tbuckley/cabot-search huggingface dataset:
Bilateral Adrenal Pheochromocytoma and Medullary Thyroid Carcinoma
Authors: Joseph D. Sapira, Michael Altman, Klaas Vandyk, Alvin P. Shapiro
Journal: New England Journal of Medicine (1965)

ALTHOUGH the first case of pheochromocytoma associated with thyroid carcinoma was reported in 19321 it was not until 1952 that this combination of neoplasms was mentioned as occurring with unusual frequency.2 In 1961 Sipple3 presented a case of his own and reviewed 51 , 4 5 6 7 cases from the literature. He suggested that the observed incidence of thyroid carcinoma in patients with pheochromocytoma was much greater than might be expected. Since then, 9 other cases with the combination of pheochromocytoma and carcinoma of the thyroid gland have been reported. The present paper outlines an additional case and offers a brief review of the . . .
Endoscopic placement of self-expanding stents in patients with symptomatic anastomotic leakage after colorectal resection for cancer: long-term results
Authors: Antonietta Lamazza, Antonio Sterpetti, Alessandro De Cesare, Alberto Schillaci, Angelo Antoniozzi, Enrico Fiori
Journal: Endoscopy (2015)

Anastomotic leak after colorectal resection for cancer is a challenging clinical problem. The postoperative quality of life in these situations is significantly impaired. We prospectively analyzed the effect of placing a self-expanding metal stent (SEMS) at the level of the leak, with or without proximal diverting ileostomy, in 22 patients with symptomatic anastomotic leakage after colorectal resection. The stents were placed successfully in all 22 patients. An proximal ileostomy was created in 15 patients under general anesthesia. The anastomotic leak healed, without evidence of residual stricture or major incontinence, in 19 patients (86 %). In 3 patients, the leak did not heal; in 2 patients with recurrent rectovaginal fistula, the size of the leak decreased significantly, allowing successful flap transposition; and only 1 patient required a permanent stoma. SEMS placement is a valid adjunct to the treatment of patients with symptomatic anastomotic leakage after colorectal resection.
PTU-167 Differences in Barrett’S Oesophagus in an Ethnically Diverse South London Population
Authors: R Hewett, J-Y Kang, A Poullis
Journal: Gut (2013)

<h3>Introduction</h3> Barrett’s oesophagus (BO) is a metaplastic change of the lining of the oesophagus; the normal squamous epithelium is replaced by specialised columnar epithelium. BO is a risk factor for oesophageal adenocarcinoma, which is increasing in incidence in developed countries<sup>1</sup>. Risk factors for BO are age, being white Caucasian and male gender<sup>2</sup>. To our knowledge, no differences have previously been found between the mean length of Barrett’s segment or the mean age of BO patients in differing ethnic groups <h3>Methods</h3> We performed a retrospective analysis of electronic patient records at St George’s Hospital, which serves a large ethnically diverse population. Patients with a diagnosis of BO were identified from gastroscopy records dating from 2009 to 2012. Demographic information was collected for every patient. Patients of Indian sub-continent Asian (ISA) origin were identified using surname as previously described3. We looked at length of Barrett’s, gender and age in ISAs, compared to other ethnic groups <h3>Results</h3> 499 procedures were identified where the diagnosis was BO. Multiple reports for individual patients were excluded, identifying 378 patients with an endoscopic diagnosis of BO. Mean age of the sample was 67 years (SD 14.4). 11% of the sample were of ISA origin, 89% were of non-ISA origin. No significant difference was found in the mean length of the Barrett’s segment between males and females. However, male patients with BO were younger than females (65.5 years vs. 70.2 years; p = 0.003). No significant difference was found in the mean Barrett’s length or mean age between ISAs and non-ISAs. Patients of ISA origin were not found to have any significant difference between mean length of Barrett’s segment or mean age. Patients of non-ISA origin had no significant difference was in mean Barrett’s length between males and females, but there was a statistically significant difference between mean age of male Barrett’s patients (65.1 y) and female Barrett’s patients (70.7 y: p = 0.01) in this group <h3>Conclusion</h3> In our ethnically diverse population, male patients with Barrett’s oesophagus are younger than female patients. Furthermore, this difference occurs only in patients of non-Indian sub-continent origin. This implies that there may be an environmental factor in the UK which confers an accelerated progression of Barrett’s oesophagus in male patients. Further study in this area is warranted <h3>Disclosure of Interest</h3> None Declared. <h3>References</h3> Shaheen &amp; Ransohoff. Gastroesophageal reflux, Barrett oesophagus, and esophageal cancer: scientific review. <i>JAMA</i> 2002: 287: 1972–1981 Ford <i>et al.</i> Ethnicity, Gender, and Socioeconomic Status as Risk Factors for Esophagitis and Barrett’s Esophagus. <i>American Journal of Epidemiology</i> 2005: 162: 454–460 Kang <i>et al.</i> Diverticular disease of the colon: ethnic differences in frequency. <i>Aliment.Pharmacol.Ther.</i> 2004: 19: 765–769
Effect of the Gulf War on Infant and Child Mortality in Iraq
Authors: Alberto Ascherio, Robert Chase, Tim Coté, Godelieave Dehaes, Eric Hoskins, Jilali Laaouej, Megan Passey, Saleh Qaderi, Saher Shuqaidef, Mary C. Smith, Sarah Zaidi
Journal: New England Journal of Medicine (1992)

Increased malnutrition and morbidity among Iraqi children after the onset of the Persian Gulf war have been reported by several fact-finding missions. The magnitude of the effect of the war and the economic embargo on child mortality remains uncertain, however.We conducted a survey of 271 clusters of 25 to 30 households each, chosen as a representative sample of the Iraqi population. The households were selected and the interviews conducted by an international team of public health professionals independent of Iraqi authorities. In each household all women 15 to 49 years of age were interviewed, and the dates of birth and death of all children born on or after January 1, 1985, were recorded.The study population included 16,076 children, 768 of whom died during the period surveyed (January 1, 1985, to August 31, 1991). The age-adjusted relative mortality for the period after the war began, as compared with the period before the war, was 3.2 (95 percent confidence interval, 2.8 to 3.7). No material change in the relative risk was observed after adjustment for region of residence, maternal education, and maternal age. The increase in mortality after the onset of the war was higher among children 1 to less than 12 months old (relative risk, 4.1; 95 percent confidence interval, 3.3 to 5.2) and among those 12 to less than 60 months old (relative risk, 3.8; 95 percent confidence interval, 2.6 to 5.4) than among those less than 1 month old (relative risk, 1.8; 95 percent confidence interval, 1.4 to 2.4). The association between the war and mortality was stronger in northern Iraq (relative risk, 5.3) and southern Iraq (relative risk, 3.4) than in the central areas (relative risk, 1.9) or in Baghdad (relative risk, 1.7).These results provide strong evidence that the Gulf war and trade sanctions caused a threefold increase in mortality among Iraqi children under five years of age. We estimate that more than 46,900 children died between January and August 1991.
AORTIC VASCULAR INFLAMMATION BY 18-FDG PET/MRI IS RELATED TO CORONARY PLAQUE BURDEN BY QUANTITATIVE CORONARY CT ANGIOGRAPHY IN PSORIASIS
Authors: Aditya A. Joshi, Mohammad Tarek Kabbany, Mark Ahlman, Joseph Lerman, Tsion Aberra, Balaji Natarajan, Taufiq Salahuddin, Justin Rodante, Martin Playford, Marcus Chen, David Bluemke, Nehal Mehta
Journal: Journal of the American College of Cardiology (2016)
Abstract 4264: CD133/prominin-1 regulates the tumorigenicity of oral squamous carcinoma cells-derived cancer initiating cells
Authors: Yu-Syuan Chen, Jeng-Fan Lo, Cheng-Chia Yu
Journal: Cancer Research (2010)

Abstract Background: Oral squamous carcinoma cell (OSCC) is a lethal cancer with clinical, pathological, phenotypical, and biological heterogeneity. Previously, we enriched a subpopulation of oral cancer derived cancer initiating cells (OC-CICs) by tumor sphere formation approach, and identified CD133 as a putative CICs marker. However, the function of CD133 in OC-CICs remains unclear. Herein, we determined the critical role of CD133, an important CICs marker, in the maintenance of stemness characteristics and tumorigenic phenotype in OC-TICs. Methods: First, side population (SP) assay, a methodology to identify CICs in cancer cells, was performed to characterize the existence of OC-CICs. Next, we want to evaluate the expression of CD133 in OC-CIC isolated from SP cells transcriptionally and translationally. Lentiviral-mediated stable overexpression and down-regulation of CD133 expression in OSCCs and OC-CICs was established. Consequently, we investigated the effect of CD133 down-regulation or overexpression on stemness properties and tumorigenicity of OSCCs and OC-CICs, respectively. Results: We identified that CD133 was significantly up-regulated in SP cells of OSCCs. Stable overexpression of CD133 enhanced the CICs properties in OSCCs. In opposite, down-regulation of CD133 significantly reduced the self-renewal ability, side population cells, and expression of stemness genes of OC-CICs. Additionally, down-regulation of CD133 enhanced the differentiation capability but inversely diminished “stemness” gene expression of OC-CICs. Finally, knockdown of CD133 in OSCC or OC-CICs lessened both in vitro malignant abilities including cell migration/cell invasion/anchorage independent growth and in vivo tumor growth by xenotransplantation assay. Conclusion: We showed that SP cells with CICs properties existed in OSCCs. CD133 contributes to the maintenance of stemness and tumorigenicity of OC-CICs. Silencing CD133 might be a potential therapeutic target for OSCC by eliminating CICs. 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 4264.
P187 Does greater physician involvement with interventional procedure coding improve coding outcome?
Authors: A. R. L. Medford, A. Pillai
Journal: Thorax (2011)

<h3>Background</h3> The Royal College of Physicians of London Health Informatics Unit has developed the Professional Record Keeping Standards. Trusts have a financial incentive to code activity accurately under Payment by Results. Coding inaccuracy is well described by the Audit Commission varying from 0.3% to 52% across Acute Trusts in England, with the potential for gross financial disparity, with particular inaccuracy in interventional specialties.1 We have previously noted a 14.6% coding inaccuracy rate for endobronchial ultrasound-guided transbronchial needle aspiration (EBUS-TBNA).2 Given that the specific EBUS-TBNA tariff is approximately six times the conventional bronchoscopy tariff, EBUS-TBNA is a good model to illustrate the potential financial effects. <h3>Hypothesis</h3> Greater physician involvement with a prospective coding cross-checking system would improve coding outcome for EBUS-TBNA and financial disparity. <h3>Methods</h3> From November 2010 to June 2011, 52 consecutive patients underwent EBUS-TBNA in a UK teaching hospital. After every procedure, anonymised patient details were emailed securely to the Trust Coding Lead. Every month, the Trust Informatics Lead would email the final coding outcomes and tariffs for all the EBUS-TBNA patients. These were cross-checked against a prospective anonymised procedure database. Primary outcome was coding accuracy. Data were compared to a previous EBUS-TBNA coding study<sup>2</sup> as a control (no coding intervention) using contingency table analysis with Fishers Exact Test and a p value of &lt;0.05 was deemed significant (GraphPad Prism 5 software). Differences in financial loss were calculated using a tariff of £504 for conventional bronchoscopy and £3404 for EBUS-TBNA (E63.2+T87.4). <h3>Results</h3> All 52 patients were coded correctly with no financial loss. From the previous study of 52 patients, 8 (14.4%) were coded incorrectly which was significant (OR 20.1, 1.1–357.5, p=0.006, Fishers Exact). Financial loss to the NHS Trust was calculated as £23 200, projected to £40 000 per year. <h3>Conclusion</h3> Greater physician engagement with coders improves coding outcomes. This is of particular importance in interventional specialties where the potential for financial loss is of a higher magnitude. A simple prospective cross-checking system can achieve better outcomes with no extra cost and minimal effort.
443P Phase III trial of afatinib vs erlotinib in patients (pts) with squamous cell carcinoma (SCC) of the lung (LUX-Lung 8): EGFR molecular aberrations and survival outcomes
Authors: K. Park, W. Li, C. Zhou, E. Felip, M. Cobo, G.D. Goss, J.-C. Soria, K. Syrigos, N. Krämer, V.K. Chand, F. Solca, S. Lu
Journal: Annals of Oncology (2015)
Case 34-1997
Authors: Lillian E.C. McMahon, Eugene J. Mark
Journal: New England Journal of Medicine (1997)

Presentation of CaseA 22-year-old man was admitted to the hospital because of respiratory distress and fever.The patient was known to have sickle cell disease but had had few problems during childhood except for priapism, which required surgical treatment. He had had malaria but had been otherwise generally well. He had received a single blood transfusion in his native Ghana before coming to this country 31 months before admission.In Boston the sickle cell crises became more frequent and more severe and often appeared to be precipitated by cold weather. The patient was admitted on multiple occasions to his . . .
Abstract 181: MIR-18b decreases self-renewal of glioblastoma cancer stem-like cells through targeting NOTCH2, NEDD9, and MEKK1
Authors: Xiaobing He, Francesco DiMeco, Angelo Vescovi, Jason Heth, Karin Muraszko, Xing Fan
Journal: Cancer Research (2012)

Abstract Glioblastoma (GBM) is the most common malignant brain tumor in human with extremely poor prognosis and new treatment for this deadly disease is desperately needed. Cancer Stem-like cells (CSCs) have been prospectively isolated from GBM and shown required for tumor propagation. We and others have demonstrated recently that differentiation of GBM neurospheres decreases GBM cell propagation both in vitro and in vivo (Zhu et al, Cancer Research, 71:6061-72, 2011). In the current study, we found that miR-18b was up-regulated upon differentiation of GBM neurosphere. When we introduced miR-18b into GBM neurospheres by lentivirus, we found that miR-18b decreases clonogenesis and growth of three different GBM neurosphere lines, indicating that GBM CSC population was reduced by miR-18b. Mechanistically, we found that miR-18b down-regulates luciferase activity of 3′-UTR reporters of NOTCH2, NEDD9, and MEKK1. Furthermore, protein expression of NOTCH2, NEDD9, and MEKK1 are also decreased by miR-18b, suggesting that NOTCH2, NEDD9 and MEKK1 are the direct targets of miR-18b in GBM CSCs. In addition, we have demonstrated previously that NOTCH regulates GBM CSC propagation through pAKT (Fan et al, Stem Cells, 28:5-16, 2010). Here, we found that pAKT and pERK1/2 were also down-regulated in miR-10b infected GBM neurosphere lines, indicating that miR-18b reduces GBM CSC propagation through NOTCH2/pAKT pathways. Taken together, we have demonstrated that miR-18b functions as a tumor suppressor and decreases GBM CSC propagation through targeting NOTCH2, NEDD9, and MEKK1, indicating that miR-18b can be a potential therapeutic molecule to target GBM CSCs and improve GBM treatment. 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 181. doi:1538-7445.AM2012-181
Alleviation of Systemic Manifestations of Castleman's Disease by Monoclonal Anti-Interleukin-6 Antibody
Authors: Joseph T. Beck, Su-Ming Hsu, John Wijdenes, Regis Bataille, Bernard Klein, David Vesole, Katherine Hayden, Sundar Jagannath, Bart Barlogie
Journal: New England Journal of Medicine (1994)

Castleman's disease (angiofollicular lymphoid hyperplasia) is a heterogeneous group of lymphoproliferative disorders of uncertain cause1. Two pathologic types, hyaline vascular and plasma-cell disease, have been recognized. The plasma-cell variant of Castleman's disease may be localized or multicentric. Multicentric disease is a systemic lymphoproliferative disorder characterized by lymphadenopathy, hepatosplenomegaly, and constitutional symptoms. Anemia, hypoalbuminemia, and hypergammaglobulinemia are also common. Interleukin-6, a cytokine with pleiotropic effects on the immune system, hematopoiesis, and acute-phase reactions, is a putative growth factor in multiple myeloma and may also be central to the pathophysiology of Castleman's disease2–7. Administration of a murine anti-interleukin-6 monoclonal . . .
Clinical Trial Reimbursement Reform Sought
Authors: T. Parkins
Journal: JNCI Journal of the National Cancer Institute (1993)

Journal Article Clinical Trial Reimbursement Reform Sought Get access Troy Parkins Troy Parkins Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 85, Issue 19, 6 October 1993, Pages 1549–1551, https://doi.org/10.1093/jnci/85.19.1549 Published: 06 October 1993
Abstract 5393: Prodrug activator gene therapy mediated by prostate-specific replicating retrovirus vectors
Authors: Shuichi Kamijima, Takahiro Kimura, Kazunori Haga, Kei Hiraoka, Akihito Inagaki, Christopher R. Logg, Chinghai Kao, Bernard H. Bochner, Tomohiko Ichikawa, Noriyuki Kasahara
Journal: Cancer Research (2011)

Abstract Replicating murine leukemia virus (RMLV)-based vectors can propagate specifically within actively dividing cancer cells and achieve highly efficient and tumor-selective gene delivery. However, in view of the known potential for retroviral integration-mediated genotoxicity, additional mechanisms to target the virus specifically to cancer cells are desirable. To further improve their tumor specificity and safety profile, we have developed RMLV vectors regulated by two different tissue-specific promoters. We generated GFP-expressing RMLV vectors ACE-emd (wild type), ACE-At-emd (regulated by ARR2PB promoter, a synthetic variant of the probasin promoter which exhibits high specificity for androgen receptor (AR)-positive prostate cancer cells) and ACE-PSES-emd (regulated by PSES promoter, an androgen-independent promoter which is highly active in PSA/PSMA-positive prostate cancer cells, both in the presence and absence of androgen). We also developed ACE-yCD, ACE-At-yCD and ACE-PSES-yCD carrying the yeast cytosine deaminase (yCD) prodrug-activator gene, which converts the nontoxic prodrug 5-fluorocytosine (5FC) into the chemotoxin 5-fluorouracil. These vectors were first in vitro tested in both prostate (LNCaP, MDA PCa 2b and PC-3) and non-prostate (293T) cell lines in the presence and absence of androgen. RMLV vector ACE-At-emd exhibited high specificity and robust replication in AR-positive prostate cancer cell lines, but only in the presence of androgen. RMLV vector ACE-PSES-emd exhibited high specificity for PSA/PSMA-positive prostate cancer cell line both in the presence and absence of androgen. For in vivo studies, male nude mice were inoculated subcutaneously with LNCaP cells (AR-positive, PSA/PSMA-positive) in Matrigel. RMLV vectors expressing GFP were injected intratumorally, and tumors were analyzed by flow cytometry 2 and 4 weeks after vector injection. The results showed that both ARR2PB- and PSES-regulated RMLV vectors achieve efficient gene delivery to LNCaP s.c. tumors in vivo. Cytotoxic activity of RMLV-yCD vectors was examined in vitro in LNCaP cells in the presence and absence of 5FC after virus infection. Cell-specific expression of each vector correlated with reduced cell viability compared to uninfected cells after 5FC treatment. We are now conducting studies to evaluate therapeutic efficacy vs. potential genotoxicity of these vectors for prodrug-activator gene therapy in vivo. 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 5393. doi:10.1158/1538-7445.AM2011-5393
REAL-WORLD EXPERIENCE OF BIOLIMUS A9-ELUTING STENTS AND COMPARISON WITH EVEROLIMUS-ELUTING XIENCE PRIME STENTS IN ALL-COMER REGISTRIES: PRELIMINARY REPORT FOR PATIENT-ORIENTED AND STENT-RELATED 2-YEAR OUTCOMES FROM THE MULTICENTER PROSPECTIVE BIOLIMUS-KOREA-3000 REGISTRY AND EXCELLENT-PRIME REGISTRY
Authors: Chan Soon Park, Chi-Hoon Kim, Jung-Kyu Han, Han-Mo Yang, Kyung Woo Park, Hae-Young Lee, Hyun-Jae Kang, Bon Kwon Koo, Hyosoo Kim
Journal: Journal of the American College of Cardiology (2016)
IB-05 * TUMOR-PROCESSED OSTEOPONTIN/SPP1 SHAPES MICROGLIA POLARIZATION AND IMMUNE MICROENVIRONMENT OF GLIOMA
Authors: B. Kaminska, P. Wisniewski, M. Kijewska, A. Ellert-Miklaszewska, D. Pszczolkowska, P. Gajdanowicz, A. Gieryng
Journal: Neuro-Oncology (2014)

Malignant gliomas attract resident microglia and macrophages and re-program these cells into pro-invasive, immunosuppressive cells. It results in formation of tumor supportive microenvironment and evasion of antitumor responses. The analysis of marker genes in microglia and macrophages infiltrating experimental gliomas indicates different kinetics and functions of various myeloid subpopulations during glioma progression. Signals responsible for recruitment and polarization of tumor infiltrating myeloid cells are poorly known. Proteomic analysis of glioma secretome revealed a presence of osteopontin (SPP1) and lactadherin (MGF-E8) in microglia-activating fractions. Both proteins stimulated microglia via αvβ3 integrin signaling that results in activation of PI-3K/Akt and FAK, enhancement of microglial migration, phagocytosis and transcriptional responses. Inhibition of ligand-integrin interactions with short interfering peptides abolished pro-invasive polarization in glioma-microglia co-cultures. We found that SPP1, highly overexpressed in glioma cells, was specifically processed by sequential thrombin and metalloproteinase-dependent cleavage. This type of processing results in losing SPP1 pro-inflammatory activity leaving intact its pro-tumorigenic activity and does not occur in non-transformed cells. Knockdown of SPP1 in glioma cells strongly reduced growth of intracranial gliomas. The number of infiltrating microglia/macrophages (Iba1+) was not affected, but amoeboid transformation, expression of the alternative phenotype markers and angiogenesis were reduced in SPP1-depleted gliomas. Interestingly, infiltrating Iba1+ cells did not undergo pro-invasive polarization. Moreover, SPP1-depleted tumors were infiltrated with T cytotoxic lymphocytes, while accumulation of T regulatory cells was significantly reduced. The expression of SPP1 is up-regulated in human glioblastoma and inversely correlated with patient's survival. Our findings demonstrate that glioma-derived and specifically processed osteopontin/SPP1 polarizes glioma-infiltrating microglia and contributes to transformation of tumor microenvironment. This defines osteopontin/SPP1 a new biomarker and target for glioma therapy, and shows that targeting glioma-microglia interactions within tumor microenvironment is a promising strategy to fight these tumors. Studies were supported by a grant 2012/04/A/NZ3/00630 from the National Science Center.