tbuckley/cabot-search huggingface dataset:
SAT0296 European Society of Cardiology/European Respiratory Society Guidelines and Detect Algorithm Right Heart Catheterisation Recommendations: A Real-Life Comparison: Table 1
Authors: F. Lumetti, V. Serra, F. Mozzani, G. Delsante, A. Ariani
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> Pulmonary arterial hypertension (PAH) is one of the most common Sistemic Sclerosis (SSc) related cause of death. Right heart catheterisation (RHC) is the gold standard to detect a PAH. Nevertheless RHC is an invasive diagnostic procedure not always accepted by patients. The European Society of Cardiology/European Respiratory Society (ESC/ERS) has suggested several consensus guidelines to identify high risk PAH subjects [1]. ESC/ERS RHC recommendation are based on patients9 syntoms and echocardiographic parameters such as tricuspid regurgitant jet (TR) velocity and right atrium (RA) area. Recently the DETECT study [2] has presented an evidence-based detection algorithm for PAH in SSc. The DETECT algorithm is divided in two steps determining referral to RHC. In the first one non ecocardiographic tests (FVC/DLCO ratio, current/past telangiectasias, serum ACA, serum NTproBNP, serum urate and right axis deviation on ECG) are taken into account. TR velocity and RA are the echocardiographic parameters assessed in step 2. <h3>Objectives</h3> To compare RHC recommendations according to ESC/ERS guidelines and DETECT algorithm in a group of SSc patients followed up in our rheumatological clinic. <h3>Methods</h3> We included 39 consecutive patients admitted to the Unit of Internal Medicine and Rheumatology of the Azienda Ospedaliero-Universitaria di Parma (Italy) between April and October 2013. Each patient had a SSc diagnosis (according to the EULAR/ACR classification criteria) established three or more years ago and was assessed with the above mentioned non-echocardiographic and echocardiographic tests. <h3>Results</h3> Table 1 shows patients with RHC recommended (or not) according to ESC/ERS guidelines and DETECT algorithm. A concordant recommendation was found in 61,5% of patients; 20,5% of patients had a RHC recommended only by ESC/ERS guidelines while 18,0% of patients had a RHC referral according to DETECT algorithm. Moreover 15,4% of patients met ESC/ERS criteria for RHC but had not a referral to echocardiography conforming to DETECT algorithm. Pretty much the same ESC/ERS RHC referral was noticed in patients with a DETECT Step2 score &gt;44. <h3>Conclusions</h3> In our cohort of patients we observed a RHC recommendation concordace between ESC/ERS guidelines and DETECT algoritm in less than two-thirds of patients. In the near future DETECT algorithm validity should be carefully assessed to have unambiguous evidence-based guidelines to identify PAH high-risk SSc patients. <h3>References</h3> Galiè N et al. Eur. Heart J. 2009;30(20):2493–2537. Coghlan JG, et al. Ann Rheum Dis 2013. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.6034
NOTES-Cholecystectomy may be a viable alternative to conventional laparoscopic cholecystectomy: A systematic review and meta-analysis of the published comparative studies
Authors: MS Sajid, N Ladwa, C Leaver, KK Singh, M Sayegh
Journal: Endoscopy (2012)

Objective: The objective of this article was to systematically analyse the published studies comparing the cholecystectomy by national orifice transluminal endoscopic surgery (NOTES-cholecystectomy) versus conventional four port laparoscopic cholecystectomy (CLC).
Ventilation–Perfusion Lung Scan and Helical Computed Tomographic Findings in a Patient with Behçet’s Disease
Authors: MURAT FANI BOZKURT, FIGEN BAŞARAN DEMIRKAZK, SALIH EMRI, BIRAY CANER
Journal: Clinical Nuclear Medicine (2001)

FANI BOZKURT, MURAT M.D.; BAŞARAN DEMIRKAZK, FIGEN M.D.; EMRI, SALIH M.D.; CANER, BIRAY M.D. Author Information
Abstract LB-78: A New Paradigm: the Inflammatory Breast Cancer Research Foundation BioBank
Authors: Carol McWilliams
Journal: Cancer Research (2011)

Abstract The Inflammatory Breast Cancer Research Foundation is a non-profit 501(c) (3) incorporated in 1994, whose mission is to assist scientists and researchers in indentifying the definitive causes of inflammatory breast cancer, and in finding more effective treatments for this highly aggressive form of breast cancer. The organization aims to support research in order to reach an unambiguous definition of inflammatory breast cancer (IBC) and assure that all cases of IBC will be correctly diagnosed, possible sub-types more easily identified, and better treatment outcomes as a result. Research has been hampered by the lack of an easily accessible, well-documented IBC cohort, and IBC cell lines are limited. However, the Inflammatory Breast Cancer Research Foundation has established a BioBank and Clinical Database. The BioBank contains non-tumor DNA, blocks and slides from diagnostic pathology, and medical records describing clinical and pathologic findings at diagnosis providing an invaluable resource. A unique characteristic of this BioBank is the inclusion of specimens and records from deceased patients who had rapid disease progression and resistance to treatment. This data provides valuable comparison for future study. 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 LB-78. doi:10.1158/1538-7445.AM2011-LB-78
Abstract 793: Evolutionary therapy modeling for multidrug resistance: A novel concept of false drug
Authors: Yoonseok Kam, Zayar Khin, Robert A. Gatenby
Journal: Cancer Research (2012)

Abstract The emergence of drug resistance is almost inevitably encountered during systematic cancer therapies resulting in treatment failure and tumor progression. The multidrug resistance (MDR), mediated by xenobiotic metabolism, is among the most well-known and well-studied mechanisms for drug resistance. Although MDR emergence is an evolutionary process, cancer therapies rarely incorporate evolutionary dynamics into their design. Here we present a study to develop a cancer treatment strategy targeting the metabolic cost of MDR and its evolutionary consequence. Through a new therapeutic strategy that reduces the fitness and proliferation of resistant cells by forcing them to use excess energy, we expect to stabilize the tumor volume by maintaining a constant population of sensitive cells and suppressing emergence of resistance. P-glycoprotein (PGP) is the best-known multidrug transporter responsible for MDR and lowers the intracellular drug concentration by an active drug export. A doxorubicin-resistant cell line MCF-7/dox showed significant overexpression of PGP pump when compared to MCF-7/wt, the parental drug-sensitive cell line. We focused on the metabolic energy cost due to the overexpression of the pump protein and its activity which requires about 2 ATP for each molecule of drug extruded. We hypothesized that the cost requires diversion of some resources which are, therefore, not available for proliferation thus reducing the evolutionary fitness of resistant cells. As expected, MCF-7/dox showed higher glycolytic activity and higher glucose demand for the growth and survival compared to the parental cell line MCF-7/wt. Due to the increased glucose consumption, MCF-7/dox appeared to be less competitive in a mixed culture with MCF-7/wt when the glucose resource was limited. We were able to increase the glycolytic activity further by applying other PGP substrates including verapamil at a non-cytotoxic dose. From these results, we propose a novel therapy using a “false drug,” which is not cytotoxic but nevertheless exported by PGP. The expenditure of resources required to extrude the false drug without any survival benefit is expected to further reduce the fitness of the MDR phenotype. When the mixed population was treated with verapamil at a non-lethal dosage, the drug-resistant population was significantly decreased further than when verapamil was not present. 2-deoxy glucose (2-DG), a glycolysis inhibitor, showed synergistic effect with verapamil in further reducing the MCF-7/dox population size. 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 793. doi:1538-7445.AM2012-793
A7
Authors: A. H. Gobuty, E. E. Kim, L. P. Kasi, Pjura G.A. Hilda Aquino, W. N. Floyd, N. K. Allan
Journal: Clinical Nuclear Medicine (1984)

Gobuty, A. H.; Kim, E. E.; Kasi, L. P.; Aquino, Pjura G.A. Hilda; Floyd, W. N.; Allan, N. K. Author Information
Abstract P2-14-07: Predictors of Employment Outcomes in Breast Cancer (BrCa) Patients: An Analysis from E2Z02 (ECOG's SOAPP Study)
Authors: AJ Tevaarwerk, J-w Lee, MC Sesto, CS Cleeland, LI Wagner, VTS Chang, M. Fisch
Journal: Cancer Research (2010)

Abstract Cancer survivors are more likely to be unemployed than healthy counterparts (de Boer et al, JAMA 2009). BrCa patients comprise roughly one-fourth of the survivor population and face challenges in their ability to work. Age and cancer therapy may increase the risk for unemployment (Hassett et al, Cancer 2009). We analyzed data from E2Z02 to examine factors affecting employment in BrCa patients. Methods: E2Z02 prospectively enrolled patients with breast, colon, lung and prostate cancer irrespective of therapy or stage. We limited this analysis to white or black BrCa patients with age at registration ≥65 yrs (those over 65 were excluded as likely to be retired; other minorities were excluded due to small numbers). Patients and oncologists answered the MDASI-ECOG regarding symptoms; additional baseline data regarding disease and treatment were collected. Change in employment was assessed by “Has your employment status changed due to illness?’ [Answer = Yes/No]; and level of employment by “What is your current employment status?” [Answer = full-time; part-time; not in the workforce]. We developed a multivariate logistic regression model for each employment outcome (change in employment, level of employment). Explanatory variables included treatment number (TNs), age (≥45 vs 46-65 yrs), race (white vs black), stage (nonmetastatic vs metastatic), therapy status (off vs on), and ECOG PS (0 vs 1 vs 2-4). TNs were counted as 0 (no medical therapy [MT] or radiotherapy [RT]), 1 (either) or 2 (both). MT encompassed both hormone and chemotherapy. Results: E2Z02 accrued 3123 patients from 3/06 to 5/08 at academic (n=6) and community (n=32) medical oncology clinics (see demographics table); 50% of E2Z02 patients had BrCa. Patients with nonmetastatic BrCa (OR 2.16, 95% CI 1.53-3.05), off therapy (OR 1.79, 95% CI 1.31-2.44), and white race (OR 1.64, 95% CI 1.10-2.46) had a higher chance of remaining employed than their counterparts. Patients with PS 0 were more likely to remain employed compared to patients with PS 1 (OR 1.85 95%CI 1.36-2.5) or PS 2-4 (OR 2.61, 95% CI 1.25-5.44). Age and TNs were not significant. As to the level of employment, nonmetastatic patients (OR=1.60, 95% CI = 1.17-2.21) and patients with better PS (P&amp;lt;0.0001) worked more hours in the workforce than their counterparts. Conclusions: This analysis identifies additional risk factors for employment changes in BrCa patients. Further research is needed to understand the complex relationship between race, other predictors and employment status. These findings could define a group of BrCa survivors at risk for changes in employment outcomes, and potentially allow for targeted interventions. Citation Information: Cancer Res 2010;70(24 Suppl):Abstract nr P2-14-07.
Enrollment in US health insurance exchanges tops seven million
Authors: M. McCarthy
Journal: BMJ (2014)

More than seven million people have enrolled in private health insurance plans through the health insurance exchanges established by the US Affordable Care Act, the White House announced on Tuesday 1 April.

The exchanges, a major component of the 2010 health reform law, were designed as marketplaces where individuals and families could compare and buy private insurance plans with standardized benefits—and find out whether they qualified for free care under Medicaid or tax …
Abstract 4314: A mouse model of cerebral cavernous malformations
Authors: Guili Yang, Huijie Wei, Zhenying Han, Zhisong Zhang, Biyan Duan, Jianning Zhang, Lu-yuan Li
Journal: Cancer Research (2011)

Abstract Cerebral cavernous malformations (CCM) are prevalent cerebral vascular lesions involving aberrant angiogenesis that can lead to hemorrhage, epilepsy, and other neurological manifestations. CCM consists of brittle, proliferating caverns filled with blood and lined with endothelial cells. However, the underlying mechanism of CCM development is poorly understood. The cytokine vascular endothelial cell growth inhibitor (VEGI; TNFSF15; TL1A) is an endogenous negative regulator of angiogenesis produced largely by endothelial cells and exerts a specific inhibitory activity on the proliferation of endothelial cells. We found that the production of VEGI by the endothelium is nearly completely diminished in the CCM tissues. In sharp contrast, the expression of VEGI is readily detectable on the vasculature in nearby brain tissues. On the other hand, angiogenic factors such as vascular endothelial cell growth factor (VEGF) is known to be highly expressed in CCM lesions. We show here that an imbalance of angiogenesis promoters and inhibitors, namely, the down-regulation of VEGI and up-regulation of VEGF, are attributable to the development of CCM. We have constructed a mouse CCM model by implanting mouse endothelial cell line bEnd3 cells in the brain of a female BALB/C mouse. The cavernous blood vessels formed in the model closely resemble those observed in CCM and thus may be used to study the pathology and treatment options of CCM. 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 4314. doi:10.1158/1538-7445.AM2011-4314
The Presence of Alveolar Structures in Breast Tumors is Associated with Drug Resistance Gene Upregulation and Poor Chemotherapy Response
Authors: E.V. Denisov, N.V. Litviakov, M.V. Zavyalova, S.V. Vtorushin, M.M. Tsyganov, T.S. Gerashchenko, E.Y. Garbukov, E.M. Slonimskaya, V.M. Perelmuter, N.V. Cherdyntseva
Journal: Annals of Oncology (2013)
PTH-068 Reducing The Outpatient Burden Of 2 Week Wait Upper Gi Referrals
Authors: S Singh, H Dhaliwal, R Keld
Journal: Gut (2014)

<h3>Introduction</h3> The two week wait (2WW) referral leads to significant burden on outpatient clinics. This delays appointments for patients that may not fit the 2WW criteria. Only 5% of patients referred as 2WW will have an upper GI malignancy and it may not be necessary for all these patients to be reviewed urgently in clinic. Previously at our hospital, most upper GI 2WW referrals were booked an OGD (performed by any available endoscopist) in addition to a clinic appointment on receipt of the referral. In order to streamline the service, in January 2013 patients were triaged to either an OGD or a clinic appointment. The index OGD’s are now done on consultant’s list (Gastroenterologist and Upper GI Surgeon) with a clinical assessment at their OGD appointment. Further management is protocol based and dependant upon the assessment and OGD findings. The aim of this study was to determine if this change in practice is effective and safe. <h3>Methods</h3> Patients referred as a 2WW in January and February 2012 were compared to those referred in January, February, August and September 2013. Only patients triaged directly to OGD were included (77/143 (54%) in 2012 and 180/291 (62%) in 2013). 14 patients were excluded from further analysis due to non-attendance. <h3>Results</h3> Total cancer detection for all referrals was 8% in 2012 and 9% in 2013. In patients selected for a direct OGD referral, 7 upper GI cancers were diagnosed in 2012 and 14 in 2013. After the OGD, 4 (5%) patients in 2012 were immediately discharged back to the GP, compared to 33 (20%) in 2013 (p = 0.003). Of those attending clinic post OGD, 9 patients (13%) were given a routine appointment in 2012 compared to 50 (37%) in 2013 (p = 0.0002). Comparing the two years, there was a 32% reduction in the requirement of urgent outpatient appointments (83% had urgent OPD in 2012 compared to 51% in 2013, p = 0.0001). Of those discharged in 2013, 85% had documentation of the current symptoms at time of OGD and in 94%, treatment advice was provided to the GP. One patient was discharged after an OGD showing grade B oesophagitis and symptom improvement with PPI. Unfortunately, a re-referral 8 weeks later for worsening symptoms found oesophageal cancer on OGD. <h3>Conclusion</h3> The introduction of consultant assessment as a first contact for all OGD 2WW referrals has led to a significant reduction in the requirement of urgent outpatient clinic appointments by one third. Waiting times for all clinic referrals have reduced significantly, amounting to 54% reduction in the number of patients waiting more than 9 weeks for a first appointment. Cancer detection is comparable to the previous model of care. Patients with ongoing symptoms at the time of endoscopy need follow up. In hindsight the missed cancer should have had an oesophageal biopsy, but this is clinical judgement and we do not believe the new service accounted for this delay. <h3>Disclosure of Interest</h3> None Declared.
Tartrate-Resistant Acid Phosphatase Isoform 5B (TRACP 5B) As Serum Marker of Bone Metastases From Non-Small Cell Lung Cancer (NSCLC) and Breast Cancer. Preliminary Results
Authors: F. Lumachi, A. Del Conte, F. Mazza, S.M.M. Basso, G.B. Chiara
Journal: Annals of Oncology (2015)
P5-14-10: Ethnic Differences in the Association between Tumor Size and Lymph Node Status among Breast Cancer Patients in South East Asia.
Authors: N Saxena, HM Verkooijen, Pathy N Bhoo, EL Siew, P Iau, SC Lee, CH Yip, M Hartman
Journal: Cancer Research (2011)

Abstract Background: South East Asia consists of three major ethnic groups, i.e. Chinese, Malays and Indians. Previous work from our breast cancer research group showed that Malay ethnicity is an independent predictor of poor survival. In this study we evaluate whether (part of) these ethnic survival disparities may be due to ethnic differences in the association of tumor size and lymph node involvement. Methods: We included all patients diagnosed with breast cancer at the National University Hospital (Singapore) and University of Malaya Medical Center (Kuala Lumpur) between 1990 and 2007, for whom information on tumor size and axillary lymph node status was available (n = 3805). Ethnic differences in the association between tumor size and lymph node involvement were studied and logistic regression analysis was performed to determine the independent effect of ethnicity on the association of tumor size and lymph node involvement. Results: 1474 patients were categorized as T1 (&amp;gt;0 to 2 cm), 1777 as T2 (2.1 to 5 cm) and 554 as T3 (&amp;gt;5 cm). Within the small tumor size range (&amp;gt;0 to 2 cm) the Malays were significantly more likely to present with node positive disease as compared to the other ethnic groups (36.9% as compared to 24.5% for Chinese and 25.9% for Indians, p value &amp;lt;0.001). Similarly, for tumors measuring 2.1-5 cm, Malays were more likely than Chinese and Indians to have lymph node involvement (59.5%, 50.2% and 52.1%, respectively p value 0.016). After adjustment for age, Progesterone Receptor (PR) status, grade and treatment received, Malay ethnicity was an independent predictor of lymph node involvement, with adjusted Odds Ratio's of 1.4 (95% CI 1.0 to 2.1) for T1 tumors and 1.4 (95% CI 1.1 to 1.9) for T2 tumors compared to Chinese women. Conclusion: Malay patients are more likely to present with lymph node metastasis especially for the small and midsized tumors as compared to the Chinese and Indians. This could reflect differences in tumor biology between the three ethnic groups with the Malays possibly having more aggressive disease than the others. Citation Information: Cancer Res 2011;71(24 Suppl):Abstract nr P5-14-10.
Abstract 5019: Loss of the ETS transcription factor ESE3 induces epithelial-mesenchimal transition and generates cells with stem cell-like properties
Authors: Domenico Albino, Nicole Longoni, Erica Ortelli, Paolo Kunderfranco, Anastasia Malek, Carlo V. Catapano, Giuseppina MR Carbone
Journal: Cancer Research (2010)

Abstract ETS transcription factors have emerged as important elements in the pathogenesis of prostate cancer. Most ETS factors promote cell proliferation, survival and transformation, while few others act as tumor suppressors. We have recently reported that the epithelial-specific ETS factor ESE3 is frequently down-regulated in prostate cancer, affects negatively cell proliferation and survival, and acts as tumor suppressor in prostate epithelial cells. ESE3 signatures extracted from prostate cancer clinical samples indicated a broad dedifferentiation program. Thus, we hypothesized that ESE3 maintains the differentiation state of prostate epithelial cells and that its loss leads to cell transformation. In this study, we report that stable knock-down of ESE3 in immortalized human prostate epithelial LHS cells (LHS-ESE3kd) resulted in the induction of epithelial-mesenchymal transition (EMT) with the acquisition of a fibroblast-like appearance. Concomitantly, LHS-ESE3kd cells acquired also ability to grow in anchorage-independent conditions in soft-agar and to form prostatosheres in sphere-forming assays. Expression of various stem-cell markers was also increased in LHS-ESE3kd compared to LHS cells. In a panel of prostate cell lines the ability to form prostatospheres was inversely correlated with ESE3 expression level, providing further support to the idea that the gene is an important regulator of the stem cell compartment. Consistently, re-expression of ESE3 in DU145 cells, which do not express ESE3, induced morphological changes consistent with a mesenchymal-epithelial transition, reduced the ability of the cells to migrate and to form prostatospheres. Cancer stem cells are reportedly to be drug resistant and drugs like taxol can select for drug-resistant cells with stem cell properties. We observed that resistance to taxol was inversely correlated with ESE3 expression in prostate cell lines. Furthermore, treatment of LHS-ESE3kd cells with taxol increased sphere formation, consistent with an enlargement of the stem-cell compartment by the ESE3 knock-down and increased selection by the drug. Collectively, these findings implicate that ESE3 controls the differentiation state and stem cell properties of prostate epithelial cells and that loss of ESE3 can be an important event in prostate tumorigenesis. 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 5019.