANIFFA, A. B. HAWTHORNE, J. I. S. REES
Journal: Clinical Nuclear Medicine (2001)

GANATRA, RAKESH H.; HANIFFA, M. A.; HAWTHORNE, A. B.; S. REES, J. I. Author Information
Abstract 3934: HCV core protein upregulates the expression of vascular endothelial growth factor via the nuclear factor-α/hypoxia-inducible factor-1α axis under hypoxic conditions
Authors: Mitsuhiko Abe, Hironori Koga, Takafumi Yoshida, Hiroshi Masuda, Hideki Iwamoto, Masahiro Sakata, Shinichiro Hanada, Toru Nakamura, Eitaro Taniguchi, Takumi Kawaguchi, Hirohisa Yano, Takuji Torimura, Takato Ueno, Michio Sata
Journal: Cancer Research (2012)

Abstract Aim: Hepatitis C virus (HCV) core protein critically contributes to hepatocarcinogenesis, which is often observed in liver cirrhosis. Since the liver cirrhosis microenvironment is affected by hypoxia, we focused on the possible driving force of HCV core protein on signal relay from hypoxia-inducible factor (HIF)-1α to vascular endothelial growth factor (VEGF). Methods: Human hepatocellular carcinoma cells stably overexpressing HCV core (Core cells) and NS5A (NS5A cells) were established; empty vector-transfected (EV) cells were used as controls. Hypoxia was induced by oxygen deprivation or by using cobalt chloride (CoCl2). YC-1 was used to inhibit HIF-1α expression. Protein analyses for cultured cells and liver tissues obtained from CoCl2-treated HCV core-transgenic (Core-Tg) mice were performed by Western blot and/or immunocytochemistry. Cellular mRNA levels were evaluated by quantitative real-time RT-PCR. Results: Under hypoxia, the sustained expression of HIF-1α, but not HIF-2α, was profoundly observed in Core cells but, was faint in EV and NS5A cells. Immunocytochemistry revealed increased HIF-1α in the nucleus. HIF-1α mRNA levels were significantly higher in Core cells than in EV cells under both normoxia and hypoxia. The HIF-1α-targeted VEGF and Bcl-xL expressions were increased in Core cells under hypoxia and abolished by YC-1 treatment. Hypoxic liver samples of Core-Tg mice indicated significant increases in both HIF-1α and VEGF expression compared to the wild type. Conclusions: HCV core protein has the distinct potential to transcriptionally upregulate and sustain HIF-1α expression under hypoxia, thereby contributing to increased VEGF expression, a key regulator in the hypoxic milieu of liver cirrhosis. 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 3934. doi:1538-7445.AM2012-3934