tbuckley/cabot-search huggingface dataset:
AB0060 Cross-Talk between the Adipogenic and the Chondrogenic Programs Elicited by A Glycosaminoglycan Mixture
Authors: N. Granados, P.D. Petrov, C. Chetrit, D. Martínez-Puig, A. Palou, M.L. Bonet
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> Mesenchymal stem cells (MSCs) are multipotent cells able to differentiate into chondrocytes, osteoblasts and adipocytes in a competitively balanced manner. MSCs play a role in the homeostasis of adipose tissue and joint tissues and provide potential for intervention in both obesity and degenerative joint disease (osteoarthritis). Nutritional and pharmacological factors influencing the differentiation fate of MSCs are of interest. <h3>Objectives</h3> To test the impact of a mixture of glycosaminoglycans (GAGs) used in osteoarthritis management (Oralvisc™, Bioiberica S.A., Palafolls, Spain) on the differentiation fate of multipotent cells. <h3>Methods</h3> Primary mouse embryo fibroblasts (MEFs), which like MSCs have the potential to differentiate into different mesenchymal cell types, were used as a model system. Post-confluent monolayer MEF cultures maintained in growth medium (non-stimulated conditions) or hormonally stimulated to differentiate into adipocytes were chronically exposed to a GAG mixture, its individual components or vehicle. In some experiments, bone morphogenetic protein 2 (BMP2), a known inducer of chondrogenic differentiation of MEFs, was used for comparison. The impact on adipocyte appearance, gene expression of chondrogenic markers, and gene expression of metabolic and adipokine genes was studied. <h3>Results</h3> Exposure to the GAG mixture, but not its individual components, suppressed spontaneous adipogenesis of MEFs, as it prevented the appearance of lipid-filled cells and the expression of adipogenic marker genes (Pparg, Cebpa, Fasn) in the non-stimulated cultures. The GAG mixture and BMP2 elicited strikingly similar time-course changes in the expression of both chondrogenic-related genes, with an early transient induction of Pref-1 followed by a marked induction of aggrecan, and adipogenic-related genes, with a generalized down-regulation coincident with aggrecan gene induction. HA did not reproduce these effects. Exposure to the GAG mixture did not prevent hormonally induced adipogenesis, but changed gene expression of MEFs in the adipose state, triggering a down-regulation of lipogenic genes (Cebpa, Fasn), an up-regulation of oxidative metabolism-related genes (Ppargc1a, Mtco2), and a down-regulation of genes coding for two insulin resistance-related adipokines (resistin and retinol binding protein 4); again, these effects were not elicited by individual components of the mixture alone. <h3>Conclusions</h3> A GAG mixture can tip the adipogenic/chondrogenic fate balance of multipotent mesenchymal cells towards chondrogenesis and, under adipogenic conditions, favor the differentiation of adipocytes with a more favorable metabolic and secretory gene expression profile. Synergism between individual GAGs in the mixture is involved in these effects. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.5516
Abstract 3383: Hepatocyte growth factor upregulation and signaling is associated with carcinogenesis and mesenchymal characteristics in hepatocellular carcinoma
Authors: Olorunseun O. Ogunwobi, Chen Liu
Journal: Cancer Research (2011)

Abstract Advanced hepatocellular carcinoma (HCC) is an important cause of cancer mortality worldwide. Epithelial-mesenchymal transition (EMT) has been shown to be an important biological process in cancer progression and metastasis. We have focused on elucidating factors that may induce EMT to promote carcinogenesis and subsequent metastasis in HCC using the BNL CL.2 (BNL) and BNL 1ME A. 7R.1 (1MEA) cell lines. BNL cells are normal hepatocytes whereas the 1MEA cells are HCC cells derived from transformation of the BNL cells. Their morphological characteristics were examined. Expression levels of hepatocyte growth factor (HGF), markers of EMT and mediators of HGF signaling were determined in the cell lines and their functional characteristics were compared. BNL cells were treated with HGF and effects on EMT-marker and mediators of HGF signaling were analyzed. BNL cells display characteristic epithelial morphology whereas 1MEA cells display mesenchymal characteristics when examined following H&amp;E staining. qPCR revealed that 1MEA cells express more HGF (200-fold) than BNL cells and confirmed by immunoblotting. There was associated decreased expression of E-cadherin, albumin, AAT and increased expression of fibronectin, collagen-1 and vimentin. There was also increased expression of COX-2, ERK, Akt, phosphorylated ERK and Akt and 1MEA cells formed numerous colonies in soft agar unlike BNL cells. Treatment of BNL cells with HGF led to decreased expression of E-cadherin and increased expression of fibronectin, vimentin, increased migration and increased expression of COX-2, ERK and Akt. We conclude that development of HCC is associated with upregulation of HGF which promotes the acquisition of morphological and molecular mesenchymal characteristics, carcinogenesis and upregulation of COX-2, ERK, Akt and phosphorylated ERK and Akt. Consequently, HGF signaling may be targeted for therapy in advanced and metastatic HCC. 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 3383. doi:10.1158/1538-7445.AM2011-3383
Abstract 1777: The skin cancer chemotherapeutic agent PEP005 is a substrate for the epidermal multidrug transporter (ABCB1) and targets tumor vasculature
Authors: Luowei Li, Suneet Shukla, Andrew Lee, Suresh Ambudkar, Stuart H. Yuspa
Journal: Cancer Research (2010)

Abstract Ingenol-3-angelate (PEP005), extracted from Euphorbia peplus, is currently in clinical trials for eradicating basal cell carcinoma (BCC), actinic keratosis and squamous cell carcinoma (SCC) in situ by topical application. Although structurally related to phorbol esters and a PKC activator, topical PEP005, but not phorbol 12-myristate 13-acetate (PMA), inhibited the growth of subcutaneous tumors derived from PAM212 (mouse SCC) and B16 (mouse melanoma). PEP005 and PMA both induced acute neutrophilic inflammation on mouse skin, but only PEP005 caused subcutaneous hemorrhage and vascular damage. Both PEP005 and PMA activated Erk1/2 in epidermis, but PEP005 also activated Erk1/2 in skin dermal fibroblasts and endothelial cells. Pretreatment with topical cyclosporin A (CsA), verapamil or XR9576, modulators of P-glycoprotein (P-gp), prevented PEP005-induced hemorrhage but not neutrophil infiltration. CsA also impaired Ing3A's anti-cancer activity while the anti-inflammatory dexamethasone did not. PEP005, but not PMA, blocked photoaffinity labeling of human P-gp with [125I]-Iodoaryazidoprazosin and inhibited P-gp mediated drug resistance to HCT-15 cells. The intracellular levels of PEP005 were significantly lower in P-gp expressing cells and treatment with XR9576 increased the levels to those of cells that do not express P-gp, demonstrating that PEP005 binds to and is transported by P-gp. Taken together, our results suggest that P-gp mediated absorptive transport, dermal penetration and vascular damage contribute to the anti-cancer activity of PEP005 in vivo. 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 1777.
18F-FDG–Avid Brunner Gland Hyperplasia
Authors: Seol Hoon Park, Kwang-Min Park, Jae Seung Kim
Journal: Clinical Nuclear Medicine (2014)

Brunner gland hyperplasia, a rare duodenal tumor, usually presents with benign features. A 68-year-old man with a history of anemia presented with a polypoid duodenal mass that was detected by CT and esophagogastroduodenoscopy. This mass showed high F-FDG avidity on PET/CT and was histopathologically confirmed as Brunner gland hyperplasia. We suggest that Brunner gland hyperplasia should be considered in the differential diagnosis of F-FDG-avid duodenal tumors.
A Virus (RMTDV) Derived From Chemically Induced Rat Mammary Tumors, I. Isolation and General Characteristics&lt;xref ref-type="fn" rid="FN2"&gt;2&lt;/xref&gt;&lt;xref ref-type="fn" rid="FN3"&gt;3&lt;/xref&gt;
Authors: V V Bergs, M Bergs, H C Chopra
Journal: JNCI Journal of the National Cancer Institute (1970)
Melphalan, prednisone, and lenalidomide versus melphalan, prednisone, and thalidomide in untreated multiple myeloma
Authors: Sonja Zweegman, Bronno van der Holt, Ulf-Henrik Mellqvist, Morten Salomo, Gerard M. J. Bos, Mark-David Levin, Heleen Visser-Wisselaar, Markus Hansson, Annette W. G. van der Velden, Wendy Deenik, Astrid Gruber, Juleon L. L. M. Coenen, Torben Plesner, Saskia K. Klein, Bea C. Tanis, Damian L. Szatkowski, Rolf E. Brouwer, Matthijs Westerman, M. (Rineke) B. L. Leys, Harm A. M. Sinnige, Einar Haukås, Klaas G. van der Hem, Marc F. Durian, E. (Vera) J. M. Mattijssen, Niels W. C. J. van de Donk, Marian J. P. L. Stevens-Kroef, Pieter Sonneveld, Anders Waage
Journal: Blood (2016)
Abstract 1635: Effect of dietary fish oil on rat colonic prostaglandin (PG) E2 metabolism
Authors: Yan Jiang, Jianwei Ren, Ian Waters, William L. Smith, Dean E. Brenner
Journal: Cancer Research (2012)

Abstract PGE2, an eicosanoid generated from arachidonic acid (AA) by the cyclooxygenase function of prostaglandin H synthases (PGHS)-1 and 2, has been linked to the risk of many cancers including colorectal carcinogenesis. Targeting colonic PGE2 homeostasis by utilizing nutritional products such as fish oil may reduce endogenous PGE2 that, in turn, may decrease subsequent inflammatory events that lead to carcinogenesis. Rats were fed high fat fish oil diets contained different ratios of eicosapentaenoic acid (EPA) and n-6 fatty acid. The colon was horizontally divided into three equal length transections, first (proximal end), second (transverse) and third (distal end). Enzymes involved in PGE2 metabolism (15-hydroxyprostaglandin dehydrogenase (15-PGDH) and PGE synthase (mPGES)) were measured using quantitative PCR and semi-quantitative Western Blotting. GC-MS analysis was performed to detect fatty acid levels in serum and colon. LC-MS/MS analysis was used to examine eicosanoid levels. Our results showed that the colonic epithelial mucosa contained less PGE2 per mg of protein than did the whole colon. Colonic PGE2 and several eicosanoids including 13-Hydroxyoctadecadienoic acid(13HODE), 5-Hydroxyeico-satetraenoic acid (5 HETE), 15-Hydroxyeicosatetraenoic acid (15 HETE) and 12-Hydroxyeicosatetraenoic acid (12 HETE) were distributed differentially in different part of the colon. Dietary fish oil intake increased tissue levels of EPA in the colon. PGHS-2 gene was affected the most by dietary fish oil among all the genes tested in normal colon. Fish oil dose-dependently decreased PGHS-2 mRNA expression in all three colon sections. mRNA expression of 15-PGDH was higher in the third colonic section than the first two sections; however it was not altered by dietary fish oil. In conclusion, different parts of the colon have different eicosanoid profiles. The decreases in PGE2 in normal colon observed with fish oil feeding do not appear to be related to expression of PGHS-1, mPGES and 15-PGDH but are most closely correlated with PGHS-2 despite that PGHS-2 levels are already low in the normal colon. These data support the concept of anatomic variability in colonic carcinogenesis. 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 1635. doi:1538-7445.AM2012-1635
The Effect of the Rice Diet on the Level of the Blood Pressure in Essential Hypertension
Authors: Dorothea G. Loofbourow, Annie L. Galbraith, Robert Sterling Palmer
Journal: New England Journal of Medicine (1949)

INTEREST in the influence of diet on the course of hypertension has existed for at least half a century. In 1904, in France, Ambard and Beaujard1 advocated the use of a low-salt diet for the treatment of hypertension. In the early 1920's in this country Allen and Sherrill2 and O'Hare and Walker3 reported on the use of low-salt diets in hypertension. These workers believed that the effect was produced by restriction of the chloride ion. Addison4 was among the first to suggest that the sodium ion was the important element, and came to the conclusion that "One has forced on . . .
Abstract LB-262: Excessive Wnt activity is insufficient for intestinal tumor growth or regeneration without gp130/Jak2/Stat3 signaling.
Authors: Toby Phesse, Michael Buchert, Matthias Ernst
Journal: Cancer Research (2013)

Abstract The majority of sporadic and familial colorectal cancers (CRC) arise from unregulated, excessive activation of the WNT signaling pathway as a result of impairment mutations in the tumor suppressor gene APC. Meanwhile, controlled activation of WNT signaling is required for intestinal regeneration in response to injury and ensures intestinal homeostasis. Thus far, however, therapeutic targeting of the WNT pathway has proven difficult in human disease. Here, we show genetically that activation of the cytokine-dependent gp130/Jak/Stat3 pathway augments intestinal regeneration in wild-type mice and promotes intestinal tumorigenesis in Apc mutant mice. Conversely, genetic restriction of gp130/Jak/Stat3 signaling suppresses regeneration and inhibits tumor burden despite persistent, excessive WNT activity. Moreover, therapeutic administration of the Jak2-kinase specific inhibitor AZD1480 in mouse models of either sporadic or inherited CRC effectively blocked de novo tumor initiation and progression. Likewise, AZD1480 suppressed the growth of human APC mutant, but not of isogenic APC wild-type, CRC cell lines in vitro and as tumor xenografts. We identify Stat3-dependent Bmi1 induction and the resulting repression of p16 and p21 as the mechanism by which the gp130/Jak/Stat3 pathway modulates the cellular response to excessive WNT signaling. We therefore propose that the gp130/Jak2/Stat3 pathway is rate-limiting selectively for the growth of APC mutant tumors, and that it provides a readily exploitable target for the therapeutic treatment of CRC. Citation Format: Toby Phesse, Michael Buchert, Matthias Ernst. Excessive Wnt activity is insufficient for intestinal tumor growth or regeneration without gp130/Jak2/Stat3 signaling. [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 LB-262. doi:10.1158/1538-7445.AM2013-LB-262
Abstract 3460: Reactive oxygen species generated by cadmium play a role in the upregulation of aldo-keto reductase 1C3 in RPMI 2630 nasal carcinoma cells
Authors: Yoon Jin Lee, Soo-Hark Hur, Hae Seon Nam, Moon Kyun Cho, Sang Han Lee
Journal: Cancer Research (2010)

Abstract Cadmium (Cd) is a carcinogenic metal which induces oxidative stress through the generation of reactive oxygen species (ROS). Therefore, the ability of cells to up-regulate their antioxidant enzymes is fundamental in the protection of cells and tissues from oxidative damage. In probing the possible survival mechanism of cancer cells to Cd-induced oxidative stress, we examined the ability of Cd to regulate the level of aldo-keto reductase 1C3 (AKR1C3), which has an anti-oxidative role that catalyzes the reductive detoxification of reactive aldehydes and ketones. Exposure of cells to Cd induced a dose- and time-dependent increase in the AKR1C3 expression in the RPMI 2640 nasal septum carcinoma cells, and this up-regulation was blocked by the free radical scavenger N-acetylcysteine (NAC). Additionally, we confirmed that Cd triggered a rapid increase in the intracellular ROS levels, and this increase was inhibited by pretreatment with NAC, which suggests that the up-regulation of AKR1C3 expression involves ROS signaling. Furthermore, pretreatment of cells with LY294002, a pharmacologic inhibitor of phosphatidylinositol-3-kinase (PI3K), suppressed the Cd-augmented AKR1C3 expression; however, inhibition of PKC or MEK1/2 signaling with Go6976 or PD98059, respectively, did not alter Cd-induced AKR1C3 expression. Collectively, these data suggest that Cd can modulate the expression of the AKR1C3 by activation of PI3K via the generation of ROS in RPMI2640 cells, which would contribute to adaptive response to oxidative stress. 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 3460.
ELONGATION OF MITRAL VALVE CHORDAE TENDINEAE IS ASSOCIATED WITH INCREASED LEAFLET SURFACE AREA IN PATIENTS WITH DEGENERATIVE MITRAL REGURGITATION
Authors: Kikuko Obase, Lynn Weinert, Andrew Hollatz, Farhan Farooqui, Joseph Roberts, Mohammed M. Minhaj, Valluvan Jeevanandam, Avery Tung, Mark Chaney, Roberto Lang
Journal: Journal of the American College of Cardiology (2015)
American Academy of Neurology Guidelines and the Neurologic Determination of Death—Reply
Authors: David M. Greer, Panayiotis N. Varelas, Eelco F. M. Wijdicks
Journal: JAMA Neurology (2016)

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 Neurology HomeNew OnlineCurrent IssueFor Authors Podcast 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 Neurology journal
O108 NATURALLY OCCURRING HBV CORE DELETION MUTANTS ENCODE CORE-POLYMERASE FUSION PROTEINS WHICH BIND TO MICRORNAS PERTURBING THE REGULATORY FUNCTION AND ENHANCING HEPATOMA CELL GROWTH
Authors: C.-T. Yeh, Y.-H. Huang, Y.-H. Tseng, W.-R. Lin, G. Hung, T.-C. Chen, W.-C. Lee
Journal: Journal of Hepatology (2014)
Abstract LB-373: Lymphatic vessels and neoformed microvessels density in primary oral squamous cell carcinoma and associated lymph nodes
Authors: Sílvia F. Sousa, Frederico O. Gleber-Netto, Helenisa H. Oliveira-Neto, Aline C. Batista, Carolina C. Gomes, Ricardo S. Gomez, Maria Cássia F. Aguiar
Journal: Cancer Research (2011)

Abstract The aim of this study was to evaluate the density of lymphatic vessels (LVD) and neoformed microvessels (MVD) in primary oral squamous cell carcinoma (OSCC) and associated lymph nodes, metastatic or not, and the association of such densities with clinicopathological behavior and metastasis presence. Since vascular endothelial growth factor C (VEGF-C) induces tumor lymphangiogenesis and lymphatic metastasis, this protein was also analyzed in tumor parenchyma. For evaluation of primary tumor, thirty-six paraffin-embedded samples of OSCC were investigated. The tumors were histologically graded and all clinical data of the patients, as tumor size and nodal metastasis were obtained from the medical records. Intratumoral and peritumoral lymphatic (LVD) and neoformed (MVD) vessels were identified by immunohistochemistry using D2–40 and CD105 antibodies respectively. The sum of intra and peritumoral lymphatic and neoformed microvessels was determined as total LVD and total MVD in a magnification of 400x. The same method of count was applied in the analysis of vascular density in lymph nodes. The immunoexpression of VEGF-C was determined by percentage of strongly positive tumour cells. Intratumoral lymphatic vessel density mean was 2.95±3.30, peritumoral mean was 2.96±2.23 and total LVD mean was 5.86±4.81. MVD intratumoral mean was 7.40±4.55, peritumoral mean was 6.25±3.92 and total MVD mean was 13.66±7.30. Intratumoral LVD was significantly lower in poor differentiated tumors (p&amp;lt;0,05). Total MVD was higher in cases with lymph node involvement (p&amp;lt;0.05). An association between VEGF-C positivity and metastasis was also observed (p&amp;lt;0,05). The LVD and MVD in metastatic lymph nodes were significantly higher than in non metastatic lymph nodes (p&amp;lt;0,001). In conclusion lower LVD and higher MVD were associated with high grade malignancy and presence of metastasis. In addition, the metastatic lymph nodes demonstrated a significantly higher vascular density comparatively to non metastatic lymph nodes and the influence of this finding in occurrence of distance metastasis should be investigated in further studies. 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-373. doi:10.1158/1538-7445.AM2011-LB-373
Abstract 1948: Pvt1-encoded microRNA miR-1204 in tumorigenesis of human ovarian and breast cancer
Authors: Jing Huang, Eric A. Collisson, Bill Gibb, Lakshmi Jakkula, Steven Martin, Joe w. Gray
Journal: Cancer Research (2010)

Abstract Amplification at chromosome 8q24 is one of the most frequent genomic abnormalities in human cancers and is associated with reduced survival duration in ovarian and breast cancers. Recently, microRNAs (miRNAs) at 8q24 have been identified in the PVT1 locus. Herein, we explored the biological functions of one miRNA, miR-1204, residing within the exon1B of PVT1. Mature hsa-mir-1204 is over-expressed in PVT1 amplified ovarian and breast cancer cell lines (HEY, OVCAR8, SUM-159PT and MDA-MB231). In vitro treatment with antagomir against hsa-mir-1204 inhibited cell proliferation and induced apoptosis in the four PVT1 amplified ovarian and breast cancer lines. Conversely, over-expression of miR-1204 promoted cell growth in PVT1 non-amplified ovarian and breast cancer lines (OV90 and MCF10A) and cooperated with c-Myc to potentiate Rat1A cell colony growth in soft agar assays. Since an inverse expression pattern is often present between miRNA and its target genes, we used computational approaches (miRanda, TargetScan, Pita) to identify distinct miR-1204 candidate target genes from two independent expression microarray datasets, one with significantly down-regulated genes by PVT1 copy number gain in 147 breast tumors and the other involving genes significantly repressed by miR-1204 overexpression and derepressed by silencing of miR-1204 in ovarian and breast cancer cells. Thirty putative target genes of miR-1204 were empirically verified by Q-RT-PCR method, and this group of genes was enriched with genes regulating cell death, cell growth and proliferation, cell cycle, cellular assembly and organization. Combined, these data suggest that human miR-1204 contributes to ovarian and breast tumor proliferation and survival and down-regulates distinct targets including multiple tumor suppressor genes and serves as a potential therapeutic target against tumors with 8q24 amplification. 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 1948.