tbuckley/cabot-search huggingface dataset:
NCI's Proposed Breast Cancer Screening Guidelines
Authors: Kara Smigel
Journal: JNCI Journal of the National Cancer Institute (1993)

Journal Article NCI's Proposed Breast Cancer Screening Guidelines Get access Kara Smigel Kara Smigel Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 85, Issue 20, 20 October 1993, Pages 1627–1628, https://doi.org/10.1093/jnci/85.20.1627 Published: 20 October 1993
Abstract 5090: The role of p32 in brain metastasis
Authors: Karin Staflin, Valentina Fogal, Antonio Fernandez-Santidrian, Erkki Ruoslahti, Brunhilde Felding-Habermann
Journal: Cancer Research (2010)

Abstract Brain metastases are among the most feared complication in cancer. To develop effective and targeted therapies for treatment of brain metastases, we need a better understanding of the mechanisms that control cancer cell growth within the brain microenvironment. We previously found evidence that brain metastatic cells have increased rates of oxidative phosphorylation and redox potential compared to tumor cells from extracranial lesions. Here we sought to identify mechanisms involved, and to identify potential targets for the inhibition of metastatic growth in the brain. Many of the genes involved in transformation such as Myc, AKT, and p53 have extensive effects on the metabolism, suggesting that tumors might be susceptible to antimetabolic drugs. One of the proteins that has been shown to be upregulated in many solid tumors is the protein p32. P32 is a multi-compartmental and multi-functional protein which has a regulatory function in oxidative phosphorylation, in addition to being involved in the regulation of apoptosis and autophagy. We found p32 expressed in human cancer cells capable of seeding brain metastases in immune deficient mice, and we hypothesized that p32 contributes to cell survival and proliferation within the brain microenvironment. We knocked down p32 in brain homing variants of the MDA-MB-231 and MDA-MB-435 metastasis cell models. Following luciferase tagged tumor cells by non-invasive bioluminescence imaging revealed that stable p32 knockdown greatly reduced metastatic activity in both MDA-MB-231 brain specific variant and the MDA-MB 435 cell line. Furthermore, our genomic profiling of p32 knock-down and control cells identified candidate genes in the respiration chain involved in p32-dependent tumor cell survival and growth that may impact progression to brain metastasis. Thus, the expression and functionality of p32 in tumor cells capable of colonizing the brain appears associated with changes in crucial pathways that enable the tumor cells to proliferate and survive within the brain microenvironment. 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 5090.
Kinetics of Tc-99m Sestamibi and Tc-99m Tetrofosmin in a Case of Parathyroid Adenoma
Authors: LUIGI MANSI, PIER FRANCESCO RAMBALDI, GIUSEPPE MARINO, BIAGIO PECORI, ENRICO DEL VECCHIO
Journal: Clinical Nuclear Medicine (1996)

The uptake of Tc-99m tetrofosmin (TF) is reported in a case of parathyroid adenoma. A 65-year-old woman was studied on different days with TF, Tc-99m sestamibi (MIBI) and Tl-201 chloride (TI). TF and MIBI injections were preceded by oral administration of potassium perchlorate. Clear identification of the adenoma was observed in all scans. No further information was obtained using a subtraction technique with Tc-99m pertechnetate. Regarding the thyroid/parathyroid ratio, different kinetics between TF and MIBI appear to be demonstrated. In particular, thyroid washout was observed with MIBI but not with TF.
AB0403 Cigarette smoking and coffee consumption independently influence the risk of developing cardiovascular disease in systemic lupus erythematosus
Authors: J. Amaya-Amaya, J. L. Pérez-Fernández, N. Molano-González, R. D. Mantilla, A. Rojas-Villarraga, J. M. Anaya
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Cardiovascular disease (CVD) is a major cause of morbidity and mortality in patients with systemic lupus erythematosus (SLE), a 50-fold than general population. Traditional risk factors, such as, cigarette smoking and dyslipidemia, are known but they cannot fully account for the increased risk. Instead, non-traditional risk factors, related to disease are also contributing. Varied results have been reported on the association between coffee drinking and CVD in the general population, with controversial results. Coffee consumption has not been evaluated systematically in SLE patients with CVD. <h3>Objectives</h3> We aimed to determine the prevalence and associated risk factors for CVD in a Latin American population with SLE. <h3>Methods</h3> This was a cross-sectional study in which consecutive patients with SLE (ACR 1997 update) seen on an outpatient basis were assessed for CVD including arterial hypertension, coronary artery disease, peripheral arterial disease, cerebrovascular disease and thrombosis. Factors associated with its occurrence were examined by bivariate and multivariate regression analyses. <h3>Results</h3> Out of a total of 310 patients, 113 (36.5%) presented with CVD. The most frequent condition was hypertension (69%). Dyslipidemia (28% vs. 12%), ever smoking (51% vs. 37%), coffee consumption (70.5% vs. 55.2%) and pleural effusion (32% vs. 19%) were positively associated with CVD (Table). Logistic regression analyses disclosed an independent effect of coffee consumption and cigarette smoking on CVD regardless of gender and duration of disease. <h3>Conclusions</h3> A high rate of CVD was observed in our patient population. Awareness of the observed risk factors should encourage preventive population strategies for CVD in patients with SLE aimed to facilitate the suppression of cigarette smoking and coffee consumption as well as to the tight control of dyslipidemia. <h3>References</h3> Magder LS, Petri M. Am J Epidemiol. 2012;176(8):708-19 Zhang Z, et al. Am J Clin Nutr. 2011;93(6):1212-9 Di Castelnuovo A, et al. Eur J Intern Med. 2012;23(1):15-25 Kahlenberg JM, Kaplan MJ.Arthritis Res Ther. 2011;13(1):203 <h3>Disclosure of Interest</h3> None Declared
Detection of a Liver-Membrane Autoantibody in HBsAg-negative Chronic Active Hepatitis
Authors: Uwe Hopf, Karl-Hermann Meyer zum Büschenfelde, Wolfgang Arnold
Journal: New England Journal of Medicine (1976)

Investigation of humoral immunity against hepatocellular membrane antigens in patients with chronic active hepatitis and other liver diseases showed two different immunofluorescence patterns of IgG on hepatocyte membranes. A linear pattern was seen in HBsAg-negative hepatitis, but HBsAg-positive cases and some of protracted, acute hepatitis B had a granular pattern. In patients with IgG bound to hepatocytes, continuing necrosis of parenchymal liver cells was seen. Conversely, hepatocytes without bound IgG were found in cases of chronic active hepatitis in remission, acute viral hepatitis without HBsAg and chronic persistent hepatitis, in "healthy" HBsAg-carriers and in patients with fatty liver or alcoholic cirrhosis. A liver-membrane autoantibody in serum, proved by fixation on membranes of isolated rabbit hepatocytes, could be demonstrated only in HBsAg-negative chronic active hepatitis with elevated IgG-concentrations. The results support the existence of different pathogenetic types of chronic active hepatitis, a so-called autoimmune type and a hepatitis virus-B-induced type.
Abstract 4551: 111In-NLS-Nimotuzumab: A potent auger electron-emitting radiotherapeutic agent for EGFR-overexpressing breast cancer
Authors: Aisha Fasih, Ray Reilly, Ilia Tikhomirov
Journal: Cancer Research (2010)

Abstract Objective: To evaluate the cytotoxicity of nimotuzumab (Nmab), a monoclonal antibody specific for EGFR labeled with 111In and modified with nuclear localization sequence (NLS) peptides for importation into the nucleus of human breast cancer (BC) cells, where the emitted Auger electrons are most damaging to DNA and lethal. Methods: NMab was derivatized with sulfo-SMCC to introduce maleimide groups for reaction with NLS-peptides (CGYGPKKKRKVGG) and benzyl-DTPA (bn-DTPA) for complexing 111In. NLS substitution was quantified by a band shift on SDS-PAGE and bnDTPA substitution by an 111In-binding assay. The immunoreactivity (Kd) of NLS-Nmab was determined by the displacement of binding of 111In-Nmab to MDA-MB-468 BC cells (106 EGFR/cell). Internalization and nuclear importation were determined in MDA-MB-468 and MCF-7 (104 EGFR/cell) BC cells by subcellular fractionation at 37 oC and 4 oC up to 3 h. Clonogenic survival (CS) was measured in MDA-MB-468 and MCF-7 cells exposed to 2 to 40 nM (450-900 KBq/mL) of 111In-NLS-Nmab for 3 days. Results: Nmab was modified with 8.5±0.2 NLS and 2.1±2.1 bn-DTPA groups. The Kd for binding of 111In-NLS-Mab to MDA-MB-468 cells was 9.8±0.9 nM. NLS-Nmab was labeled with 111In to a radiochemical purity of 99.2±0.1% (specific activity 350±9 MBq/mg). The proportion of cell-bound 111In internalized into MDA-MB-468 cells at 3 h was 27.8±0.8% at 37 oC and 4.4±0.2 at 4 oC. Nuclear uptake was 31.2±2.6% for 111In-NLS-Nmab and 16.0±0.6% for 111In-Nmab (P&amp;lt;0.001). Binding and nuclear uptake were 20-fold and 6-fold lower, respectively for MCF-7 cells. The CS of MDA-MB-468 cells exposed to 111In-NLS-Nmab (20 nM) was 2.8±0.2% compared to 21.0±5.3% for 111In-Nmab (P=0.004) and 60.0±7.0% for Nmab (P=0.001). The CS of MCF-7 cells exposed to 111In-NLS-Nmab (40 nM) was 82.6±6.4% vs. 80.0±1.6% for 111In-Nmab (p&amp;gt;0.05) and 95±19.4% for Nmab (p&amp;gt;0.05). Conclusion: 111In-NLS-Nmab is a promising targeted radiotherapeutic agent for EGFR-overexpressing BC as evidenced by a 20-fold increased toxicity towards MDA-MB-468 cells compared to Nmab but lack of toxicity towards MCF-7 cells with 10-fold lower EGFR expression similar to that on most normal epithelial cells. Supported by the Canadian Breast Cancer Research Alliance (Grant 019513). 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 4551.
American Cardiology: The History of a Specialty and its College
Authors: A. Hollman
Journal: BMJ (1996)

W Bruce Fye Johns Hopkins University Press, £20, pp 489 ISBN 0 8018 5292 7

Bruce Fye's book originated as the 40th anniversary narrative of the American College of Cardiology, but Dr Fye has wisely described the college's story within the much wider framework of the history of cardiology in the United States. The result is an absorbing and very well written chronicle of, for example, how new technology catalysed the growth of cardiology, and of how warring factions in various organisations battled with each other to promote their own version of the true way ahead. I found it exciting reading.

It was the electrocardiograph that enabled physicians to become differentiated as …
Synergistic Growth Inhibition with a PI3 Kinase/mTOR Inhibitor Plus Lapatinib.
Authors: T. Speicher, W. Hackl, A. Lipton
Journal: Cancer Research (2009)

Abstract The mammalian target of rapamycin, mTOR, is a member of the phosphatidylinositol 3-kinase (PI3-K) /Akt family and plays a key role in cell growth and survival. The PI3-K/mTOR pathway is activated by many growth factor receptors in human tumor cells. In addition, the PI3-K pathway is constitutively activated by mutation in one-third of breast cancers. Therefore, blockade of the PI3-K/mTOR pathway may sensitize breast cancers to HER-2/neu inhibition. BEZ235 (Novartis Pharma AG) is a potent, oral, dual PI3-K/mTOR inhibitor currently in Phase I clinical trials. The purpose of this study was to assess the in vitro effects of combining a dual PI3-K/mTOR inhibitor (BEZ235, Novartis Pharma AG) and a lapatinib-like dual inhibitor of EGFR and HER-2/neu (GW2974) on the growth of HER-2/neu-transfected MCF-7 human breast cancer cells. Cells were exposed to the lapatinib-like compound [GW2974 (0.05-5.0µM)] or the dual PI3-K/mTOR inhibitor [BEZ235 (0.5-3nM)] alone or in combination for 3 days (12 different dose combinations were tested). Cell growth was determined using the colorimetric MTT tetrazolium dye assay. The Chou-Talalay method of isobologram analysis was performed to determine the inhibitory effect. Dose-dependent growth inhibition was observed in HER-2/neu-transfected MCF-7 cells after 3 days exposure to GW2974 (IC50: 5.0 mM) or BEZ235 (IC50: 2.2 nM). Exposure to the combination of GW2974 (0.05-0.50 mM) and BEZ235 (0.50-1.0 nM) resulted in synergistic growth inhibition in HER-2/neu-transfected MCF-7 human breast cancer cells. In summary, the combination of lapatinib plus PI3-K/mTOR warrants further investigation as a therapeutic strategy for breast cancer. Citation Information: Cancer Res 2009;69(24 Suppl):Abstract nr 6114.
Humanitarian power has been hijacked and must regain its reputation for neutrality
Authors: Gabriele Rossi
Journal: BMJ (2013)

Attacks on its staff have led Médecins Sans Frontières (Doctors Without Borders) recently to stop offering humanitarian assistance in Somalia altogether. <b>Gabriele Rossi</b> says that humanitarianism must be uncoupled from political and military activity and rebuild its reputation of impartiality
Abstract 3560: The chromatin architecture at gucocorticoid receptor binding sites.
Authors: Craig J. Burd, James M. Ward, Adam B. Burkholder, David C. Fargo, Trevor K. Archer
Journal: Cancer Research (2013)

Abstract Steroid hormone receptors are transcription factors that are implicated in the development and progression of several cancer types. It is clear that receptor activity is deregulated in these disease states. Using the glucocorticoid receptor (GR) as a model factor for transcriptional initiation, we aimed to understand the role chromatin structure plays in defining the specific genetic programs initiated by receptor activation. Using Formaldehyde Assisted Isolation of Regulatory Elements (FAIRE), we examined the chromatin state at GR binding locations. FAIRE-seq data indicated an enrichment of signal, suggesting a more open chromatin state, surrounding the GR binding sites even in the absence of hormone. This enrichment is only seen at binding sites and not at unutilized response elements. This data is in line with recent developments indicating accessibility as a determinant of receptor binding. However, further characterization of binding regions suggests consistent nucleosome occupancy at these binding locations. Taken together, these data suggest that receptor binding may be determined by a very specific chromatin architecture that is defined by a transitional accessibility state. Citation Format: Craig J. Burd, James M. Ward, Adam B. Burkholder, David C. Fargo, Trevor K. Archer. The chromatin architecture at gucocorticoid receptor binding sites. [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 3560. doi:10.1158/1538-7445.AM2013-3560
Duodenal perforation due to toothpick perforation, an uncommon cause of chronic abdominal pain
Authors: B. Robert, E. Bartoli, M. Fumery, M. Eoche, C. Chivot, F. Demasure, H. Mancheron, T. Yzet
Journal: Endoscopy (2012)

A 55-year-old woman presented with a 3-month history of chronic left upper quadrant abdominal pain. She had no previous medical history. Her symptoms were not associated with nausea or emesis. Physical examination showed an afebrile patient with left upper quadrant abdominal tenderness. Laboratory tests demonstrated an elevated white cell count of 15000/µL (normal range 4000 – 10000/µL). C reactive protein was 50 mg/dL (normal < 5 mg/mL). Liver function tests were normal. Images from ultrasonography exploration were considered normal.
Abstract 2686: RSK2/CREB/Fascin-1 signaling is important for tumor metastasis.
Authors: Dan Li, Lingtao Jin, Gina Alesi, Young Mee Kim, Dongsheng Wang, Benjamin H Lee, Jack Taunton, Kelly R Magliocca, Zhuo Georgia Chen, Sumin Kang
Journal: Cancer Research (2013)

Abstract Metastasis is the leading cause of death in patients with breast, lung or head and neck cancers. However, the molecular mechanisms underlying metastases in these cancers remain unclear. We found that the p90 ribosomal S6 kinase 2 (RSK2)-cAMP response element-binding (CREB) pathway is commonly activated in diverse metastatic human cancer cells, leading to upregulation of a CREB transcription target Fascin-1. We also observed that the protein expression patterns of RSK2 and Fascin-1 correlate in primary human tumor tissue samples from HNSCC patients. Moreover, knockdown of RSK2 disrupts filopodia formation and bundling in highly invasive cancer cells, leading to attenuated cancer cell invasion in vitro and tumor metastasis in vivo, while expression of Fascin-1 significantly rescues these phenotypes. Furthermore, targeting RSK2 by a small molecule RSK inhibitor FMK-MEA effectively attenuated the invasive and metastatic potential of cancer cells in vitro and in vivo, respectively. Together, our findings for the first time link the RSK2-CREB signaling to filopodia formation and bundling by upregulating Fascin-1, providing a pro-invasive and pro-metastatic advantage to human cancers; protein effectors of RSK2-CREB-Fascin-1 pathway represents promising biomarkers and therapeutic targets in clinical prognosis and treatment of metastatic human cancers. Citation Format: Dan Li, Lingtao Jin, Gina Alesi, Young Mee Kim, Dongsheng Wang, Benjamin H Lee, Jack Taunton, Kelly R Magliocca, Zhuo Georgia Chen, Sumin Kang. RSK2/CREB/Fascin-1 signaling is important for tumor metastasis. [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 2686. doi:10.1158/1538-7445.AM2013-2686
Detection of Epstein–Barr Viral Genomes in Reed–Sternberg Cells of Hodgkin's Disease
Authors: Lawrence M. Weiss, Lucile A. Movahed, Roger A. Warnke, Jeffrey Sklar
Journal: New England Journal of Medicine (1989)

We used slot blot hybridization, Southern blot hybridization, and in situ hybridization to investigate the presence of Epstein–Barr virus (EBV) genomes in biopsy tissues from patients with Hodgkin's disease. Slot blot hybridization performed on DNA of tissue specimens from 16 patients revealed that biopsy tissue from 3 (19 percent) contained EBV DNA. Southern blot hybridization with a DNA probe containing the 500-base-pair tandem repeated sequences located at the termini of the EBV genome confirmed the findings of the slot blot hybridization in the three positive tissue specimens and indicated the monoclonality of the EBV-infected cells in such tissues. In situ hybridization performed on the three positive specimens and on two from a previous study localized EBV nucleic acid to the Reed-Sternberg cells and variants in all specimens, with intense hybridization to Reed–Sternberg cells in two, less intense but consistent hybridization to Reed–Sternberg cells in two, and focal hybridization to Reed–Sternberg cells in one. We conclude that EBV genomes are present within Reed–Sternberg cells and variants in some patients with Hodgkin's disease and that the infected cells are monoclonal. (N Engl J Med 1989; 320:502–6.)
DIASTOLIC DYSFUNCTION BY DOPPLER ECHOCARDIOGRAM IS ASSOCIATED WITH MAJOR ADVERSE EVENTS IN ADULT FONTAN PATIENTS
Authors: Makoto Mori, Kayoko Shioda, Maria Pernetz, Robert Elder, Alicia Rangosch, Wendy Book, Fred Rodriguez, Anurag Sahu, Brian Kogon, Michael McConnell, Camden Hebson, Maan Jokhadar
Journal: Journal of the American College of Cardiology (2015)
EL VACIAMIENTO GÁSTRICO ESTÁ ENLENTECIDO EN LA NOTES TRANSGÁSTRICA COMPARADO CON OTROS ACCESOS DE LA NOTES Y LAPAROSCOPIA: ESTUDIO ALEATORIZADO EN UN MODELO PORCINO DE SUPERVIVENCIA
Authors: H Córdova, A Rodríguez D'Jesús, C Guarner-Argente, G Martínez-Pallí, R Navarro-Ripoll, C Rodríguez de Miguel, M Beltrán, J Comas, MA Martínez, S Delgado, A Lacy, CC Thompson, J Llach, G Fernández-Esparrach
Journal: Endoscopy (2010)

Métodos: aleatorización en cuatro grupos: NOTES transgástrica (TG), transrectal (TR), transvaginal (TV) y laparoscopia (Lap). Los accesos TG, TR y TV se realizaron con técnicas antisépticas, mientras la Lap fue realizada en condiciones estériles. Se realizó 30 minutos de exploración abdominal en todos los grupos. Al final de la cirugía, la cápsula endoscópica (CE) activada fue liberada dentro del antro gástrico con la ayuda del endoscopio y un asa de polipectomía. El tiempo de supervivencia fue 14días.
Abstract 5453: YK-4-279 inhibits ETS-positive prostate cancer cell metastasis in a mouse xenograft model.
Authors: Said Rahim, Sarah Justvig, Sung-Hyeok Hong, Yali Kong, Milton L. Brown, Colm Morrissey, Jeffrey A. Toretsky, Aykut Uren
Journal: Cancer Research (2013)

Abstract Chromosomal translocations involving the ETS family of transcription factors are found in a majority of prostate cancers, including the most clinically aggressive forms. These translocations produce a chimeric gene, which fuses the promoter region of an androgen responsive gene to the coding region of ETS factors, most frequently ETV1 or ERG. Over-expression of ETS factors in prostate cancer cells results in a more invasive phenotype. The high prevalence of these rearrangements, and their biological significance represents a novel therapeutic target for the treatment of prostate cancer. We recently demonstrated that the small molecule YK-4-279 inhibits ERG and ETV1 biological activity in fusion-positive prostate cancer cells leading to decreased motility and invasion in-vitro. Here we present our findings in an in-vivo mouse xenograft model. SCID-beige mice were subcutaneously injected with LNCaP and PC-3 xenografts. Mice were treated with YK-4-279 and its effect on primary tumor size and lung metastasis was observed. YK-4-279 treatment resulted in reduced metastasis of the tumor from primary site to lungs. YK-4-279 also affected expression of ETV1 target genes such as MMP7 and MMP13. ETS fusion-negative PC-3 xenografts were unresponsive to YK-4-279. Our results demonstrate that YK-4-279 decreases tumor growth and inhibits metastasis in fusion-positive prostate cancer cell xenografts. Therefore, YK-4-279 may have an impact on preventing metastasis in prostate cancer patients, which is a leading cause of death. Citation Format: Said Rahim, Sarah Justvig, Sung-Hyeok Hong, Yali Kong, Milton L. Brown, Colm Morrissey, Jeffrey A. Toretsky, Aykut Uren. YK-4-279 inhibits ETS-positive prostate cancer cell metastasis in a mouse xenograft model. [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 5453. doi:10.1158/1538-7445.AM2013-5453