tbuckley/cabot-search huggingface dataset:
Abstract 4242: A humanized tumor mouse model to characterize the interaction of human disseminated cancer cells with the human immune system
Authors: Melanie Werner-Klein
Journal: Cancer Research (2012)

Abstract Most primary cancers can be surgically removed, but many patients will die from metastatic disease months to years after initial therapy. Adjuvant therapies are increasingly tailored to exploit characteristics of the primary tumor however they usually improve the survival of less than 10% of breast cancer patients. It has been recently shown that dissemination is an early event and that disseminated cancer cells (DCC) differ genetically from the primary tumor. Therefore a model is needed which i) provides a human, autologous immune system and ii) allows the expansion of DCC, which belong to the rarest cells in the human body (1-2 cells per 106 bone marrow cells in positive patients), in order to investigate the interaction of these particular cell populations. Here we show that a humanized tumor mouse model can be established using hematopoietic stem cells (HSC) and DCC isolated from diagnostic BM-aspirates of melanoma and mammary carcinoma patients. Bone marrow samples are obtained prior to tumor resection. HSC are purified and engrafted by intra-femoral injection into NOD-scidIL2Rg-/- (NSG) mice and show long-term reconstitution (&amp;gt;24 weeks) of lymphoid and myeloid lineages, also upon serial transplantation. DCC enriched from diagnostic BM-aspirates or lymph node samples can be transplanted and are able to establish tumors in NSG mice, even at low cell numbers (&amp;lt;10 cells) in 50 to 70% of DCC-containing samples. Since human melanoma and mammary carcinomas are, in later stages, characterized by wide-spread metastasis, involving bone, lung and liver, we currently focus on whether and how the humanized immune system enables the systemic cancer spread of DCC derived tumors. 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 4242. doi:1538-7445.AM2012-4242
INSULIN COMA THERAPY
Authors: JOSEPH E. LIFSCHUTZ
Journal: American Journal of Psychiatry (1954)

Insulin coma therapy has been used at this hospital since October 1951. Up to June, 1954, 89 patients had received a full course of therapy. A very closely matched group of control patients was obtained, with following conclusions: 1. The insulin coma group showed essentially the same number of improved patients as the control group. Figures for the control group were actually slightly better. 2. The results in the group diagnosed catatonic schizophrenia were much better for the control group than for the insulin treated group. There was no difference in the other diagnostic categories. 3. Where EST was used it was at least as effective as insulin coma therapy. 4. Insulin does not increase the rate of improvement in patients diagnosed either acutely or chronically ill. 5. Although more severely ill patients are given insulin coma therapy, their improvement rate is the same as the control group. It is our conclusion that the insulin coma therapy has been of little value in itself in the improvement of patients who have had it. We would venture to state that the results we have obtained, which only equal the results of a very similar group not getting insulin, were due to somatic and psychotherapeutic efforts simulataneous with the insulin coma therapy. Psychiatric hospitalization averaged 3 months longer per patient in the insulin group. Our conclusions do not warrant this excess period in the hospital.
SEX DIFFERENCES IN ANTITHROMBOTIC THERAPY: OBSERVATIONS FROM THE GLORIA-AF REGISTRY PROGRAM
Authors: Christine Teutsch, Gregory Y.H. Lip, Hans-Christoph Diener, Sergio Dubner, Jonathan Halperin, Changsheng Ma, Kenneth Rothman, Nils Schoof, Amelie Elsaesser, Menno Huisman
Journal: Journal of the American College of Cardiology (2016)
STATEWIDE INITIATIVES IMPROVE THE CARE AND OUTCOMES OF PATIENTS WITH OUT-OF-HOSPITAL CARDIAC ARREST AT HOME AND IN PUBLIC LOCATIONS: RESULTS FROM THE HEARTRESCUE PROJECT
Authors: Christopher B. Fordyce, Carolina M. Hansen, Kristian Kragholm, James G. Jollis, Mayme L. Roettig, Matthew E. Dupre, Lance B. Becker, Claire C. Corbett, Lisa Monk, R. Darrell Nelson, David A. Pearson, Clark Tyson, Sean Van Diepen, Monique L. Anderson, Bryan McNally, Christopher B. Granger
Journal: Journal of the American College of Cardiology (2016)
Abstract LB-334: Imaging caspase dependent cell death as a surrogate for efficacy of cancer therapeutics
Authors: Stefanie Galbán, Michael Lafferty, Lisa M. Sharkey, Katrina A. Schinske, Rahim F. Merchant, Brian D. Ross, A Rehemtulla
Journal: Cancer Research (2011)

Abstract Induction of cell death in malignant lesions still represents the major goal in the treatment of cancer patients. Imaging of apoptosis would enhance the development of optimal dosing, schedule and combination therapies. Here we used a luciferase biosensor (Promega) and developed a bioluminescent assay system with optimized signal to noise for the detection of cell death in vitro and in living animals. Using D54-MG cells stably expressing the reporter, we demonstrate that TRAIL treatment resulted in a 100–200 fold induction of bioluminescence activity which correlated with cell death as demonstrated by increased cleavage of Caspase-3. Furthermore inhibition of apoptosis using the pan caspase inhibitor Z-VAD-FMK resulted in inhibition of reporter activity. The utility of this cell death reporter was further demonstrated in human glioma xenografted tumors wherein induction of apoptosis was correlated with reporter activation. The high signal to noise and dynamic range of reporter activity provides for a sensitive and quantitative surrogate for evaluation of experimental therapeutics. In addition, the ability to image repeatedly provides a unique opportunity to understand the dynamics of cell death in response to specific drugs or combination therapies. We are also investigating the application of this technology in a high throughput screening of compound and targeted siRNA libraries in diverse cells and in pre-clinical cancer mouse models. 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-334. doi:10.1158/1538-7445.AM2011-LB-334
AB0935 Metabolic syndrome in PSA patients is not associated with disease activity:
Authors: J. Stolfa
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Metabolic syndrome (MetS) is regarded as one of the extraarticular manifestations of psoriasis (Pso) and psoriatic arthritis (PsA). Its etiology is as yet not well understood. The major component of MetS is insulin resistance, which is, among others associated with chronic inflammation [1]. So we put a question, if chronic inflammation in active PsA could contribute to the development of the MetS. <h3>Objectives</h3> To ascertain if the occurrence of MetS is associated with higher clinical or humoral activity of the disease. <h3>Methods</h3> 103 consecutive patients with PsA were followed for two years and their clinical activity was assessed clinically using ``disease activity index in PsA``(DAPsA) [2] and humoral activity through C-reactive protein (CRP) twice a year for 2 – 4 years. The parameters of MetS were checked once a year. So we had 4 – 6 controls available. The pats were dividend in two groups: those with MetS (MetS+) and without MetS (MetS-). Then the average values of DAPsA and CRP in both groups were calculated and compared. <h3>Results</h3> The average values of DAPsA, as well as CRP did not differ substantially in both groups - see table 1. <h3>Conclusions</h3> On the basis of this study we cannot confirm the association of the activity of PsA as assessed clinically or using laboratory parameter (CRP).The drawback of this small, preliminary study is that it did not take into account the severity of psoriasis and the pharmacotherapy. <h3>References</h3> Boehncke WH, Buerger C, Boehncke S. Co-morbidities in psoriasis vulgaris. Hautarzt 2009; 60:116-21 Schoels M, Aletaha D, Funovits J, et al. Application of the DAREA/DAPSA score for assessment of disease activity in psoriatic arthritis. Ann Rheum Dis 2010;69:1441-1447 <h3>Disclosure of Interest</h3> J. Stolfa Grant/Research support from: Supported by Ministery of Health of Czech Republic Grant Number 000 000 23728
LP48 : SVR12 results after 12-weeks boceprevir, peginterferon and ribavirin in the dutch acute hepatitis C in HIV study (DAHHs)
Authors: S. Hullegie, M. Claassen, G. van den Berk, J. van der Meer, D. Posthouwer, F. Lauw, J. Arends, P. Koopmans, C. Richter, A. van Eeden, W. Bierman, E. Leyten, B. Rijnders
Journal: Journal of Hepatology (2015)
Abstract 3029: Biochemical evidence towards the existence of an oncogenic Hsp90 complex
Authors: Anna Rodina, Kamalika Moulick, James Ahn, Hongliang Zong, Leandro Cerchietti, Erica Gomes DaGama, Eloisi Caldas-Lopes, Kristin Beebe, Fabiana Perna, Katerina Hatzi, Ly Vu, Xinyang Zhao, Danuta Zatorska, Tony Taldone, Peter Smith-Jones, Mary Alpaugh, Steven Gross, Nagavarakishore Pillarsetty, Thomas Ku, Jason Lewis, Steven Larson, Ross Levine, Hediye Erdjument-Bromage, Monica Guzman, Stephen Nimer, Ari Melnick, Len Neckers, Gabriela Chiosis
Journal: Cancer Research (2012)

Abstract To maintain homeostasis, cells employ intricate molecular machineries comprised of thousands of proteins programmed to execute well-defined functions. Dysregulation of these pathways, through protein mis-expression or mutation, provides biological advantages that confer the malignant phenotype. At the molecular level, this requires cells to invest energy in maintaining the stability and function of these proteins, and for this reason cancer cells co-opt molecular chaperones, including Hsp90. Hsp90 is recognized to play important roles in maintaining the transformed phenotype - the chaperone and its associated co-chaperones assist in the correct folding of cellular proteins, collectively referred to as “client proteins,” many of which are effectors of signal transduction pathways controlling cell growth, differentiation, the DNA damage response, and cell survival. Tumor cell addiction to these proteins (i.e. through mutations, aberrant expression, improper cellular translocation, etc) thus makes them critically reliant on Hsp90. While Hsp90 is expressed in all cells and tissues, it was shown that tumors preferentially contain Hsp90 that is in a higher order multi-chaperone complex with high affinity for certain Hsp90 inhibitors, while normal tissues harbor a latent, uncomplexed Hsp90 that has low affinity for these inhibitors. We here extend this model and propose that Hsp90 forms biochemically distinct complexes in cancer cells. In this view, a major fraction of cancer cell Hsp90 retains “house keeping” chaperone functions similar to normal cells, whereas a functionally distinct Hsp90 pool enriched or expanded in cancer cells specifically interacts with oncogenic proteins required to maintain tumor cell survival. Perhaps this Hsp90 fraction represents a cell stress specific form of chaperone complex that is expanded and constitutively maintained in the tumor cell context. Our data suggest that it may execute functions necessary to maintain the malignant phenotype. One such role is to regulate the folding of mutated (i.e. mB-Raf) or chimeric proteins (i.e. Bcr-Abl). We here also present experimental evidence for an additional role; that is, to facilitate scaffolding and complex formation of molecules involved in aberrantly activated signaling complexes. 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 3029. doi:1538-7445.AM2012-3029
Abstract P2-09-22: Predictive Significance of the Proportion of ER-or PgR-Positive Tumor Cells in Neoadjuvant Chemotherapy for Operable HER2-Negative Breast Cancer
Authors: T Osako, R Nishimura, Y Okumura, M Hayashi, N. Arima
Journal: Cancer Research (2010)

Abstract Background Estrogen receptor (ER) and progesterone receptor (PgR) status are predictive for clinical and pathological response in neoadjuvant chemotherapy for operable breast cancer. However, it remains unclear how the proportion of ER-or PgR-positive staining tumor cells affect responses to neoadjuvant chemotherapy. The purpose of this study was to examine the correlation of the proportion of ER-or PgR-positive staining tumor cells with the clinical and pathological responses to neoadjuvant chemotherapy for operable HER2-negative breast cancer. Patients and Methods From April 2002 to May 2010, 101 patients received neoadjuvant chemotherapy containing epirubicin and taxane in our clinic. We assessed menopausal status, tumor size, lymph node status, histological grade, ER, PgR, p53 and Ki-67. In this study, we defined the positivity of ER and PgR as more than or equal to 1% of the positive staining tumor cells according to ASCO/CAP announcement in April 2010. Furthermore, patients with ER-positive tumor were divided into two groups at 30% of ER positive staining tumor cells. Results A clinical response was seen in 82% of all patients and a pathological complete response (pCR) was seen in 17%. Of the 101 patients, 60 (59%) had ER-positive tumors and 38 (63%) of the patients had tumors with more than 90% of ER-positive staining cells. Also, 52 (51%) had PgR-positive tumors. Fourteen (34%) of the 41 patients with ER-negative tumors achieved a pCR and 15 (31%) of the 49 patients with PgR-negative tumors achieved a pCR. Patients with more than 30% of ER-or more than 1% of PgR-positive staining tumor cells did not achieve a pCR. There was no significant correlation of pCR with menopausal status, tumor size, grade and Ki-67. In univariate analysis, a pCR was associated with ER status (p=0.0001), PgR status (p=0.0001), and chemotherapy regimens (p=0.014). Multivariate analysis revealed that ER status was a significant factor for pCR, and patients with ER-negative tumors were 20.1 times more likely to achieve a pCR than those with more than or equal to 30% tumors staining tumor cells (p=0.005; 95% confidential interval, 2.5-16.5). Conclusion We demonstrated a predictive significance of the proportion of ER-or PgR-positive tumor cells in neoadjuvant chemotherapy for operable HER2- negative breast cancer. ER-negativity (&amp;lt;1%) is significantly predictive to achieve a pCR in multivariate analysis. Conversely, it seems very possible that patients with more than 30% ER-or more than 1% PgR-positive staining tumor cells do not achieve a pCR. It is important to take the proportion of ER-and PgR-positive staining tumor cells into consideration in the treatment of breast cancer. Citation Information: Cancer Res 2010;70(24 Suppl):Abstract nr P2-09-22.
Abstract 4962: Assessing serum miRNA as putative biomarkers for serous epithelial ovarian cancer
Authors: Casina W. Kan, Michael A. Hahn, Deborah J. Marsh, Viive M. Howell
Journal: Cancer Research (2011)

Abstract Serous epithelial ovarian cancer (EOC) is the most lethal gynecological malignancy; due in part to vague and non-specific symptoms resulting in delayed diagnosis. The biomarker in routine clinical use for EOC is CA-125, with the OVA1 test (Quest Diagnostics) recently available to aid in predicting the likelihood that an ovarian mass is malignant. Current diagnostic tests have limitations which may be improved by expansion of biomarker panels. MicroRNAs (miRNAs) are a class of small non-coding RNA molecules that regulate important cellular processes. They exhibit distinct expression profiles in cancers and have recently been discovered in serum and other body fluids. Tumor miRNAs may be shed into the circulation, raising the possibility of their use as serum biomarkers for the detection of EOC. Exiqon LNA miRNA microarrays were performed using RNA from cell line models of serous EOC. Over-expressed miRNAs were selected as candidates for assessment in serum. These were measured in RNA extracted from serum of patients with serous EOC (n=30) and healthy age-matched volunteers (n=30) by quantitative reverse-transcription polymerase chain reaction (qRT-PCR). As there are currently no routine methods for the normalization of miRNA in serum, a group of highly and uniformly expressed miRNAs with no reported involvement in cancer was selected for assessment as endogenous controls. Five miRNAs, miR-182, miR-96 and miR-200a, miR-200b and miR-200c were identified as highly expressed in a panel of serous EOC cell lines consistent with previous reports, and therefore selected for investigation as putative serous EOC biomarkers. In addition, miR-92a, miR-103, miR-638 and RNU48 were selected as candidate endogenous controls given that they were consistently expressed at high levels in the cell line panel. qRT-PCR data will be presented on the expression of these 8 candidate miRNAs and RNU48 either with or without pre-amplification of target sequence. In conclusion, miR-92a, miR-103 and miR-638 were observed to show little variation between patients and healthy volunteer serum. These results identify the potential for these miRNAs to be used as endogenous controls for the expression of miRNA in serum. Reliable detection of specific miRNAs in serum from women with serous EOC may improve the detection of this malignancy. 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 4962. doi:10.1158/1538-7445.AM2011-4962
Hydatid Cyst of the Interventricular Septum
Authors: M O Demirkol, N Kurtoğlu, C Keleş, M Sişmanoğlu, F Turan
Journal: Clinical Nuclear Medicine (2001)

ONUR DEMIRKOL, MEHMET M.D.,*; KURTOĞLU, NURI M.D.,†; KELEŞ, CÜNEYT M.D.,‡; ŞIŞMANOĞLU, MESUT M.D.‡; TURAN, FIKRET M.D.† Author Information
FRI0312 Biological Therapy Survival Rate in A Canadian Cohort of Rheumatoid Arthritis Patients
Authors: E. Rioux, M.-J. Rioux, I. Fortin
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> In recent years, major advance has been made in the treatment of rheumatoid arthritis (RA). The efficacy of tumor necrosis factor-α (TNF-α) inhibitor has been demonstrated in different controlled clinical trials and observational studies. However, some patients have inadequate response to TNF-α inhibitors and may switch to an alternative treatment from a different class of drugs, such as abatacept (ABA), tocilizumab (TCZ) and rituximab (RTX). ABA, TCZ and RTX are indicated for use after inadequate response to traditional disease-modifying antirheumatic drugs (DMARD) or TNF-α inhibitors for the treatment of RA. <h3>Objectives</h3> The objective of this study was to assess in Canadian clinical practice the survival rate in patients with RA treated with a TNF-α inhibitor such as etanercept (ETN) and adalimumab (ADA) and alternative treatments such as ABA, TCZ and RTX. <h3>Methods</h3> Charts of all RA patients taking ETN, ADA, ABA, TCZ and RTX at the Centre de Rhumatologie de l9Est du Québec were reviewed and detailed data including 28-joint disease activity score (DAS28-ESR), start and end date and motive for discontinuation were recorded. Survival estimation was explored using Kaplan-Meier analysis and the log rank test was used to check for differences between the Kaplan-Meier curves using the statistical software R. <h3>Results</h3> A total of 474 RA patients starting treatment with ETN, ADA, ABA, TCZ or RTX were enrolled in this study. 158 patients were on ETN, 128 patients were on ADA, 73 patients were on ABA, 54 patients were on TCZ and 61 patients were on RTX therapies. Overall, DAS28-ESR decreased from 4.37 at baseline to 2.80 at month 24 for ETN, from 4.37 to 2.98 for ADA, from 4.58 to 4.06 for ABA, from 5.31 to 3.24 for TCZ and from 4.65 to 2.97 for RTX. After 24 months, using Kaplan-Meier curves plotted for all treatments, 56% of patients are still on ETN, 39% of patients are still on ADA, 38% of patients are still on ABA, 55% of patients are still on TCZ and 67% of patients are still on RTX. However, for biologic-naïve patients, 57% of patients are still on ETN, 48% of patients are still on ADA, 63% of patients are still on ABA, 73% of patients are still on TCZ and 100% of patients are still on RTX (n=2) at month 24. Statistical tests of comparison between treatment revealed significant differences (log-rank: p=0.000125). <h3>Conclusions</h3> The present study suggests that the survival rate for biologic-naïve patients is higher than on patients who failed to respond to their previous biologic. It also suggests that RTX has a better survival rate than ETN, ADA, ABA and TCZ in second line treatment. Also, ADA, ABA and TCZ has better profile when used as a first-line agent. <h3>References</h3> Girolomoni et al., 2012, Karlsson et al., 2008, Hublein et al., 2012, Strand et al., 2013 <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.3681
Endoscopic snare polypectomy of a pedunculated adenocarcinoma of the duodenal bulb arising from a hyperplastic polyp
Authors: J. Gerada, D. Babic, J. Degaetano, J. Pocock
Journal: Endoscopy (2012)

Primary non-ampullary adenocarcinoma of the duodenum is a rare occurrence, arising mainly from adenomatous polyps [1]. We report the first case of a pedunculated adenocarcinoma of the duodenal bulb, arising from a hyperplastic polyp, treated with endoscopic snare polypectomy.