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<?xml-stylesheet type="text/xsl" href="http://www.neuroblastomafoundation.org/utility/FeedStylesheets/atom.xsl" media="screen"?><feed xmlns="http://www.w3.org/2005/Atom" xml:lang="en"><title type="html">Neuroblastoma Research</title><subtitle type="html" /><id>http://www.neuroblastomafoundation.org/blogs/research/atom.aspx</id><link rel="alternate" type="text/html" href="http://www.neuroblastomafoundation.org/blogs/research/default.aspx" /><link rel="self" type="application/atom+xml" href="http://www.neuroblastomafoundation.org/blogs/research/atom.aspx" /><generator uri="http://communityserver.org" version="4.1.40407.4157">Community Server</generator><updated>2012-02-01T04:41:59Z</updated><entry><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 rel="alternate" type="text/html" href="/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" /><id>/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</id><published>2012-02-04T11:46:08Z</published><updated>2012-02-04T11:46:08Z</updated><content type="html">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;</content><author><name>Anonymous</name><uri>http://www.neuroblastomafoundation.org/members/Anonymous/default.aspx</uri></author><category term="PLoS One" scheme="http://www.neuroblastomafoundation.org/blogs/research/archive/tags/PLoS+One/default.aspx" /></entry><entry><title>Acitretin, an Enhancer of Alpha-Secretase Expression, Crosses the Blood-Brain Barrier and Is Not Eliminated by P-Glycoprotein.</title><link rel="alternate" type="text/html" href="/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" /><id>/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</id><published>2012-02-04T11:46:08Z</published><updated>2012-02-04T11:46:08Z</updated><content type="html">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;</content><author><name>Anonymous</name><uri>http://www.neuroblastomafoundation.org/members/Anonymous/default.aspx</uri></author><category term="Neurodegener Dis" scheme="http://www.neuroblastomafoundation.org/blogs/research/archive/tags/Neurodegener+Dis/default.aspx" /></entry><entry><title>The dopamine metabolite aminochrome inhibits mitochondrial complex I and modifies the expression of iron transporters DMT1 and FPN1.</title><link rel="alternate" type="text/html" href="/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" /><id>/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</id><published>2012-02-04T11:46:07Z</published><updated>2012-02-04T11:46:07Z</updated><content type="html">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;</content><author><name>Anonymous</name><uri>http://www.neuroblastomafoundation.org/members/Anonymous/default.aspx</uri></author><category term="Biometals" scheme="http://www.neuroblastomafoundation.org/blogs/research/archive/tags/Biometals/default.aspx" /></entry><entry><title>Novel GαS-Protein Signaling Associated with Membrane-Tethered Amyloid Precursor Protein Intracellular Domain.</title><link rel="alternate" type="text/html" href="/blogs/research/archive/2012/02/04/novel-g-s-protein-signaling-associated-with-membrane-tethered-amyloid-precursor-protein-intracellular-domain.aspx" /><id>/blogs/research/archive/2012/02/04/novel-g-s-protein-signaling-associated-with-membrane-tethered-amyloid-precursor-protein-intracellular-domain.aspx</id><published>2012-02-04T11:45:40Z</published><updated>2012-02-04T11:45:40Z</updated><content type="html">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;</content><author><name>Anonymous</name><uri>http://www.neuroblastomafoundation.org/members/Anonymous/default.aspx</uri></author><category term="J Neurosci" scheme="http://www.neuroblastomafoundation.org/blogs/research/archive/tags/J+Neurosci/default.aspx" /></entry><entry><title>An extension of the single threshold design for monitoring efficacy and safety in phase II clinical trials.</title><link rel="alternate" type="text/html" href="/blogs/research/archive/2012/02/03/an-extension-of-the-single-threshold-design-for-monitoring-efficacy-and-safety-in-phase-ii-clinical-trials.aspx" /><id>/blogs/research/archive/2012/02/03/an-extension-of-the-single-threshold-design-for-monitoring-efficacy-and-safety-in-phase-ii-clinical-trials.aspx</id><published>2012-02-03T11:06:05Z</published><updated>2012-02-03T11:06:05Z</updated><content type="html">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;</content><author><name>Anonymous</name><uri>http://www.neuroblastomafoundation.org/members/Anonymous/default.aspx</uri></author><category term="Stat Med" scheme="http://www.neuroblastomafoundation.org/blogs/research/archive/tags/Stat+Med/default.aspx" /></entry><entry><title>Childhood cancer incidence and survival 2003-2005, Thailand: study from the thai pediatric oncology group.</title><link rel="alternate" type="text/html" href="/blogs/research/archive/2012/02/03/childhood-cancer-incidence-and-survival-2003-2005-thailand-study-from-the-thai-pediatric-oncology-group.aspx" /><id>/blogs/research/archive/2012/02/03/childhood-cancer-incidence-and-survival-2003-2005-thailand-study-from-the-thai-pediatric-oncology-group.aspx</id><published>2012-02-03T11:06:05Z</published><updated>2012-02-03T11:06:05Z</updated><content type="html">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;</content><author><name>Anonymous</name><uri>http://www.neuroblastomafoundation.org/members/Anonymous/default.aspx</uri></author><category term="Asian Pac J Cancer Prev" scheme="http://www.neuroblastomafoundation.org/blogs/research/archive/tags/Asian+Pac+J+Cancer+Prev/default.aspx" /></entry><entry><title>Cellular consequences of the expression of Alzheimer's disease-causing presenilin 1 mutations in human neuroblastoma (SH-SY5Y) cells.</title><link rel="alternate" type="text/html" href="/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" /><id>/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</id><published>2012-02-03T11:06:05Z</published><updated>2012-02-03T11:06:05Z</updated><content type="html">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;</content><author><name>Anonymous</name><uri>http://www.neuroblastomafoundation.org/members/Anonymous/default.aspx</uri></author><category term="Brain Res" scheme="http://www.neuroblastomafoundation.org/blogs/research/archive/tags/Brain+Res/default.aspx" /></entry><entry><title>Protection of prenylated flavonoids from mori cortex radicis (Moraceae) against nitric oxide-induced cell death in neuroblastoma SH-SY5Y cells.</title><link rel="alternate" type="text/html" href="/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" /><id>/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</id><published>2012-02-03T11:06:04Z</published><updated>2012-02-03T11:06:04Z</updated><content type="html">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;</content><author><name>Anonymous</name><uri>http://www.neuroblastomafoundation.org/members/Anonymous/default.aspx</uri></author><category term="Arch Pharm Res" scheme="http://www.neuroblastomafoundation.org/blogs/research/archive/tags/Arch+Pharm+Res/default.aspx" /></entry><entry><title>Arylpiperazine Dopamineric Ligands Protect Neuroblastoma Cells from Nitric Oxide (NO)-Induced Mitochondrial Damage and Apoptosis.</title><link rel="alternate" type="text/html" href="/blogs/research/archive/2012/02/03/arylpiperazine-dopamineric-ligands-protect-neuroblastoma-cells-from-nitric-oxide-no-induced-mitochondrial-damage-and-apoptosis.aspx" /><id>/blogs/research/archive/2012/02/03/arylpiperazine-dopamineric-ligands-protect-neuroblastoma-cells-from-nitric-oxide-no-induced-mitochondrial-damage-and-apoptosis.aspx</id><published>2012-02-03T11:06:04Z</published><updated>2012-02-03T11:06:04Z</updated><content type="html">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;</content><author><name>Anonymous</name><uri>http://www.neuroblastomafoundation.org/members/Anonymous/default.aspx</uri></author><category term="ChemMedChem" scheme="http://www.neuroblastomafoundation.org/blogs/research/archive/tags/ChemMedChem/default.aspx" /></entry><entry><title>Tumor-initiating cells in childhood neuroblastoma--letter.</title><link rel="alternate" type="text/html" href="/blogs/research/archive/2012/02/03/tumor-initiating-cells-in-childhood-neuroblastoma-letter.aspx" /><id>/blogs/research/archive/2012/02/03/tumor-initiating-cells-in-childhood-neuroblastoma-letter.aspx</id><published>2012-02-03T11:06:04Z</published><updated>2012-02-03T11:06:04Z</updated><content type="html">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;</content><author><name>Anonymous</name><uri>http://www.neuroblastomafoundation.org/members/Anonymous/default.aspx</uri></author><category term="Cancer Res" scheme="http://www.neuroblastomafoundation.org/blogs/research/archive/tags/Cancer+Res/default.aspx" /></entry><entry><title>Tumor-initiating cells in childhood neuroblastoma--response.</title><link rel="alternate" type="text/html" href="/blogs/research/archive/2012/02/03/tumor-initiating-cells-in-childhood-neuroblastoma-response.aspx" /><id>/blogs/research/archive/2012/02/03/tumor-initiating-cells-in-childhood-neuroblastoma-response.aspx</id><published>2012-02-03T11:06:04Z</published><updated>2012-02-03T11:06:04Z</updated><content type="html">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;</content><author><name>Anonymous</name><uri>http://www.neuroblastomafoundation.org/members/Anonymous/default.aspx</uri></author><category term="Cancer Res" scheme="http://www.neuroblastomafoundation.org/blogs/research/archive/tags/Cancer+Res/default.aspx" /></entry><entry><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 rel="alternate" type="text/html" href="/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" /><id>/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</id><published>2012-02-03T11:05:52Z</published><updated>2012-02-03T11:05:52Z</updated><content type="html">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;</content><author><name>Anonymous</name><uri>http://www.neuroblastomafoundation.org/members/Anonymous/default.aspx</uri></author><category term="Int J Biol Sci" scheme="http://www.neuroblastomafoundation.org/blogs/research/archive/tags/Int+J+Biol+Sci/default.aspx" /></entry><entry><title>Influence of a 50 Hz magnetic field and of all-trans‑retinol on the             proliferation of human cancer cell lines.</title><link rel="alternate" type="text/html" href="/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" /><id>/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</id><published>2012-02-02T12:01:00Z</published><updated>2012-02-02T12:01:00Z</updated><content type="html">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;</content><author><name>Anonymous</name><uri>http://www.neuroblastomafoundation.org/members/Anonymous/default.aspx</uri></author><category term="Int J Oncol" scheme="http://www.neuroblastomafoundation.org/blogs/research/archive/tags/Int+J+Oncol/default.aspx" /></entry><entry><title>Shifting from Population-wide to Personalized Cancer Prognosis with Microarrays.</title><link rel="alternate" type="text/html" href="/blogs/research/archive/2012/02/02/shifting-from-population-wide-to-personalized-cancer-prognosis-with-microarrays.aspx" /><id>/blogs/research/archive/2012/02/02/shifting-from-population-wide-to-personalized-cancer-prognosis-with-microarrays.aspx</id><published>2012-02-02T12:00:59Z</published><updated>2012-02-02T12:00:59Z</updated><content type="html">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;</content><author><name>Anonymous</name><uri>http://www.neuroblastomafoundation.org/members/Anonymous/default.aspx</uri></author><category term="PLoS One" scheme="http://www.neuroblastomafoundation.org/blogs/research/archive/tags/PLoS+One/default.aspx" /></entry><entry><title>Calpastatin upregulation in Mycoplasma hyorhinis-infected cells is promoted by the mycoplasma lipoproteins via the NF-κB pathway.</title><link rel="alternate" type="text/html" href="/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" /><id>/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</id><published>2012-02-01T11:41:59Z</published><updated>2012-02-01T11:41:59Z</updated><content type="html">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;</content><author><name>Anonymous</name><uri>http://www.neuroblastomafoundation.org/members/Anonymous/default.aspx</uri></author><category term="Cell Microbiol" scheme="http://www.neuroblastomafoundation.org/blogs/research/archive/tags/Cell+Microbiol/default.aspx" /></entry></feed>
