tbuckley/cabot-search huggingface dataset:
Abstract 1994: Smurf2 mediates ubiquitination and degradation of YY1 to suppress B-cell proliferation and lymphomagenesis.
Authors: Charusheila Ramkumar, Hang Cui, Yahui Kong, Stephen Jones, Rachel Gerstein, Hong Zhang
Journal: Cancer Research (2013)

Abstract Current treatment of diffuse large B-cell lymphoma (DLBCL), the most common type of non-Hodgkin's lymphoma, has improved patient survival significantly. However, 40-50% of DLBCL patients still die from this disease. There is a critical need to better understand the specific molecular pathways that are perturbed in DLBCL for the development of new and effective therapeutic approaches. We show that mice deficient in the E3 ubiquitin ligase Smurf2 spontaneously develop B-cell lymphomas that resemble human DLBCL with molecular features of germinal center B cells. We discover that Smurf2 mediates ubiquitination and degradation of YY1, a key germinal center transcription factor. Importantly, Smurf2 deficiency enhances YY1-mediated transactivation of c-Myc and B-cell proliferation. Furthermore, the expression of Smurf2 is significantly decreased in primary human DLBCL samples compared to normal B cells, and low levels of Smurf2 expression correlate with poor survival prognosis in DLBCL patients. The Smurf2-YY1-c-Myc regulatory axis represents a novel pathway perturbed in DLBCL that suppresses B-cell proliferation and lymphomagenesis, suggesting Smurf2 as a new therapeutic paradigm for DLBCL. Citation Format: Charusheila Ramkumar, Hang Cui, Yahui Kong, Stephen Jones, Rachel Gerstein, Hong Zhang. Smurf2 mediates ubiquitination and degradation of YY1 to suppress B-cell proliferation and lymphomagenesis. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1994. doi:10.1158/1538-7445.AM2013-1994 Note: This abstract was not presented at the AACR Annual Meeting 2013 because the presenter was unable to attend.
PATHOLOGY OF LEFT MAIN ATHEROSCLEROSIS: IMPLICATIONS FOR PERCUTANEOUS CORONARY INTERVENTIONS
Authors: Emanuel Harari, Fumiyuki Otsuka, Kazuyuki Yahagi, Christoph Lutter, Hiroyoshi Mori, Tobias Koppara, Maria Romero, Frank Kolodgie, Elena Ladich, Michael Joner, Renu Virmani
Journal: Journal of the American College of Cardiology (2016)
AB0122 The Effect of GV1001, a Peptide Vaccine, in Animal Model of Rheumatoid Arthritis
Authors: I.A. Choi, J.-Y. Choi, S. Jung, F. Basri, S. Park, E.Y. Lee
Journal: Annals of the Rheumatic Diseases (2015)

<h3>Background</h3> GV1001 is a 16-mer peptide developed as a cancer vaccine to prime the immune system to recognize telomerase. Besides its role as a cancer vaccine, GV1001 has anti-inflammatory effects in in-vitro experiments using macrophage or monocyte. <h3>Objectives</h3> We evaluated the effect of GV1001 to inhibit joint inflammation in animal model of RA. <h3>Methods</h3> 7-9 week old BDA/1 mice (Harlan, Netherlands) were used to induce collagen induced arthritis (CIA). Mice were immunized with bovine type II collagen on day 1 and boosted on day 21. Treatments with GV1001 (0.2 nM, 1 nM, 2 nM, 5 nM, and 10 nM) or placebo were started on day 21, three times in alternative week (on day 21, 23, 25 and day 35, 37, 39). Weight and arthritis index of the mice using a standardized grading scale (0–3) were monitored from day 21. Observation finished on day 42, harvesting mouse serum for further analysis. The second experiment was proceeded with 0.2 nM GV1001 group, 0.2 nM control peptide and arthritis control without treatment in the same schedule to harvest splenocytes. Control peptide was one of the scrambled peptides of GV1001, consist of the same amino acids with a different sequence (PEP164; PKRPSFIEALTRPLR). <h3>Results</h3> Mean arthritis index lower tendencies in 0.2 nM GV1001 group compared to placebo group without statistical significance (p=0.1). Serum IL-6 level was significantly lower in 1 nM and 0.2 nM GV1001 group (p&lt;0.01, both) compared to placebo group. In-vitro T cell re-stimulation with collagen, the level of interferon-gamma in 0.2 nM GV1001 treated group was significantly lower than placebo group (p&lt;0.001) and control peptide group (p&lt;0.01). <h3>Conclusions</h3> Protective effect of GV1001 was not dose dependent and suspected to be related with T cell immune reaction in animal models of RA. These results suggest that GV1001 can modulate immune response in RA patients and has a potential to be used as immunotherapy, such as an RA vaccine. <h3>Acknowledgements</h3> KAEL-GemVax Co., Ltd provided GV1001 peptide and educational grant KAEL-GemVax had no role in the study design and conduct of the study; the collection, management, analysis, and interpretation of the data. <h3>Disclosure of Interest</h3> None declared
Acquired Phagocyte Dysfunction
Authors: P. R. Craddock, Y. Yawata, L. VanSanten, S. Gilberstadt, S. Silvis, H. S. Jacob
Journal: New England Journal of Medicine (1974)

Cachectic patients infused with hypertonic amino acids and dextrose ("parenteral hyperalimentation") are subject to severe hypophosphatemia and recurrent fungal and bacterial septicemia. We observed a relation between the two. Severe hypophosphatemia, induced in a total of 18 mongrel dogs, resulted in a 50 per cent depression of chemotactic, phagocytic and bactericidal activity of their granulocytes. There was a concomitant reduction in leukocyte ATP content. The motility defect was corrected if cellular ATP was repleted by phosphate supplementation of animals in vivo or by incubation of leukocytes with adenosine and phosphate in vitro. Analogously, severe hypophosphatemia in a hyperalimented patient was associated with a 45 per cent impairment of chemotactic responsiveness and was reversed by similar in vivo and in vitro manipulations. The studies provide an additional explanation for the high rate of sepsis in patients undergoing hyperalimentation therapy, secondary to an acquired granulocyte dysfunction induced by hypophosphatemia. (N Engl J Med 290:1403–1407, 1974)
Abstract 215: Neural precursor cells induce cell death of high-grade astrocytomas through stimulation of TRPV1.
Authors: Michael Synowitz, Kristin Stock, Jitender Kumar, Stefania Petrosino, Roberta Imperatore, Ewan St J Smith, Peter Wend, Bettina Purfürst, Ulrike A Nuber, Ulf Gurok, Vitali Matyash, Joo-Hee Wälzlein, Sridhar R Chirasani, Gunnar Dittmar, Benjamin F Cravatt, Stefan Momma, Gary R Lewin, Alessia Ligresti, Luciano De Petrocellis, Luigia Cristino, Joerg Christian Tonn, Vincenzo Di Marzo, Helmut Kettenmann, Rainer Glass
Journal: Cancer Research (2013)

Abstract Primary astrocytomas of grade 3 or 4 according to the classification system of the World Health Organization (high-grade astrocytomas or HGAs) are preponderant among adults and are almost invariably fatal despite the use of multimodal therapy. Here we show that the juvenile brain has an endogenous defense mechanism against HGAs. Neural precursor cells (NPCs) migrate to HGAs, reduce glioma expansion and prolong survival time by releasing endovanilloids that activate the vanilloid receptor (transient receptor potential vanilloid subfamily member-1 or TRPV1) on HGA cells. TRPV1 is highly expressed in tumor and weakly expressed in tumor-free brain. TRPV1 stimulation triggers tumor cell death through the branch of the endoplasmic reticulum stress pathway that is controlled by activating transcription factor-3 (ATF3). The antitumorigenic response of NPCs is lost with aging. NPC-mediated tumor suppression can be mimicked in the adult brain by systemic administration of the synthetic vanilloid arvanil, suggesting that TRPV1 agonists have potential as new HGA therapeutics. Citation Format: Michael Synowitz, Kristin Stock, Jitender Kumar, Stefania Petrosino, Roberta Imperatore, Ewan St J Smith, Peter Wend, Bettina Purfürst, Ulrike A Nuber, Ulf Gurok, Vitali Matyash, Joo-Hee Wälzlein, Sridhar R Chirasani, Gunnar Dittmar, Benjamin F Cravatt, Stefan Momma, Gary R Lewin, Alessia Ligresti, Luciano De Petrocellis, Luigia Cristino, Joerg Christian Tonn, Vincenzo Di Marzo, Helmut Kettenmann, Rainer Glass. Neural precursor cells induce cell death of high-grade astrocytomas through stimulation of TRPV1. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 215. doi:10.1158/1538-7445.AM2013-215
Spontaneous Regression of Chest Wall Malignant Lymphoma
Authors: KIKUO MACHIDA, YUSUKE INOUE, NORINARI HONDA, MAKOTO HOSONO, TAKEO TAKAHASHI, AKIO KASHIMADA
Journal: Clinical Nuclear Medicine (2003)

MACHIDA, KIKUO M.D., PH.D.; INOUE, YUSUKE M.D.; HONDA, NORINARI M.D.; HOSONO, MAKOTO M.D., PH.D.; TAKAHASHI, TAKEO M.D.; KASHIMADA, AKIO M.D. Author Information
Diabetes UK responds to comments by Asimakopoulou and colleagues
Authors: L. Ansari
Journal: BMJ (2014)

Asimakopoulou and colleagues suggest that Diabetes UK’s type 2 diabetes awareness campaign failed to offer those at risk of type 2 diabetes something practical they could do about it.1 2 3 This is simply incorrect. The advertising specifically recommended that people who were worried should get their risk assessed at a pharmacy or GP surgery, or use our online risk score.

Neither is it correct that people already know that a family history of diabetes is a risk factor for type 2 diabetes. Market research that we commissioned ahead of the campaign showed that, unprompted, barely one in 10 people identified family history as …
Exercise Renal Scintigraphy Shows Renal Ischemia in a Transplanted Kidney
Authors: Stefano Fanti, Michele Mirelli, Tiziano Curti, Maurizio Levorato, Roberto Franchi, Maurizio Dondi, Gabriele Testi, Nino Monetti
Journal: Clinical Nuclear Medicine (2002)

Exercise renography is essentially a research method to investigate hypertension and has very limited clinical application. Captopril renography has long been used to study renal artery stenosis causing hypertension with good results. The authors describe a patient with a transplanted kidney supplied by reversal of flow via the external iliac artery. A “steal phenomenon” of the kidney related to ambulation was considered likely. Ischemia of the transplanted kidney was revealed by exercise renography, which showed parenchymal trapping of radiotracer as a result of exercise.
AB0585 High prevalence of psoriatic arthritis in the middle of norway
Authors: M. Hoff, A. Kavanaugh, P. Romundstad, A. M. Gulati, G. Haugeberg
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> Studies indicate that the prevalence of psoriatic arthritis (PsA) range from 0.02-0.25 % in various parts of the world [1] <h3>Objectives</h3> To explore the prevalence of PsA based on the Norwegian population survey "Helse undersøkelsen i Nord Trøndelag" (HUNT-3) performed in 2006-08. <h3>Methods</h3> In HUNT 3 an invitation letter was mailed to all 94,194 adult inhabitants (aged &gt; 20 yrs) in the county Nord-Trøndelag. A total of 50,806 (54%) responded and answered a questionnaire (Q1) and underwent a brief medical examination. Q1 included questions if patients suffered from psoriasis, rheumatoid arthritis (RA) and ankylosing spondylitis (AS). Patients answering they suffer from psoriasis further answered a second questionnaire (Q2) specific about psoriasis including if they had PsA In order to identify as many patients with PsA as possible we then used the following criteria to identify individual's potential to have PsA: Persons who answered "Yes" or "I do not know" at the question: "Do you have PsA" in Q2. Persons answering that they had psoriasis and RA (Q1). Persons answering that they had psoriasis and AS (Q1). In addition we included persons answering they had psoriasis and cardiovascular disease, but had not filled out Q2. This approach identified 1,238 patients from HUNT 3. The diagnosis for each identified individual was validated by an experienced rheumatologist (MH) reviewing the medical hospital records in the county. The evaluation was based on joint involvement, serology, X-ray and skin involvement. Treatment and organ manifestations were noticed and the CASPAR criteria were applied. Patients found to have PsA who did not fulfill the CASPAR criteria were evaluated by two rheumatologists (MH and GH). <h3>Results</h3> Finally a total of 338 patients were found to have PsA. Mean age was 54 yr, 57.4% were female and disease duration 9,2 yr. 52.1% were current or previous users of MTX and 18.6% of anti-TNF therapy. 95.6 % fulfilled the Caspar criteria. All the 15 patients evaluated to have PsA without fulfilling the Caspar criteria had psoriasis and arthritis but data on serology was not available. The total prevalence of PsA (per 1,000) was 6.7 (95% CI 5.9-7.4). Age and gender were distributed as shown in table 1. <h3>Conclusions</h3> The prevalence of PsA in the middle of Norway appears to be higher than previously reported both in Norway [2] and other countries[1]. The reason for this is unknown and may include environmental factors, life style factors and genetic differences. Further studies are warranted to explore for these differences in prevalence of PsA. <h3>References</h3> Setty AR et al. Curr Rheumatol Rep2007;9(6):449. Madland TM et al. J Rheumatol 2005;32(10):1918 <h3>Disclosure of Interest</h3> M. Hoff: None Declared, A. Kavanaugh : None Declared, P. Romundstad: None Declared, A. Gulati: None Declared, G. Haugeberg Grant/research support from: Unrestricted research grant from Pfizer
REFRACTORY CARDIOGENIC SHOCK SECONDARY TO POST-PARTUM MULTIVESSEL SPONTANEOUS CORONARY ARTERY DISSECTION RESCUED WITH BIVENTRICULAR ASSIST DEVICES
Authors: Mahmoud Farhoud, Gabriela Orasanu, Salil Deo, Benjamin Medalion, Michael Zacharias, Mahazarin Ginwalla, Guilherme Oliveira, Soon Park, Basar Sareyyupoglu, Chantal Elamm
Journal: Journal of the American College of Cardiology (2016)
Gardner's Syndrome With Bone Scintigraphic and CT Demonstration
Authors: B D Nguyen, B B Chin, D P Beall
Journal: Clinical Nuclear Medicine (1998)

Gardner's syndrome is a familial autosomal dominant disorder characterized by the triad of colonic polyposis, osteomatosis, and soft tissue tumors. It is associated with adenoma of the pituitary gland, adrenal gland, parathyroid gland and duodenum, along with potential carcinoma of the duodenum and thyroid gland. The authors present a case with multi-system involvement from Gardner's syndrome demonstrated with bone scintigraphy and CT.
Abstract 255: GRB7 – a novel target in triple-negative breast cancer
Authors: Orsi Giricz, Stephanie C. Pero, David N. Krag, Joseph A. Sparano, Paraic A. Kenny
Journal: Cancer Research (2011)

Abstract Triple-negative breast tumors lack expression of estrogen and progesterone receptors and HER2, rendering them non-responsive to the most effective targeted therapies in breast cancer. These tumors are typically more aggressive than other breast cancer subtypes and, consequently, have a poor prognosis. In a clinical trial of triple-negative breast cancer patients treated with anthracyclines and taxanes, we and others have recently determined that high levels of GRB7 are predictive of tumor recurrence. GRB7 is a cytoplasmic adaptor protein that interacts with receptor tyrosine kinases and integrins, transducing information to their downstream signaling cascades. In this study, we have tested the hypothesis that triple-negative breast cancer cell lines are dependent on GRB7 for migration, invasion and colony formation in 3D culture. Using a highly specific peptide inhibitor (G7-18NATE), we found that the GRB7 inhibition significantly impaired each of these phenotypes in four triple-negative breast cancer cell lines: MDA-MB-468, MDA-MB-231, HCC70 and T4-2. In addition, we have tested whether GRB7 inhibition may sensitize these cell lines to the chemotherapies used in the initial clinical trial. Combination treatment with G7-18NATE and doxorubicin or docetaxel resulted in cooperative cell growth inhibition in each of the four cell lines. Co-treatment lowered the IC40 of both chemotherapeutic agents, and it proved to be synergistic in all cases (Combination Index values &amp;lt;1) These data implicate GRB7 as a key mediator of migration, invasion, colony growth and chemoresistance of triple-negative breast cancer cells and suggest that GRB7 itself, or GRB7-dependent pathways, may prove to be important targets therapeutic. This work was supported in part by Susan G. Komen for the Cure (KG091136). 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 255. doi:10.1158/1538-7445.AM2011-255
Abstract LB-284: Retinoblastoma tumor suppressor protein phosphorylation and inactivation depend on direct interaction with Pin1
Authors: Flavio Rizzolio, Chiara Lucchetti, Isabella Caligiuri, Irene Marchesi, Mariella Caputo, Giuseppe Toffoli, Andres J. Szanto, Luigi Bagella, Matteo Castronovo, Antonio Giordano
Journal: Cancer Research (2012)

Abstract It is well known that alterations in the pathway controlling pRb phosphorylation account for more than 50% of tumors. Here, we report a striking experimental demonstration that, in cancer cells, pRb phosphorylation by CDK/cyclin proteins depends on Pin1 activity. We propose, for the first time, a detailed mechanism regarding pRb phosphorylation and activity, thereby significantly advancing the basic understanding of cell cycle control. We conclude that at the beginning-middle of G1, CDKs phosphorylate pRb pocket domain, thus allowing its interaction with Pin1. Next, in mid-late G1, the new complex pRb-Pin1 allows CDKs to complete pRb phosphorylation, and therefore allows the expression of S phase entry genes (Cell Death &amp; Differentiation, in press). We believe our finding will have broad implications on target therapy for cancer patients. In fact, cancer cells can inactive pRb by overexpressing only Pin1, without affecting the well-known CDK pathways. Since Pin1 is overexpressed in most tumors, this suggests a new approach to treating cancer patients by utilizing Pin1 inhibitors in combination with or without CDK inhibitors. 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 LB-284. doi:1538-7445.AM2012-LB-284
Abstract 4421: Curucmin suppresses myeloid-derived suppressor cells and inhibits gastric cancer growth
Authors: Shuiping Tu, Huanyu Jin, Jingdong Shi, Ya Suo, Anna Liu, Gang LU, Chung S. Yang
Journal: Cancer Research (2011)

Abstract Myeloid-derived suppressor cells (MDSCs) are accumulated in the spleen and tumor and contribute to tumor growth, angiogenesis and progression. In this study, we examined the effects of curcumin, a compound from turmeric, on MDSCs and gastric cancer growth in vivo. BABL/C nude mice injected subcutaneously with gastric cancer MKN-45 cells were fed with control diet or 2% curcumin diet or received curucmin through daily i.p. injection at 50mg/kg body weight. Cell apoptosis were determined by Flow cytometer and TUNEL staining. Protein expressions were determined by Western Blot and Immunohistochemistry staining. The frequencies of myeloid-derived suppress cells in the mice were analyzed by Flow cytometer. Cytokines were determined by ELISA. Tumors growth was significantly inhibited by both 2% curucumin diet and curcumin i.p. injection treatment. The frequencies of MDSCs in the spleen, blood and tumor tissues were significantly decreased in the tumor-bearing mice after a 5-days or a 4-weeks treatment with curcumin (in diet or by i.p. injection) compared to control treatment. MDSCs isolated from the spleen of curcumin-treated mice secreted lower levels of IL-6, compared to that from untreated mice. The treatment of MDSCs isolated from the spleen of the untreated tumor-bearing mice with curcumin had lower levels of IL-6, compared to that of control mice. Furthermore, curcumin treatment significantly reduced IL-6 level secreted by IL-1beta-induced MDSCs. Curucmin treatment also significantly induced apoptosis of gastric cancer cells in vitro and in vivo. Our results demonstrate for the first time that cucumin could inhibit MDSCs mobilization and activation and that curcumin inhibits gastric cancer partly through suppressing MDSCs mobilization and activation. MDSCs may be a new target of cucumin for gastric cancer therapy and prevention. (The project was supported by NIH grant R21CA149865 (Tu SP)). 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 4421. doi:10.1158/1538-7445.AM2011-4421
Anterior Choroidal Artery Infarction Presenting as a Progressive Cognitive Deficit
Authors: SATYAJIT SARANGI, ELMER C. SAN PEDRO, JAMES M. MOUNTZ
Journal: Clinical Nuclear Medicine (2000)

Purpose: The authors describe a patient in whom neuroimaging using Tc-99m HMPAO SPECT, F-18 fluorodeoxyglucose (F-18 FDG) coincidence imaging, and magnetic resonance imaging (MRI) identified an anterior choroidal artery infarction. Neuroimaging played a critical role in confirming this diagnosis, because the patient had symptoms of progressive cognitive decline and satisfied the National Institute of Neurological and Communicative Disorders and Stroke–Alzheimer’s Disease and Related Disorders Association criteria for Alzheimer’s disease (AD). Methods: Tc-99m HMPAO brain SPECT was performed using a triple-head gamma camera. F-18 FDG scanning was obtained 40 minutes after intravenous injection of 5 mCi F-18 FDG using a coincidence camera. A brain MRI scan was performed using a 1.5-Tesla scanner. Results: Tc-99m HMPAO SPECT showed focal hypoperfusion to the right parahippocampal cortex. F-18 FDG coincidence imaging showed a more extensive reduction in glucose metabolism compared with SPECT. The MRI scan confirmed the presence of a small segmental choroidal artery infarction. The Tc-99m HMPAO and F-18 FDG scans were not consistent with AD. Conclusions: This case illustrates the value of the regional cerebral blood flow SPECT for evaluating memory impairment in the elderly. Decreased regional cerebral blood flow to the posterior temporoparietal region is consistent with AD, whereas regional cerebral blood flow diminution in a vascular territory is consistent with vascular dementia. In this case, the patient was clinically diagnosed with AD, and SPECT was performed to establish the baseline regional cerebral blood flow before the cholinesterase inhibitor donepezil was administered. An infarction was diagnosed on the regional cerebral blood flow brain SPECT scan, which was later confirmed by MRI. Infarctions of the parahippocampal cortex may result in memory impairment, which can appear clinically similar to AD.
P1240 CHARACTERIZATION OF HCV-1 SUBTYPES AND NATURAL RESISTANCE TO PROTEASE INHIBITORS IN LIVER AND PLASMA COMPARTMENTS OF HIV/HCV COINFECTED INDIVIDUALS
Authors: S. Bagaglio, E. Messina, H. Hasson, M. Merli, A. Lazzarin, A. Smacchia, C. Uberti-Foppa, G. Morsica
Journal: Journal of Hepatology (2014)