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<?xml-stylesheet type="text/xsl" href="http://www.neuroblastomafoundation.org/utility/FeedStylesheets/rss.xsl" media="screen"?><rss version="2.0" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:slash="http://purl.org/rss/1.0/modules/slash/" xmlns:wfw="http://wellformedweb.org/CommentAPI/" xmlns:itunes="http://www.itunes.com/dtds/podcast-1.0.dtd"><channel><title>The Neuroblastoma Foundation</title><link>http://www.neuroblastomafoundation.org/blogs/</link><description>Our mission is dedicated to improving the lives of children with neuroblastoma. It is a place for you to find answers and ask questions.  One of the primary goals of the Neuroblastoma Foundation is to ensure that parents, patients and health care professionals find the information they need to make the best treatment decisions possible for children and adults affected by neuroblastoma. </description><dc:language>en-US</dc:language><generator>CommunityServer 2008.5 SP2 (Build: 40407.4157)</generator><item><title>Ceruloplasmin deficiency reduces levels of iron and BDNF in the cortex and striatum of young mice and increases their vulnerability to stroke.</title><link>http://www.neuroblastomafoundation.org/blogs/research/archive/2012/02/04/ceruloplasmin-deficiency-reduces-levels-of-iron-and-bdnf-in-the-cortex-and-striatum-of-young-mice-and-increases-their-vulnerability-to-stroke.aspx</link><pubDate>Sat, 04 Feb 2012 11:46:08 GMT</pubDate><guid isPermaLink="false">9a7c9348-2ef3-4ddc-9fa4-361883222a9c:23711</guid><dc:creator>pubmed: neuroblastoma</dc:creator><slash:comments>0</slash:comments><description>Ceruloplasmin deficiency reduces levels of iron and BDNF in the cortex and striatum of young mice and increases their vulnerability to stroke. PLoS One. 2011;6(9):e25077 Authors: Texel SJ, Zhang J, Camandola S, Unger EL, Taub DD, Koehler RC, Harris ZL, Mattson MP Abstract Ceruloplasmin (Cp) is an essential ferroxidase that plays important roles in cellular iron trafficking. Previous findings suggest that the proper regulation and subcellular localization of iron are very important in brain cell function...(&lt;a href="http://www.neuroblastomafoundation.org/blogs/research/archive/2012/02/04/ceruloplasmin-deficiency-reduces-levels-of-iron-and-bdnf-in-the-cortex-and-striatum-of-young-mice-and-increases-their-vulnerability-to-stroke.aspx"&gt;read more&lt;/a&gt;)&lt;img src="http://www.neuroblastomafoundation.org/aggbug.aspx?PostID=23711" width="1" height="1"&gt;</description><category domain="http://www.neuroblastomafoundation.org/blogs/research/archive/tags/PLoS+One/default.aspx">PLoS One</category></item><item><title>Acitretin, an Enhancer of Alpha-Secretase Expression, Crosses the Blood-Brain Barrier and Is Not Eliminated by P-Glycoprotein.</title><link>http://www.neuroblastomafoundation.org/blogs/research/archive/2012/02/04/acitretin-an-enhancer-of-alpha-secretase-expression-crosses-the-blood-brain-barrier-and-is-not-eliminated-by-p-glycoprotein.aspx</link><pubDate>Sat, 04 Feb 2012 11:46:08 GMT</pubDate><guid isPermaLink="false">9a7c9348-2ef3-4ddc-9fa4-361883222a9c:23710</guid><dc:creator>pubmed: neuroblastoma</dc:creator><slash:comments>0</slash:comments><description>Acitretin, an Enhancer of Alpha-Secretase Expression, Crosses the Blood-Brain Barrier and Is Not Eliminated by P-Glycoprotein. Neurodegener Dis. 2012 Feb 1; Authors: Holthoewer D, Endres K, Schuck F, Hiemke C, Schmitt U, Fahrenholz F Abstract Background: ADAM10 (a disintegrin and metalloproteinase 10) has been demonstrated to act as the main physiological α-secretase. Enzymatic activity of the α-secretase on the one hand prevents the formation of toxic Aβ peptides and on the other hand promotes the...(&lt;a href="http://www.neuroblastomafoundation.org/blogs/research/archive/2012/02/04/acitretin-an-enhancer-of-alpha-secretase-expression-crosses-the-blood-brain-barrier-and-is-not-eliminated-by-p-glycoprotein.aspx"&gt;read more&lt;/a&gt;)&lt;img src="http://www.neuroblastomafoundation.org/aggbug.aspx?PostID=23710" width="1" height="1"&gt;</description><category domain="http://www.neuroblastomafoundation.org/blogs/research/archive/tags/Neurodegener+Dis/default.aspx">Neurodegener Dis</category></item><item><title>The dopamine metabolite aminochrome inhibits mitochondrial complex I and modifies the expression of iron transporters DMT1 and FPN1.</title><link>http://www.neuroblastomafoundation.org/blogs/research/archive/2012/02/04/the-dopamine-metabolite-aminochrome-inhibits-mitochondrial-complex-i-and-modifies-the-expression-of-iron-transporters-dmt1-and-fpn1.aspx</link><pubDate>Sat, 04 Feb 2012 11:46:07 GMT</pubDate><guid isPermaLink="false">9a7c9348-2ef3-4ddc-9fa4-361883222a9c:23709</guid><dc:creator>pubmed: neuroblastoma</dc:creator><slash:comments>0</slash:comments><description>The dopamine metabolite aminochrome inhibits mitochondrial complex I and modifies the expression of iron transporters DMT1 and FPN1. Biometals. 2012 Feb 3; Authors: Aguirre P, Urrutia P, Tapia V, Villa M, Paris I, Segura-Aguilar J, Núñez MT Abstract Hallmarks of idiopathic and some forms of familial Parkinson&amp;#39;s disease are mitochondrial dysfunction, iron accumulation and oxidative stress in dopaminergic neurons of the substantia nigra. There seems to be a causal link between these three conditions...(&lt;a href="http://www.neuroblastomafoundation.org/blogs/research/archive/2012/02/04/the-dopamine-metabolite-aminochrome-inhibits-mitochondrial-complex-i-and-modifies-the-expression-of-iron-transporters-dmt1-and-fpn1.aspx"&gt;read more&lt;/a&gt;)&lt;img src="http://www.neuroblastomafoundation.org/aggbug.aspx?PostID=23709" width="1" height="1"&gt;</description><category domain="http://www.neuroblastomafoundation.org/blogs/research/archive/tags/Biometals/default.aspx">Biometals</category></item><item><title>Novel GαS-Protein Signaling Associated with Membrane-Tethered Amyloid Precursor Protein Intracellular Domain.</title><link>http://www.neuroblastomafoundation.org/blogs/research/archive/2012/02/04/novel-g-s-protein-signaling-associated-with-membrane-tethered-amyloid-precursor-protein-intracellular-domain.aspx</link><pubDate>Sat, 04 Feb 2012 11:45:40 GMT</pubDate><guid isPermaLink="false">9a7c9348-2ef3-4ddc-9fa4-361883222a9c:23708</guid><dc:creator>pubmed: neuroblastoma</dc:creator><slash:comments>0</slash:comments><description>Novel GαS-Protein Signaling Associated with Membrane-Tethered Amyloid Precursor Protein Intracellular Domain. J Neurosci. 2012 Feb 1;32(5):1714-29 Authors: Deyts C, Vetrivel KS, Das S, Shepherd YM, Dupré DJ, Thinakaran G, Parent AT Abstract Numerous physiological functions, including a role as a cell surface receptor, have been ascribed to Alzheimer&amp;#39;s disease-associated amyloid precursor protein (APP). However, detailed analysis of intracellular signaling mediated by APP in neurons has been lacking...(&lt;a href="http://www.neuroblastomafoundation.org/blogs/research/archive/2012/02/04/novel-g-s-protein-signaling-associated-with-membrane-tethered-amyloid-precursor-protein-intracellular-domain.aspx"&gt;read more&lt;/a&gt;)&lt;img src="http://www.neuroblastomafoundation.org/aggbug.aspx?PostID=23708" width="1" height="1"&gt;</description><category domain="http://www.neuroblastomafoundation.org/blogs/research/archive/tags/J+Neurosci/default.aspx">J Neurosci</category></item><item><title>An extension of the single threshold design for monitoring efficacy and safety in phase II clinical trials.</title><link>http://www.neuroblastomafoundation.org/blogs/research/archive/2012/02/03/an-extension-of-the-single-threshold-design-for-monitoring-efficacy-and-safety-in-phase-ii-clinical-trials.aspx</link><pubDate>Fri, 03 Feb 2012 11:06:05 GMT</pubDate><guid isPermaLink="false">9a7c9348-2ef3-4ddc-9fa4-361883222a9c:23589</guid><dc:creator>pubmed: neuroblastoma</dc:creator><slash:comments>0</slash:comments><description>An extension of the single threshold design for monitoring efficacy and safety in phase II clinical trials. Stat Med. 2011 Jun 30;30(14):1648-64 Authors: Brutti P, Gubbiotti S, Sambucini V Abstract Tan and Machin (biStat. Med. 2002; 21:1991-2012) introduce a Bayesian two-stage design for phase II clinical trials where the binary endpoint of interest is treatment efficacy. In this paper we propose an extension of their design to incorporate safety considerations. At each stage we define the treatment...(&lt;a href="http://www.neuroblastomafoundation.org/blogs/research/archive/2012/02/03/an-extension-of-the-single-threshold-design-for-monitoring-efficacy-and-safety-in-phase-ii-clinical-trials.aspx"&gt;read more&lt;/a&gt;)&lt;img src="http://www.neuroblastomafoundation.org/aggbug.aspx?PostID=23589" width="1" height="1"&gt;</description><category domain="http://www.neuroblastomafoundation.org/blogs/research/archive/tags/Stat+Med/default.aspx">Stat Med</category></item><item><title>Childhood cancer incidence and survival 2003-2005, Thailand: study from the thai pediatric oncology group.</title><link>http://www.neuroblastomafoundation.org/blogs/research/archive/2012/02/03/childhood-cancer-incidence-and-survival-2003-2005-thailand-study-from-the-thai-pediatric-oncology-group.aspx</link><pubDate>Fri, 03 Feb 2012 11:06:05 GMT</pubDate><guid isPermaLink="false">9a7c9348-2ef3-4ddc-9fa4-361883222a9c:23588</guid><dc:creator>pubmed: neuroblastoma</dc:creator><slash:comments>0</slash:comments><description>Childhood cancer incidence and survival 2003-2005, Thailand: study from the thai pediatric oncology group. Asian Pac J Cancer Prev. 2011;12(9):2215-20 Authors: Wiangnon S, Veerakul G, Nuchprayoon I, Seksarn P, Hongeng S, Krutvecho T, Sripaiboonkij N Abstract Background: Previous population-based incidences of childhood cancer in Thailand were achieved by extrapolating from data limited to a small number of cancer registries, not from the whole country. In addition, survival of childhood cancer patients...(&lt;a href="http://www.neuroblastomafoundation.org/blogs/research/archive/2012/02/03/childhood-cancer-incidence-and-survival-2003-2005-thailand-study-from-the-thai-pediatric-oncology-group.aspx"&gt;read more&lt;/a&gt;)&lt;img src="http://www.neuroblastomafoundation.org/aggbug.aspx?PostID=23588" width="1" height="1"&gt;</description><category domain="http://www.neuroblastomafoundation.org/blogs/research/archive/tags/Asian+Pac+J+Cancer+Prev/default.aspx">Asian Pac J Cancer Prev</category></item><item><title>Cellular consequences of the expression of Alzheimer's disease-causing presenilin 1 mutations in human neuroblastoma (SH-SY5Y) cells.</title><link>http://www.neuroblastomafoundation.org/blogs/research/archive/2012/02/03/cellular-consequences-of-the-expression-of-alzheimer-s-disease-causing-presenilin-1-mutations-in-human-neuroblastoma-sh-sy5y-cells.aspx</link><pubDate>Fri, 03 Feb 2012 11:06:05 GMT</pubDate><guid isPermaLink="false">9a7c9348-2ef3-4ddc-9fa4-361883222a9c:23587</guid><dc:creator>pubmed: neuroblastoma</dc:creator><slash:comments>0</slash:comments><description>Cellular consequences of the expression of Alzheimer&amp;#39;s disease-causing presenilin 1 mutations in human neuroblastoma (SH-SY5Y) cells. Brain Res. 2012 Jan 12; Authors: Boyle JP, Hettiarachchi NT, Wilkinson JA, Pearson HA, Scragg JL, Lendon C, Al-Owais MM, Kim CB, Myers DM, Warburton P, Peers C Abstract Mutations in the presenilin 1 (PS1) gene lead to early-onset Alzheimer&amp;#39;s disease with the S170F mutation causing the earliest reported age of onset. Expression of this, and other PS1 mutations...(&lt;a href="http://www.neuroblastomafoundation.org/blogs/research/archive/2012/02/03/cellular-consequences-of-the-expression-of-alzheimer-s-disease-causing-presenilin-1-mutations-in-human-neuroblastoma-sh-sy5y-cells.aspx"&gt;read more&lt;/a&gt;)&lt;img src="http://www.neuroblastomafoundation.org/aggbug.aspx?PostID=23587" width="1" height="1"&gt;</description><category domain="http://www.neuroblastomafoundation.org/blogs/research/archive/tags/Brain+Res/default.aspx">Brain Res</category></item><item><title>Protection of prenylated flavonoids from mori cortex radicis (Moraceae) against nitric oxide-induced cell death in neuroblastoma SH-SY5Y cells.</title><link>http://www.neuroblastomafoundation.org/blogs/research/archive/2012/02/03/protection-of-prenylated-flavonoids-from-mori-cortex-radicis-moraceae-against-nitric-oxide-induced-cell-death-in-neuroblastoma-sh-sy5y-cells.aspx</link><pubDate>Fri, 03 Feb 2012 11:06:04 GMT</pubDate><guid isPermaLink="false">9a7c9348-2ef3-4ddc-9fa4-361883222a9c:23586</guid><dc:creator>pubmed: neuroblastoma</dc:creator><slash:comments>0</slash:comments><description>Protection of prenylated flavonoids from mori cortex radicis (Moraceae) against nitric oxide-induced cell death in neuroblastoma SH-SY5Y cells. Arch Pharm Res. 2012 Jan;35(1):163-70 Authors: Lee HJ, Lyu da H, Koo U, Nam KW, Hong SS, Kim KO, Kim KH, Lee D, Mar W Abstract Seven prenylated flavanoids, licoflavone C (1), cyclomulberrin (2), neocyclomorusin (3), sanggenon I (4), morusin (5), kuwanon U (6) and kuwanon E (7), and three 2-arylbenzofurans, moracin P (8), moracin O (9), and mulberrofuran Q...(&lt;a href="http://www.neuroblastomafoundation.org/blogs/research/archive/2012/02/03/protection-of-prenylated-flavonoids-from-mori-cortex-radicis-moraceae-against-nitric-oxide-induced-cell-death-in-neuroblastoma-sh-sy5y-cells.aspx"&gt;read more&lt;/a&gt;)&lt;img src="http://www.neuroblastomafoundation.org/aggbug.aspx?PostID=23586" width="1" height="1"&gt;</description><category domain="http://www.neuroblastomafoundation.org/blogs/research/archive/tags/Arch+Pharm+Res/default.aspx">Arch Pharm Res</category></item><item><title>Arylpiperazine Dopamineric Ligands Protect Neuroblastoma Cells from Nitric Oxide (NO)-Induced Mitochondrial Damage and Apoptosis.</title><link>http://www.neuroblastomafoundation.org/blogs/research/archive/2012/02/03/arylpiperazine-dopamineric-ligands-protect-neuroblastoma-cells-from-nitric-oxide-no-induced-mitochondrial-damage-and-apoptosis.aspx</link><pubDate>Fri, 03 Feb 2012 11:06:04 GMT</pubDate><guid isPermaLink="false">9a7c9348-2ef3-4ddc-9fa4-361883222a9c:23585</guid><dc:creator>pubmed: neuroblastoma</dc:creator><slash:comments>0</slash:comments><description>Arylpiperazine Dopamineric Ligands Protect Neuroblastoma Cells from Nitric Oxide (NO)-Induced Mitochondrial Damage and Apoptosis. ChemMedChem. 2012 Feb 1; Authors: Tovilovic G, Zogovic N, Harhaji-Trajkovic L, Misirkic-Marjanovic M, Janjetovic K, Vucicevic L, Kostic-Rajacic S, Schrattenholz A, Isakovic A, Soskic V, Trajkovic V Abstract The protective ability of novel arylpiperazine-based dopaminergic ligands against nitric oxide (NO)-mediated neurotoxicity is investigated. The most potent neuroprotective...(&lt;a href="http://www.neuroblastomafoundation.org/blogs/research/archive/2012/02/03/arylpiperazine-dopamineric-ligands-protect-neuroblastoma-cells-from-nitric-oxide-no-induced-mitochondrial-damage-and-apoptosis.aspx"&gt;read more&lt;/a&gt;)&lt;img src="http://www.neuroblastomafoundation.org/aggbug.aspx?PostID=23585" width="1" height="1"&gt;</description><category domain="http://www.neuroblastomafoundation.org/blogs/research/archive/tags/ChemMedChem/default.aspx">ChemMedChem</category></item><item><title>Tumor-initiating cells in childhood neuroblastoma--letter.</title><link>http://www.neuroblastomafoundation.org/blogs/research/archive/2012/02/03/tumor-initiating-cells-in-childhood-neuroblastoma-letter.aspx</link><pubDate>Fri, 03 Feb 2012 11:06:04 GMT</pubDate><guid isPermaLink="false">9a7c9348-2ef3-4ddc-9fa4-361883222a9c:23584</guid><dc:creator>pubmed: neuroblastoma</dc:creator><slash:comments>0</slash:comments><description>Tumor-initiating cells in childhood neuroblastoma--letter. Cancer Res. 2012 Feb 1;72(3):821-2 Authors: Mohlin S, Pietras A, Wigerup C, Ora I, Andäng M, Nilsson K, Olofsson T, Gisselsson D, Påhlman S PMID: 22298597 [PubMed - in process]...(&lt;a href="http://www.neuroblastomafoundation.org/blogs/research/archive/2012/02/03/tumor-initiating-cells-in-childhood-neuroblastoma-letter.aspx"&gt;read more&lt;/a&gt;)&lt;img src="http://www.neuroblastomafoundation.org/aggbug.aspx?PostID=23584" width="1" height="1"&gt;</description><category domain="http://www.neuroblastomafoundation.org/blogs/research/archive/tags/Cancer+Res/default.aspx">Cancer Res</category></item><item><title>Tumor-initiating cells in childhood neuroblastoma--response.</title><link>http://www.neuroblastomafoundation.org/blogs/research/archive/2012/02/03/tumor-initiating-cells-in-childhood-neuroblastoma-response.aspx</link><pubDate>Fri, 03 Feb 2012 11:06:04 GMT</pubDate><guid isPermaLink="false">9a7c9348-2ef3-4ddc-9fa4-361883222a9c:23583</guid><dc:creator>pubmed: neuroblastoma</dc:creator><slash:comments>0</slash:comments><description>Tumor-initiating cells in childhood neuroblastoma--response. Cancer Res. 2012 Feb 1;72(3):823-4 Authors: Hansford LM, Kaplan DR PMID: 22298598 [PubMed - in process]...(&lt;a href="http://www.neuroblastomafoundation.org/blogs/research/archive/2012/02/03/tumor-initiating-cells-in-childhood-neuroblastoma-response.aspx"&gt;read more&lt;/a&gt;)&lt;img src="http://www.neuroblastomafoundation.org/aggbug.aspx?PostID=23583" width="1" height="1"&gt;</description><category domain="http://www.neuroblastomafoundation.org/blogs/research/archive/tags/Cancer+Res/default.aspx">Cancer Res</category></item><item><title>Activated β-catenin Forces N2A Cell-derived Neurons Back to Tumor-like Neuroblasts and Positively Correlates with a Risk for Human Neuroblastoma.</title><link>http://www.neuroblastomafoundation.org/blogs/research/archive/2012/02/03/activated-catenin-forces-n2a-cell-derived-neurons-back-to-tumor-like-neuroblasts-and-positively-correlates-with-a-risk-for-human-neuroblastoma.aspx</link><pubDate>Fri, 03 Feb 2012 11:05:52 GMT</pubDate><guid isPermaLink="false">9a7c9348-2ef3-4ddc-9fa4-361883222a9c:23582</guid><dc:creator>pubmed: neuroblastoma</dc:creator><slash:comments>0</slash:comments><description>Activated β-catenin Forces N2A Cell-derived Neurons Back to Tumor-like Neuroblasts and Positively Correlates with a Risk for Human Neuroblastoma. Int J Biol Sci. 2012;8(2):289-97 Authors: Zhi F, Gong G, Xu Y, Zhu Y, Hu D, Yang Y, Hu Y Abstract Neuroblastoma is an embryonic malignancy arising from neuroblasts. The mechanisms that regulate the origination of neuroblastoma are still not very clear. In this study, we revealed that 6-bromoindirubin 3&amp;#39;-oxime (BIO), a specific GSK-3β inhibitor, promoted...(&lt;a href="http://www.neuroblastomafoundation.org/blogs/research/archive/2012/02/03/activated-catenin-forces-n2a-cell-derived-neurons-back-to-tumor-like-neuroblasts-and-positively-correlates-with-a-risk-for-human-neuroblastoma.aspx"&gt;read more&lt;/a&gt;)&lt;img src="http://www.neuroblastomafoundation.org/aggbug.aspx?PostID=23582" width="1" height="1"&gt;</description><category domain="http://www.neuroblastomafoundation.org/blogs/research/archive/tags/Int+J+Biol+Sci/default.aspx">Int J Biol Sci</category></item><item><title>Influence of a 50 Hz magnetic field and of all-trans‑retinol on the             proliferation of human cancer cell lines.</title><link>http://www.neuroblastomafoundation.org/blogs/research/archive/2012/02/02/influence-of-a-50-hz-magnetic-field-and-of-all-trans-retinol-on-the-proliferation-of-human-cancer-cell-lines.aspx</link><pubDate>Thu, 02 Feb 2012 12:01:00 GMT</pubDate><guid isPermaLink="false">9a7c9348-2ef3-4ddc-9fa4-361883222a9c:23416</guid><dc:creator>pubmed: neuroblastoma</dc:creator><slash:comments>0</slash:comments><description>Influence of a 50 Hz magnetic field and of all-trans‑retinol on the proliferation of human cancer cell lines. Int J Oncol. 2012 Jan 27; Authors: Trillo MA, Martínez MA, Cid MA, Leal J, Ubeda A Abstract In vitro exposure to power frequency magnetic fields (MF) has been reported to influence cell proliferation and differentiation. However, the nature of the response of different human cancer cell types to these fields has not been sufficiently characterized. The present work investigates the response...(&lt;a href="http://www.neuroblastomafoundation.org/blogs/research/archive/2012/02/02/influence-of-a-50-hz-magnetic-field-and-of-all-trans-retinol-on-the-proliferation-of-human-cancer-cell-lines.aspx"&gt;read more&lt;/a&gt;)&lt;img src="http://www.neuroblastomafoundation.org/aggbug.aspx?PostID=23416" width="1" height="1"&gt;</description><category domain="http://www.neuroblastomafoundation.org/blogs/research/archive/tags/Int+J+Oncol/default.aspx">Int J Oncol</category></item><item><title>Shifting from Population-wide to Personalized Cancer Prognosis with Microarrays.</title><link>http://www.neuroblastomafoundation.org/blogs/research/archive/2012/02/02/shifting-from-population-wide-to-personalized-cancer-prognosis-with-microarrays.aspx</link><pubDate>Thu, 02 Feb 2012 12:00:59 GMT</pubDate><guid isPermaLink="false">9a7c9348-2ef3-4ddc-9fa4-361883222a9c:23415</guid><dc:creator>pubmed: neuroblastoma</dc:creator><slash:comments>0</slash:comments><description>Shifting from Population-wide to Personalized Cancer Prognosis with Microarrays. PLoS One. 2012;7(1):e29534 Authors: Shao L, Fan X, Cheng N, Wu L, Xiong H, Fang H, Ding D, Shi L, Cheng Y, Tong W Abstract The era of personalized medicine for cancer therapeutics has taken an important step forward in making accurate prognoses for individual patients with the adoption of high-throughput microarray technology. However, microarray technology in cancer diagnosis or prognosis has been primarily used for...(&lt;a href="http://www.neuroblastomafoundation.org/blogs/research/archive/2012/02/02/shifting-from-population-wide-to-personalized-cancer-prognosis-with-microarrays.aspx"&gt;read more&lt;/a&gt;)&lt;img src="http://www.neuroblastomafoundation.org/aggbug.aspx?PostID=23415" width="1" height="1"&gt;</description><category domain="http://www.neuroblastomafoundation.org/blogs/research/archive/tags/PLoS+One/default.aspx">PLoS One</category></item><item><title>Calpastatin upregulation in Mycoplasma hyorhinis-infected cells is promoted by the mycoplasma lipoproteins via the NF-κB pathway.</title><link>http://www.neuroblastomafoundation.org/blogs/research/archive/2012/02/01/calpastatin-upregulation-in-mycoplasma-hyorhinis-infected-cells-is-promoted-by-the-mycoplasma-lipoproteins-via-the-nf-b-pathway.aspx</link><pubDate>Wed, 01 Feb 2012 11:41:59 GMT</pubDate><guid isPermaLink="false">9a7c9348-2ef3-4ddc-9fa4-361883222a9c:23285</guid><dc:creator>pubmed: neuroblastoma</dc:creator><slash:comments>0</slash:comments><description>Calpastatin upregulation in Mycoplasma hyorhinis-infected cells is promoted by the mycoplasma lipoproteins via the NF-κB pathway. Cell Microbiol. 2012 Jan 31; Authors: Elkind E, Vaisid T, Kornspan JD, Barnoy S, Rottem S, Kosower NS Abstract Mycoplasma hyorhinis frequently contaminates cultured cells, with effects on synthetic and metabolic pathways. We demonstrated for the first time that contamination of cells by a strain of M. hyorhinis (NDMh) results in increased levels of calpastatin (the endogenous...(&lt;a href="http://www.neuroblastomafoundation.org/blogs/research/archive/2012/02/01/calpastatin-upregulation-in-mycoplasma-hyorhinis-infected-cells-is-promoted-by-the-mycoplasma-lipoproteins-via-the-nf-b-pathway.aspx"&gt;read more&lt;/a&gt;)&lt;img src="http://www.neuroblastomafoundation.org/aggbug.aspx?PostID=23285" width="1" height="1"&gt;</description><category domain="http://www.neuroblastomafoundation.org/blogs/research/archive/tags/Cell+Microbiol/default.aspx">Cell Microbiol</category></item><item><title>Rapid Detection of Neoplastic Cells in Serous Cavity Effusions in Children with Flow Cytometry Immunophenotyping.</title><link>http://www.neuroblastomafoundation.org/blogs/research/archive/2012/02/01/rapid-detection-of-neoplastic-cells-in-serous-cavity-effusions-in-children-with-flow-cytometry-immunophenotyping.aspx</link><pubDate>Wed, 01 Feb 2012 11:41:58 GMT</pubDate><guid isPermaLink="false">9a7c9348-2ef3-4ddc-9fa4-361883222a9c:23284</guid><dc:creator>pubmed: neuroblastoma</dc:creator><slash:comments>0</slash:comments><description>Rapid Detection of Neoplastic Cells in Serous Cavity Effusions in Children with Flow Cytometry Immunophenotyping. Leuk Lymphoma. 2012 Jan 30; Authors: Shen H, Tang Y, Xu X, Wang L, Wang Q, Xu W, Song H, Zhao Z, Wang J Abstract Abstract The aim of the study was to evaluate the role of flow cytometric immunophenotyping (FCI) as a quick diagnostic tool for pediatric malignancy in serous cavity effusions (SCE). FCI results on 103 SCE in a pediatric population were compared with retrospective clinical...(&lt;a href="http://www.neuroblastomafoundation.org/blogs/research/archive/2012/02/01/rapid-detection-of-neoplastic-cells-in-serous-cavity-effusions-in-children-with-flow-cytometry-immunophenotyping.aspx"&gt;read more&lt;/a&gt;)&lt;img src="http://www.neuroblastomafoundation.org/aggbug.aspx?PostID=23284" width="1" height="1"&gt;</description><category domain="http://www.neuroblastomafoundation.org/blogs/research/archive/tags/Leuk+Lymphoma/default.aspx">Leuk Lymphoma</category></item><item><title>Suppression of p75 Neurotrophin Receptor Surface Expression with Intrabodies Influences Bcl-xL mRNA Expression and Neurite Outgrowth in PC12 Cells.</title><link>http://www.neuroblastomafoundation.org/blogs/research/archive/2012/02/01/suppression-of-p75-neurotrophin-receptor-surface-expression-with-intrabodies-influences-bcl-xl-mrna-expression-and-neurite-outgrowth-in-pc12-cells.aspx</link><pubDate>Wed, 01 Feb 2012 11:41:47 GMT</pubDate><guid isPermaLink="false">9a7c9348-2ef3-4ddc-9fa4-361883222a9c:23283</guid><dc:creator>pubmed: neuroblastoma</dc:creator><slash:comments>0</slash:comments><description>Suppression of p75 Neurotrophin Receptor Surface Expression with Intrabodies Influences Bcl-xL mRNA Expression and Neurite Outgrowth in PC12 Cells. PLoS One. 2012;7(1):e30684 Authors: Zhang C, Helmsing S, Zagrebelsky M, Schirrmann T, Marschall AL, Schüngel M, Korte M, Hust M, Dübel S Abstract BACKGROUND: Although p75 neurotrophin receptor (p75NTR) is the first neurotrophin receptor isolated, its diverse physiological functions and signaling have remained elusive for many years. Loss-of-function phenotypic...(&lt;a href="http://www.neuroblastomafoundation.org/blogs/research/archive/2012/02/01/suppression-of-p75-neurotrophin-receptor-surface-expression-with-intrabodies-influences-bcl-xl-mrna-expression-and-neurite-outgrowth-in-pc12-cells.aspx"&gt;read more&lt;/a&gt;)&lt;img src="http://www.neuroblastomafoundation.org/aggbug.aspx?PostID=23283" width="1" height="1"&gt;</description><category domain="http://www.neuroblastomafoundation.org/blogs/research/archive/tags/PLoS+One/default.aspx">PLoS One</category></item><item><title>Liposome-encapsulated curcumin suppresses neuroblastoma growth through nuclear factor-kappa B inhibition.</title><link>http://www.neuroblastomafoundation.org/blogs/research/archive/2012/01/31/liposome-encapsulated-curcumin-suppresses-neuroblastoma-growth-through-nuclear-factor-kappa-b-160-inhibition.aspx</link><pubDate>Tue, 31 Jan 2012 11:23:30 GMT</pubDate><guid isPermaLink="false">9a7c9348-2ef3-4ddc-9fa4-361883222a9c:23120</guid><dc:creator>pubmed: neuroblastoma</dc:creator><slash:comments>0</slash:comments><description>Liposome-encapsulated curcumin suppresses neuroblastoma growth through nuclear factor-kappa B inhibition. Surgery. 2012 Jan 26; Authors: Orr WS, Denbo JW, Saab KR, Myers AL, Ng CY, Zhou J, Morton CL, Pfeffer LM, Davidoff AM Abstract BACKGROUND: Nuclear factor-κB (NF-κB) has been implicated in tumor cell proliferation and survival and in tumor angiogenesis. We sought to evaluate the effects of curcumin, an inhibitor of NF-κB, on a xenograft model of disseminated neuroblastoma. METHODS: For in vitro...(&lt;a href="http://www.neuroblastomafoundation.org/blogs/research/archive/2012/01/31/liposome-encapsulated-curcumin-suppresses-neuroblastoma-growth-through-nuclear-factor-kappa-b-160-inhibition.aspx"&gt;read more&lt;/a&gt;)&lt;img src="http://www.neuroblastomafoundation.org/aggbug.aspx?PostID=23120" width="1" height="1"&gt;</description><category domain="http://www.neuroblastomafoundation.org/blogs/research/archive/tags/Surgery/default.aspx">Surgery</category></item><item><title>Chemotherapy-Associated Angiogenesis in Neuroblastoma Tumors.</title><link>http://www.neuroblastomafoundation.org/blogs/research/archive/2012/01/31/chemotherapy-associated-angiogenesis-in-neuroblastoma-tumors.aspx</link><pubDate>Tue, 31 Jan 2012 11:23:30 GMT</pubDate><guid isPermaLink="false">9a7c9348-2ef3-4ddc-9fa4-361883222a9c:23119</guid><dc:creator>pubmed: neuroblastoma</dc:creator><slash:comments>0</slash:comments><description>Chemotherapy-Associated Angiogenesis in Neuroblastoma Tumors. Am J Pathol. 2012 Jan 26; Authors: Michaelis M, Hinsch N, Michaelis UR, Rothweiler F, Simon T, Wilhelm Doerr H, Cinatl J, Cinatl J Abstract The influences of cytotoxic drugs on endothelial cells remain incompletely understood. Herein, we examined the effects of chemotherapeutic agents in experimental angiogenesis models and analyzed vessel densities in clinical neuroblastoma tumor samples. Cisplatin (20 to 500 ng/mL), doxorubicin (4 to...(&lt;a href="http://www.neuroblastomafoundation.org/blogs/research/archive/2012/01/31/chemotherapy-associated-angiogenesis-in-neuroblastoma-tumors.aspx"&gt;read more&lt;/a&gt;)&lt;img src="http://www.neuroblastomafoundation.org/aggbug.aspx?PostID=23119" width="1" height="1"&gt;</description><category domain="http://www.neuroblastomafoundation.org/blogs/research/archive/tags/Am+J+Pathol/default.aspx">Am J Pathol</category></item><item><title>Targeting mitochondria by α-tocopheryl succinate kills neuroblastoma cells irrespective of MycN oncogene expression.</title><link>http://www.neuroblastomafoundation.org/blogs/research/archive/2012/01/31/targeting-mitochondria-by-tocopheryl-succinate-kills-neuroblastoma-cells-irrespective-of-mycn-oncogene-expression.aspx</link><pubDate>Tue, 31 Jan 2012 11:23:30 GMT</pubDate><guid isPermaLink="false">9a7c9348-2ef3-4ddc-9fa4-361883222a9c:23118</guid><dc:creator>pubmed: neuroblastoma</dc:creator><slash:comments>0</slash:comments><description>Targeting mitochondria by α-tocopheryl succinate kills neuroblastoma cells irrespective of MycN oncogene expression. Cell Mol Life Sci. 2012 Jan 28; Authors: Kruspig B, Nilchian A, Bejarano I, Orrenius S, Zhivotovsky B, Gogvadze V Abstract Amplification of the MycN oncogene characterizes a subset of highly aggressive neuroblastomas, the most common extracranial solid tumor of childhood. However, the significance of MycN amplification for tumor cell survival is controversial, since down-regulation...(&lt;a href="http://www.neuroblastomafoundation.org/blogs/research/archive/2012/01/31/targeting-mitochondria-by-tocopheryl-succinate-kills-neuroblastoma-cells-irrespective-of-mycn-oncogene-expression.aspx"&gt;read more&lt;/a&gt;)&lt;img src="http://www.neuroblastomafoundation.org/aggbug.aspx?PostID=23118" width="1" height="1"&gt;</description><category domain="http://www.neuroblastomafoundation.org/blogs/research/archive/tags/Cell+Mol+Life+Sci/default.aspx">Cell Mol Life Sci</category></item><item><title>Gintonin, newly identified compounds from ginseng, is novel lysophosphatidic acids-protein complexes and activates G protein-coupled lysophosphatidic acid receptors with high affinity.</title><link>http://www.neuroblastomafoundation.org/blogs/research/archive/2012/01/31/gintonin-newly-identified-compounds-from-ginseng-is-novel-lysophosphatidic-acids-protein-complexes-and-activates-g-protein-coupled-lysophosphatidic-acid-receptors-with-high-affinity.aspx</link><pubDate>Tue, 31 Jan 2012 11:23:29 GMT</pubDate><guid isPermaLink="false">9a7c9348-2ef3-4ddc-9fa4-361883222a9c:23117</guid><dc:creator>pubmed: neuroblastoma</dc:creator><slash:comments>0</slash:comments><description>Gintonin, newly identified compounds from ginseng, is novel lysophosphatidic acids-protein complexes and activates G protein-coupled lysophosphatidic acid receptors with high affinity. Mol Cells. 2012 Jan 27; Authors: Hwang SH, Shin TJ, Choi SH, Cho HJ, Lee BH, Pyo MK, Lee JH, Kang J, Kim HJ, Park CW, Shin HC, Nah SY Abstract Recently, we isolated a subset of glycolipoproteins from Panax ginseng, that we designated gintonin, and demonstrated that it induced [Ca(2+)](i) transients in cells via G-protein...(&lt;a href="http://www.neuroblastomafoundation.org/blogs/research/archive/2012/01/31/gintonin-newly-identified-compounds-from-ginseng-is-novel-lysophosphatidic-acids-protein-complexes-and-activates-g-protein-coupled-lysophosphatidic-acid-receptors-with-high-affinity.aspx"&gt;read more&lt;/a&gt;)&lt;img src="http://www.neuroblastomafoundation.org/aggbug.aspx?PostID=23117" width="1" height="1"&gt;</description><category domain="http://www.neuroblastomafoundation.org/blogs/research/archive/tags/Mol+Cells/default.aspx">Mol Cells</category></item><item><title>Anaplastic Lymphoma Kinase (ALK) regulates initiation of transcription of MYCN in neuroblastoma cells.</title><link>http://www.neuroblastomafoundation.org/blogs/research/archive/2012/01/31/anaplastic-lymphoma-kinase-alk-regulates-initiation-of-transcription-of-mycn-in-neuroblastoma-cells.aspx</link><pubDate>Tue, 31 Jan 2012 11:23:29 GMT</pubDate><guid isPermaLink="false">9a7c9348-2ef3-4ddc-9fa4-361883222a9c:23116</guid><dc:creator>pubmed: neuroblastoma</dc:creator><slash:comments>0</slash:comments><description>Anaplastic Lymphoma Kinase (ALK) regulates initiation of transcription of MYCN in neuroblastoma cells. Oncogene. 2012 Jan 30; Authors: Schönherr C, Ruuth K, Kamaraj S, Wang CL, Yang HL, Combaret V, Djos A, Martinsson T, Christensen JG, Palmer RH, Hallberg B Abstract Neuroblastoma is a neural crest-derived embryonal tumour of the postganglionic sympathetic nervous system and a disease with several different chromosomal gains and losses, which include MYCN-amplified neuroblastoma on chromosome 2, deletions...(&lt;a href="http://www.neuroblastomafoundation.org/blogs/research/archive/2012/01/31/anaplastic-lymphoma-kinase-alk-regulates-initiation-of-transcription-of-mycn-in-neuroblastoma-cells.aspx"&gt;read more&lt;/a&gt;)&lt;img src="http://www.neuroblastomafoundation.org/aggbug.aspx?PostID=23116" width="1" height="1"&gt;</description><category domain="http://www.neuroblastomafoundation.org/blogs/research/archive/tags/Oncogene/default.aspx">Oncogene</category></item><item><title>NEU4L sialidase overexpression promotes β-catenin signalling in neuroblastoma cells, enhancing stem-like malignant cell growth.</title><link>http://www.neuroblastomafoundation.org/blogs/research/archive/2012/01/31/neu4l-sialidase-overexpression-promotes-catenin-signalling-in-neuroblastoma-cells-enhancing-stem-like-malignant-cell-growth.aspx</link><pubDate>Tue, 31 Jan 2012 11:23:19 GMT</pubDate><guid isPermaLink="false">9a7c9348-2ef3-4ddc-9fa4-361883222a9c:23115</guid><dc:creator>pubmed: neuroblastoma</dc:creator><slash:comments>0</slash:comments><description>NEU4L sialidase overexpression promotes β-catenin signalling in neuroblastoma cells, enhancing stem-like malignant cell growth. Int J Cancer. 2012 Jan 27; Authors: Tringali C, Cirillo F, Lamorte G, Papini N, Anastasia L, Lupo B, Silvestri I, Tettamanti G, Venerando B Abstract Neuroblastoma (NB) is a frequently lethal tumour that occurs in childhood and originates from embryonic neural crest cells. The malignant and aggressive phenotype of NB is strictly related to the de-regulation of pivotal pathways...(&lt;a href="http://www.neuroblastomafoundation.org/blogs/research/archive/2012/01/31/neu4l-sialidase-overexpression-promotes-catenin-signalling-in-neuroblastoma-cells-enhancing-stem-like-malignant-cell-growth.aspx"&gt;read more&lt;/a&gt;)&lt;img src="http://www.neuroblastomafoundation.org/aggbug.aspx?PostID=23115" width="1" height="1"&gt;</description><category domain="http://www.neuroblastomafoundation.org/blogs/research/archive/tags/Int+J+Cancer/default.aspx">Int J Cancer</category></item><item><title>DNA demethylation increases sensitivity of neuroblastoma cells to chemotherapeutic drugs.</title><link>http://www.neuroblastomafoundation.org/blogs/research/archive/2012/01/28/dna-demethylation-increases-sensitivity-of-neuroblastoma-cells-to-chemotherapeutic-drugs.aspx</link><pubDate>Sat, 28 Jan 2012 11:21:32 GMT</pubDate><guid isPermaLink="false">9a7c9348-2ef3-4ddc-9fa4-361883222a9c:22163</guid><dc:creator>pubmed: neuroblastoma</dc:creator><slash:comments>0</slash:comments><description>DNA demethylation increases sensitivity of neuroblastoma cells to chemotherapeutic drugs. Biochem Pharmacol. 2012 Jan 18; Authors: Charlet J, Schnekenburger M, Brown KW, Diederich M Abstract Neuroblastoma is a common embryonal malignancy in which high-stage cases have a poor prognosis, often associated with resistance to chemotherapeutic drugs. DNA methylation alterations are frequent in neuroblastoma and can modulate sensitivity to chemotherapeutic drugs in other cancers, suggesting that manipulation...(&lt;a href="http://www.neuroblastomafoundation.org/blogs/research/archive/2012/01/28/dna-demethylation-increases-sensitivity-of-neuroblastoma-cells-to-chemotherapeutic-drugs.aspx"&gt;read more&lt;/a&gt;)&lt;img src="http://www.neuroblastomafoundation.org/aggbug.aspx?PostID=22163" width="1" height="1"&gt;</description><category domain="http://www.neuroblastomafoundation.org/blogs/research/archive/tags/Biochem+Pharmacol/default.aspx">Biochem Pharmacol</category></item><item><title>Pen-2 overexpression induces Aβ-42 production, memory defect, motor             activity enhancement and feeding behavior dysfunction in NSE/Pen-2 transgenic             mice.</title><link>http://www.neuroblastomafoundation.org/blogs/research/archive/2012/01/27/pen-2-overexpression-induces-a-42-production-memory-defect-motor-activity-enhancement-and-feeding-behavior-dysfunction-in-nse-pen-2-transgenic-mice.aspx</link><pubDate>Fri, 27 Jan 2012 11:16:47 GMT</pubDate><guid isPermaLink="false">9a7c9348-2ef3-4ddc-9fa4-361883222a9c:21874</guid><dc:creator>pubmed: neuroblastoma</dc:creator><slash:comments>0</slash:comments><description>Pen-2 overexpression induces Aβ-42 production, memory defect, motor activity enhancement and feeding behavior dysfunction in NSE/Pen-2 transgenic mice. Int J Mol Med. 2011 Dec;28(6):961-71 Authors: Nam SH, Seo SJ, Goo JS, Kim JE, Choi SI, Lee HR, Hwang IS, Jee SW, Lee SH, Bae CJ, Park JY, Kim HS, Shim SB, Hwang DY Abstract Pen-2 is a key regulator of the γ-secretase complex, which is involved in the production of the amyloid β (Aβ)-42 peptides, which ultimately lead to Alzheimer&amp;#39;s disease (AD...(&lt;a href="http://www.neuroblastomafoundation.org/blogs/research/archive/2012/01/27/pen-2-overexpression-induces-a-42-production-memory-defect-motor-activity-enhancement-and-feeding-behavior-dysfunction-in-nse-pen-2-transgenic-mice.aspx"&gt;read more&lt;/a&gt;)&lt;img src="http://www.neuroblastomafoundation.org/aggbug.aspx?PostID=21874" width="1" height="1"&gt;</description><category domain="http://www.neuroblastomafoundation.org/blogs/research/archive/tags/Int+J+Mol+Med/default.aspx">Int J Mol Med</category></item></channel></rss>
