tbuckley/cabot-search huggingface dataset:
Structure and expression of TMPRSS2-ERG splice variants in prostate cancer
Authors: Ying Hu, Albert Dobi, Taduru Sreenath, Christopher Cook, Atekelt Tadase, Lakshmi Ravindranath, Jennifer Cullen, Bungo Furusato, Yongmei Chen, Rajesh Thangapazham, Ahmed Mohamed, Chen Sun, Isabell Sesterhenn, David McLeod, Gyorgy Petrovics, Shiv Srivastava
Journal: Clinical Cancer Research (2008)

A44    Purpose:  The expression of the ETS-related gene (ERG) is low or undetectable in benign prostate epithelial cells. High prevalence of ERG overexpression in prostate cancer cells due to TMPRSS2-ERG fusions suggest causal roles of ERG protein in the neoplastic process. TMPRSS2-ERG fusion junctions have been extensively studied in prostate cancer. However, virtually nothing is known about the nature of full-length transcripts and encoded proteins. This study focuses on qualitative and quantitative features of full-length TMPRSS2-ERG transcripts in prostate cancer.   Experimental Design : Full-length TMPRSS2-ERG transcripts were cloned and sequenced from a cDNA library generated from pooled RNA of sixTMPRSS2-ERG fusion positive prostate tumors.The encoded ERG proteins were analyzed in HEK293 cells. Copy numbers of TMPRSS2-ERG splice variants were determined by quantitative reverse transcription-PCR in laser capture microdissected prostate cancer cells.   Results:  Two types ofTMPRSS2-ERG cDNAs were identified: type I, which encodes full-length prototypical ERG protein (ERG1, ERG2, ERG3), and type II, encoding truncated ERG proteins lacking the ETS domain (ERG8 and a new variant,TEPC). In microdissected prostate tumor cells from122 patients, relative abundance of these variants was in the following order: ERG8 > TEPC > ERG 3 > ERG1/2 with combined overexpression rate of 62.3% in prostate cancer. Increased ratio of type I over type II splice forms showed a trend of correlation with less favorable pathology and outcome.   Conclusions:  Qualitative and quantitative features of specific ERG splice variants defined herepromise to enhance the utility of ERG as a biomarker and therapeutic target in prostate cancer
Differential Diagnosis of Common Complaints.
Authors: Robert H. Seller
Journal: Annals of Internal Medicine (1986)

* Abdominal Pain in Adults * Abdominal Pain in Children * Backache * Belching, Bloating, and Flatulence * Breast Lumps * Chest Pain * Colds, Flu and Stuffy Nose * Constipation * Cough * Diarrhea * Dizziness/Lightheadedness and Vertigo * Earache * Facial Pain * Fatigue * Fever * Forgetfulness * Headache * Heartburn, Indigestion, and Dyspepsia * Insomnia * Menstrual Irregularities * Menstrual Pain * Nausea and/or Vomiting Without Abdominal Pain * Pain in the Foot * Pain in the Lower Extremity in Adults * Pain in the Lower Extremity and Limping in Children * Pain in the Upper Extremity * Palpations * Shortness of Breath * Skin Problems * Sore Throat * Swelling of the Legs * Urethral discharge and Dysuria * Vaginal Discharge and Itching * Vision Problems and Other Common Eye Problems * Voiding Disorders and Incontinence * Weight Gain and Weight Loss
Abstract 1923: NF-κB signaling supports a sub-population of ovarian cancer tumor-initiating cells
Authors: Carrie D. House, Christina M. Annunziata
Journal: Cancer Research (2014)

Abstract Although most patients respond favorably to first-line chemotherapy, ovarian cancer remains the most lethal gynecological cancer in the United States primarily because of a high incidence of disease recurrence. The inability of traditional chemotherapy to eradicate tumor-initiating cells (TICs) is a plausible explanation for tumor relapse and we have begun to characterize TIC populations in ovarian cancer cell lines. Importantly, we are investigating the role of the NF-κB pathway in regulating this system. We have identified conditions that sustain a highly tumorigenic TIC population. Preliminary data suggest that NF-κB promotes and sustains TICs in ovarian cancer and current efforts are underway to characterize the molecular mechanisms underlying this preference. We will correlate activity of this pathway with expression of ovarian TIC protein markers such as CD133, Sox2, Nanog, and Oct-4 in TIC cell cultures and xenografts. Moreover we will use TICs to investigate effects of inhibiting this pathway on marker expression, proliferation, resistance to chemotherapy, and the ability to form tumors in mice. Clarifying the specific role of the NF-κB network in TIC populations will further our understanding of ovarian cancer initiation, progression, and relapse and may lead to improved therapeutic strategies for women in first remission, to prevent subsequent relapse to incurable disease. Citation Format: Carrie D. House, Christina M. Annunziata. NF-κB signaling supports a sub-population of ovarian cancer tumor-initiating cells. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 1923. doi:10.1158/1538-7445.AM2014-1923
Pregnancy Is a Risk Factor for Pancreatitis After Endoscopic Retrograde Cholangiopancreatography in a National Cohort Study
Authors: Sumant Inamdar, Tyler M. Berzin, Divyesh V. Sejpal, Douglas K. Pleskow, Ram Chuttani, Mandeep S. Sawhney, Arvind J. Trindade
Journal: Clinical Gastroenterology and Hepatology (2015)
Effect of Alpha-Peltatin, Beta-Peltatin, and Podophyllotoxin on Lymphomas and Other Transplanted Tumors&lt;xref ref-type="fn" rid="fn1"&gt;&lt;sup&gt;2&lt;/sup&gt;&lt;/xref&gt;
Authors: Ezra M. Greenspan, J. Leiter, M. J. Shear
Journal: JNCI Journal of the National Cancer Institute (1950)

Effect of Alpha-Peltatin, Beta-Peltatin, and Podophyllotoxin on Lymphomas and Other Transplanted Tumors Get access Ezra M. Greenspan, Ezra M. Greenspan Search for other works by this author on: Oxford Academic PubMed Google Scholar J. Leiter, J. Leiter Search for other works by this author on: Oxford Academic PubMed Google Scholar M. J. Shear M. J. Shear Chemotherapy Section, National Cancer Institute, National Institutes of Health, Public Health Service, Bethesda, Md. Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 10, Issue 6, June 1950, Pages 1295–1333, https://doi.org/10.1093/jnci/10.6.1295 Published: 01 June 1950 Article history Received: 13 April 1950 Published: 01 June 1950
ACCF/AHA/CDC Conference Report on Emerging Infectious Diseases and Biological Terrorism Threats⁎⁎The findings and conclusions in this report are those of the Conference participants and do not necessarily reflect the official position of the American College of Cardiology Foundation, the American Heart Association, and the Centers for Disease Control and Prevention
Authors: George A. Mensah, Augustus O. Grant, Carl J. Pepine, Larry M. Baddour, Leslie T. Cooper, Sandra B. Dunbar, Erika S. Froelicher, Kurt J. Greenlund, Edward L. Kaplan, Robert A. Kloner, Darwin R. Labarthe, Russell V. Luepker, Mohammad Madjid, James E. Muller, Siobhán O’Connor, Joseph P. Ornato, Rose Marie Robertson, Michael J. Roy, Prediman K. Shah, Kathryn A. Taubert, Walter R. Wilson, Zhi-Jie Zheng, Robert A. Harrington, Jonathan Abrams, Jeffrey L. Anderson, Eric R. Bates, Mark J. Eisenberg, Cindy L. Grines, Mark A. Hlatky, Robert C. Lichtenberg, Jonathan R. Lindner, Gerald M. Pohost, Richard S. Schofield, Samuel J. Shubrooks, James H. Stein, Cynthia M. Tracy, Robert A. Vogel, Deborah J. Wesley
Journal: Journal of the American College of Cardiology (2007)
Abstract 19462: N-terminal Region of Cardiac Myosin Binding Protein-C is Proinflammatory Following Myocardial Infarction
Authors: Thomas L Lynch, Christoph Liebetrau, Lukas Pyttel, Christian Troidl, Sakthivel Sadayappan
Journal: Circulation (2014)

Introduction:  Myocardial infarction (MI) promotes inflammation within the heart through the recruitment and activation of innate and adaptive cells of the immune system, contributing to the development of dilated cardiomyopathy (DCM). Cardiac myosin binding protein-C (cMyBP-C), a regulatory protein of the cardiac sarcomere, is highly degraded following MI releasing a predominant N-terminal 40kDa fragment (C0C1f) into the local heart tissue and systemic circulation. However, whether released cMyBP-C promotes proinflammatory cytokine expression and/or autoantibody (AAb) production leading to myocardial inflammation in MI patients has not been studied.   Hypothesis:  C0C1f-targeted AAbs are produced in MI patients and that C0C1f causes proinflammatory immune cell activation.   Methods and Results:  We performed indirect ELISA using sera from 631 MI patients upon arrival to the emergency department and 139 control individuals to elucidate whether C0C1f is immunogenic leading to AAb production in MI patients. AAbs targeted to C0C1f were identified in 28 MI patients by ELISA, which was confirmed by Western blot analysis. Competitive ELISA demonstrated that these AAbs were specifically targeted to C0C1f. To determine whether C0C1f leads to activation of immune cells, bone marrow derived mouse monocytes were cultured with different N-terminal regions of cMyBP-C for 3, 6, 9, and 24 hrs. After 6 hrs of incubation, recombinant mouse C0C1f produced marked elevation in the inflammatory markers TNFα, proIL1b, IL1b, and IL6 and in the adhesion markers VCAM and ICAM in mouse monocytes. After 24 hrs of incubation with C0C1f, the levels of the anti-inflammatory marker Mrc1 were noticeably reduced in mouse monocytes. Similar results were obtained using human bone marrow-derived monocytes cultured with human C0C1f.   Conclusions:  These results implicate the C0C1f fragment of cMyBP-C as proinflammatory leading to activation of innate and adaptive immune responses that may contribute to myocardial inflammation following MI.
Abstract 16853: Going Beyond Patient Satisfaction: Unmet Psychosocial Needs Following Coronary Revascularization
Authors: Matthew Manierre, Daniel J Elliott, Claudine T Jurkovitz, William S Weintraub, Steven S Martin
Journal: Circulation (2014)

Background: Hospitals routinely employ measures of patient satisfaction to understand if patient needs are being met, but they rarely look beyond patient discharge and general satisfaction. This study’s objective was to assess both satisfaction and problems that may be faced by patients after discharge from a large east coast hospital following percutaneous coronary intervention or coronary artery bypass graft. Methods: Permission was gained from almost all patients to be contacted by phone after discharge. University researchers called them 90 days after discharge to gauge both their satisfaction with post-discharge care and any problems they may have experienced. Results: A total of 365 patients accepted to participate for a response rate of 42.1%. Surveys were administered on average 134 days after discharge (SD=22.7). While the three measures of patient satisfaction used found that 95% of the patients were satisfied or very satisfied with post discharge care, many patients still reported substantial difficulties since they were discharged. In particular, 28% had problems feeling depressed or stressed, 21% reported having difficulty paying for healthcare related expenses, and 32% had difficulty keeping up with diet or exercise plans. Open ended probes expanded on the first two problems. In the case of depression and stress, many respondents struggled to acclimate to reduced autonomy and mobility. Some of these patients described substantial social strain induced by feelings of isolation and inability to meet caregiving duties for other ill family members. Financial strains were often serious, sometimes resulting in struggles with the stress of debt collectors, being unable to afford medications, and missing bills. Even more important is the finding that, in spite of the widespread prevalence of these three problems, only 53% of respondents with these problems ever reported them to someone at the hospital or the post discharge care team, and only 58% of those reported being helped. Conclusion: These results suggest that a high number of potentially fixable issues may be going unassisted. Even patients expressing high satisfaction are still frequently subject to a wide array of psychosocial stressors that can influence the recovery process.
Abstract 2676: Inhibition of bmp signaling suppresses metastasis in mammary cancer
Authors: Philip Owens, Michael W. Pickup, Sergey V. Novitskiy, Jennifer M. Giltnane, Agnes E. Gorska, Corey R. Hopkins, Charles C. Hong, Harold L. Moses
Journal: Cancer Research (2014)

Abstract Bone Morphogenetic Proteins (BMPs) are secreted cytokines/growth factors that play differing roles in cancer. BMPs are overexpressed in human breast cancers, but loss of BMP signaling in mammary carcinomas can accelerate metastasis. We show that human breast cancers display active BMP signaling, which is rarely downregulated or homozygously deleted. We hypothesized that systemic inhibition of BMP signaling in both the tumor and the surrounding microenvironment could prevent tumor progression and metastasis. To test this hypothesis, we used DMH1, a BMP antagonist in MMTV.PyVmT expressing mice. Treatment with DMH1 reduced lung metastasis and the tumors were less proliferative and more apoptotic. In the surrounding tumor microenvironment, treatment with DMH1 altered fibroblasts, lymphatic vessels and macrophages to be less tumor promoting. These results indicate that inhibition of BMP signaling may successfully target both the tumor and the surrounding microenvironment to reduce tumor burden and metastasis. Citation Format: Philip Owens, Michael W. Pickup, Sergey V. Novitskiy, Jennifer M. Giltnane, Agnes E. Gorska, Corey R. Hopkins, Charles C. Hong, Harold L. Moses. Inhibition of bmp signaling suppresses metastasis in mammary cancer. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 2676. doi:10.1158/1538-7445.AM2014-2676
Abstract 16451: Dose-Escalation Study Using Novel Continuous Flow Intracoronary Delivery of Allogeneic Cardiosphere-Derived Stem Cells: Is There a Threshold for Cell Therapy?
Authors: Eleni Tseliou, James Dawkins, Rpmain Gallet, Michelle Kreke, Rachel Smith, Ryan Middleton, Jackelyn Valle, Eugenio Cingolani, Saibal Kar, Linda Marbán, Rajendra Makkar, Eduardo Marbán
Journal: Circulation (2014)

BACKGROUND: Intracoronary (IC) infusion of cardiosphere-derived stem cells (CDCs) under stop-flow conditions has proven efficacious in producing myocardial regeneration in preclinical and clinical studies. However, the minimally-effective dose is not known, nor is it clear whether benefit is straightforwardly dependent on CDC dose. OBJECTIVE: To determine the dose-efficacy relationship of allogeneic CDCs in a large-animal chronic myocardial infarction (MI) model. METHODS: Escalating doses of allogeneic CDCs (3.125M, 6.25M, 12.5M, 25M; or vehicle as a control) were infused into the left anterior descending coronary artery using a nonocclusive guiding catheter in an anterior chronic MI minipig model. Magnetic resonance imaging (MRI) was used to assess structural and functional endpoints. RESULTS: CDCs were infused in a total of 25 animals under continuous flow at a rate of 1.25M CDCs/min. An additional 5 control animals underwent continuous flow of vehicle over 10 min. No animals experienced adverse events during or after the infusions. One month post therapy, ejection fraction (EF) was preserved at doses of 6.25M, 12.5M and 25M, but not with 3.125 M allo-CDCs or control (ΔEF = -6.7±0.9% in the placebo, -5.1±1.8% in 3.125M, -1.4±0.6% in the 6.25M, -2±1.4% in the 12.5M and -2.3±1.2% in the 25M group; p=0.04 by one way ANOVA for treatment effect). All doses of CDCs (except 3.125M) led to equivalent scar mass reductions, as assessed by MRI with Gd enhancement (p=0.0037 treated vs placebo, one-way ANOVA). Provocative electrophysiology testing at the end of the study revealed no enhanced arrythmogenic potential after cell therapy. CONCLUSIONS: Allogeneic CDCs can be safely administered with a non-occlusive method, over a wide dosage range. All doses &gt;3.125M lead to enhanced preservation of left ventricular function and tissue remodeling, but to similar degrees. Our data reveal that CDCs work by a “threshold” effect that does not obey classical drug-receptor kinetics. This finding is consistent with the extraordinary ability of seemingly-homeopathic doses to exert large, lasting benefits.
Abstract 18572: Sleep Duration is Associated with Degree of Insulin Resistance in a High Risk Population: the Baptist Employee Healthy Heart Study
Authors: Shozab S Ali, Ebenezer Oni, Ehimen C Aneni, Lara Roberson, Janisse Post, Gagandeep Nagi, Sameer Shaharyar, Omar Jamal, Rehan Malik, Muhammad Aziz, Adnan Younus, Beatriz Rosell, Henry Guzman, Ricardo Cury, Jonathan Fialkow, Arthur S Agatston, Emir Veledar, Theodore Feldman, Khurram Nasir
Journal: Circulation (2014)

Introduction: Metabolic syndrome, the clustering of multiple cardiovascular risk factors, is established as a risk factor for CVD. Shorter or longer sleep duration has been reported to be associated with increased risk of metabolic syndrome (MS) and diabetes mellitus (DM) through increased insulin resistance (IR). However, it is not known if impaired sleep alters IR in a high-risk population with known MS/DM. Methods: The Baptist Employee Healthy Heart Study is an ongoing lifestyle intervention study examining the effects of web-based interventions on reducing CVD risk in individuals with MS/DM. Sleep duration was self reported by the participants. Daily sleep duration was categorized into sleep &lt;7 hours (short), 7 to 8 hours (normal) and &gt;8 hours (long). Homeostatic model assessment of insulin resistance (HOMA-IR) was calculated from fasting insulin and fasting glucose level. Results: The population consisted of 182 participants (74% women, 49% Hispanic, mean age 52 ± 9 years). In this study the mean sleep duration was 7±5 hours and mean HOMA-IR was 5.2 ± 5.6 units. Systolic and diastolic blood pressure, BMI, waist circumference, total cholesterol level and LDL cholesterol level did not apparently differ across the groups. Both short and long sleepers tended to have lower HDL cholesterol level and higher triglyceride level (p&lt;0.05). The mean HOMA-IR was significantly higher in short and long sleepers {7-8hrs (4.09±4.8); &lt;7hrs (5.36±4.7); &gt;8hrs (9.52±10.7), p&lt;0.001}, and were more likely to have HOMA-IR in the highest quartile as compared to normal sleepers. In ordinal logistic regression, after adjustment for traditional risk factors, short and long sleepers were at 2-3 fold higher risk of increasing levels of HOMA-IR. Conclusions: In this study of high metabolic risk individuals, sleep duration was associated with increased insulin resistance and highlights the importance of improving sleep hygiene in the clinical management of high risk individuals with MS and DM.
Leaving Stalag 17
Authors: Arlene Lawson
Journal: JAMA (2002)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Changes in heart rate and heart rate variability before ambulatory ischemic events11The opinions and assertions expressed herein are those of the authors and are not to be construed as reflecting the views of the USUHS or the US Department of Defense.
Authors: Willem J Kop, Ralph J Verdino, John S Gottdiener, Shaun T O’Leary, C.Noel Bairey Merz, David S Krantz
Journal: Journal of the American College of Cardiology (2001)
The effect of hypoxia on the natural killer activity of human peripheral blood lymphocytes against cancer cells
Authors: D. Robert Siemens, Abdol-Karim Sheikhi, Eugene Chung, Hugh Pross, Charles H. Graham
Journal: Cancer Research (2006)

Proc Amer Assoc Cancer Res, Volume 47, 2006

627 

Introduction and Objective: The potential role of natural killer (NK) and lymphokine activated killer (LAK) cells in cancer immunotherapy is expanding and subsequent investigation of tumor escape mechanisms of innate immunity is an exciting area of basic science and clinical inquiry. Tumour hypoxia has been shown to be associated with malignant progression in cancer cells and an independent prognostic indicator of poor clinical outcome for patients with various cancers. We have previously shown that this hypoxia induced progression can be attenuated by low concentrations of nitric oxide (NO) mimetic agents. We therefore postulate that a hypoxic environment may also have a significant effect on the ability of immune cells to target and kill tumor cells. We determine the effect of hypoxia on natural killer cell cytotoxicity. Furthermore, we determine the role of NO to improve prostate cancer cell killing by circulating immune cells. Methods: Two human prostate cancer cell lines PC3 and DU145, as well as a natural killer cell (NK) sensitive leukemia cell line K562, were used for cytotoxicity experiments. Cells were cultured in hypoxic (1% O2) or standard (20% O2) conditions for 24 hours prior to exposure to effector immune cells. Cytotoxicity was assessed using a standard four hour chromium release assay to measure NK activity of fresh human peripheral blood lymphocytes, as well as IL-2 stimulated LAK cells. Furthermore, we investigated the effect of hypoxia on the tumor expression of ligands (MHC class 1 chain related molecules (MIC)) for NK activating receptors with flow cytometry. To determine the ability of NO to modulate effects of tumor hypoxia, we cultured the cell lines with an NO mimetic, GTN, to determine if it could inhibit the hypoxic effects on tumor cell killing. Results: Results of the cytotoxicity assays reveal that culturing cell lines in a low oxygen environment will significantly decrease NK and LAK cell killing. This reduction of cytotoxicity was found to be associated with a tumor cell shedding of MIC A, B molecules. As well, in both the leukemia and prostate cancer cell lines, the addition of low molar concentrations of GTN did significantly attenuate the hypoxia-associated decreased cell killing. Conclusions: These findings indicate hypoxia leads to cellular adaptive responses of prostate cancer cells which interfere with immune effector cell killing, due at least in part by tumor shedding of MIC. These hypoxia related effects may be inhibited by the addition of low concentrations of nitric oxide mimetics. These novel findings suggest that manipulation of nitric oxide signalling may be a beneficial adjuvant in cell based adoptive immunotherapy protocols for prostate cancer.