1. Articles in category: Pre-Clinical

    1-24 of 518 1 2 3 4 ... 20 21 22 »
    1. Chemoimmunotherapeutic effect of combined treatment with ex vivo generated antigen-presenting immune cells and conventional antitumor agents in a mouse neuroblastoma model.

      Chemoimmunotherapeutic effect of combined treatment with ex vivo generated antigen-presenting immune cells and conventional antitumor agents in a mouse neuroblastoma model.

      J Pediatr Surg. 2017 Apr 21;:

      Authors: Inoue S, Setoyama Y, Odaka A, Kitagawa D, Beck Y

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      Mentions: Treatment
    2. The second-generation ALK inhibitor alectinib effectively induces apoptosis in human neuroblastoma cells and inhibits tumor growth in a TH-MYCN transgenic neuroblastoma mouse model.

      The second-generation ALK inhibitor alectinib effectively induces apoptosis in human neuroblastoma cells and inhibits tumor growth in a TH-MYCN transgenic neuroblastoma mouse model.

      Cancer Lett. 2017 Apr 25;:

      Authors: Lu J, Guan S, Zhao Y, Yu Y, Woodfield SE, Zhang H, Yang KL, Bieerkehazhi S, Qi L, Li X, Gu J, Xu X, Jin J, Muscal JA, Yang T, Xu GT, Yang J

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      Mentions: ALK MYCN
    3. Immunoassays for the quantification of ALK and phosphorylated ALK support the evaluation of on-target ALK inhibitors in neuroblastoma.

      Immunoassays for the quantification of ALK and phosphorylated ALK support the evaluation of on-target ALK inhibitors in neuroblastoma.

      Mol Oncol. 2017 Apr 22;:

      Authors: Tucker ER, Tall JR, Danielson LS, Gowan S, Jamin Y, Robinson SP, Banerji U, Chesler L

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      Mentions: ALK
    4. Tolcapone induces oxidative stress leading to apoptosis and inhibition of tumor growth in Neuroblastoma.

      Tolcapone induces oxidative stress leading to apoptosis and inhibition of tumor growth in Neuroblastoma.

      Cancer Med. 2017 Apr 21;:

      Authors: Maser T, Rich M, Hayes D, Zhao P, Nagulapally AB, Bond J, Saulnier Sholler G

      Abstract Catechol-O-methyltransferase (COMT) is an enzyme that inactivates dopamine and other catecholamines by O-methylation.

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    5. Combined ALK and MDM2 inhibition increases antitumor activity and overcomes resistance in human ALK mutant neuroblastoma cell lines and xenograft models.

      Combined ALK and MDM2 inhibition increases antitumor activity and overcomes resistance in human ALK mutant neuroblastoma cell lines and xenograft models.

      Elife. 2017 Apr 20;6:

      Authors: Wang HQ, Halilovic E, Li X, Liang J, Cao Y, Rakiec DP, Ruddy DA, Jeay S, Wuerthner JU, Timple N, Kasibhatla S, Li N, Williams JA, Sellers WR, Huang A, Li F

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      Mentions: ALK MYCN
    6. Armed Oncolytic Adenovirus-Expressing PD-L1 Mini-Body Enhances Antitumor Effects of Chimeric Antigen Receptor T Cells in Solid Tumors

      Chimeric antigen receptor–modified T cells (CAR T cells) produce proinflammatory cytokines that increase expression of T-cell checkpoint signals such as PD-L1, which may inhibit their functionality against solid tumors. In this study, we evaluated in human tumor xenograft models the proinflammatory properties of an oncolytic adenovirus (Onc.Ad) with a helper-dependent Ad (HDAd) that expresses a PD-L1 blocking mini-antibody (mini-body; HDPDL1) as a strategy to enhance CAR T-cell killing.

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      Mentions: Antibody PD-1
    7. Butyrylcholinesterase as a Blood Biomarker in Neuroblastoma.

      Butyrylcholinesterase as a Blood Biomarker in Neuroblastoma.

      J Pediatr Hematol Oncol. 2017 Apr 03;:

      Authors: Coulter DW, Boettner AD, Kortylewicz ZP, Enke SP, Luther JA, Verma V, Baranowska-Kortylewicz J

      Abstract Blood-based biomarkers are important in the detection of the disease and in the assessment of responses to therapy.

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      Mentions: MYCN Biomarkers
    8. Impact of shared care program in follow-up of childhood cancer survivors: An intervention study

      With the growing rate of childhood cancer cure and the risks of sequelae, long-term follow-up (FU) of survivors is a central issue. Several models have been proven far from satisfactory. Shared care FU is the result of collaboration between general practitioners (GPs) and cancer centers. We sought to demonstrate the feasibility of setting up a shared care program based on the patient-centered education of GPs and to evaluate the impact of this model in an intervention study.

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    9. Therapeutic Potential of Bacteria against Solid Tumors

      Intentional bacterial infections can produce efficacious antitumor responses in mice, rats, dogs, and humans. However, low overall success rates and intense side effects prevent such approaches from being employed clinically. In this work, we titered bacteria and/or the proinflammatory cytokine TNFα in a set of established murine models of cancer.

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      Mentions: Side Effects
    10. Optimization of a Neural Stem-Cell-Mediated Carboxylesterase/Irinotecan Gene Therapy for Metastatic Neuroblastoma.

      Optimization of a Neural Stem-Cell-Mediated Carboxylesterase/Irinotecan Gene Therapy for Metastatic Neuroblastoma.

      Mol Ther Oncolytics. 2017 Mar 17;4:67-76

      Authors: Gutova M, Goldstein L, Metz M, Hovsepyan A, Tsurkan LG, Tirughana R, Tsaturyan L, Annala AJ, Synold TW, Wan Z, Seeger R, Anderson C, Moats RA, Potter PM, Aboody KS

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    11. P450 inhibitor ketoconazole increased the intratumor drug levels and antitumor activity of fenretinide in human neuroblastoma xenograft models.

      P450 inhibitor ketoconazole increased the intratumor drug levels and antitumor activity of fenretinide in human neuroblastoma xenograft models.

      Int J Cancer. 2017 Mar 24;:

      Authors: Lopez-Barcons L, Maurer BJ, Kang MH, Reynolds CP

      Abstract We previously reported that concurrent ketoconazole, an oral anti-fungal agent and P450 enzyme inhibitor, increased plasma levels of the cytotoxic retinoid, fenretinide (4-HPR) in mice.

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    12. Lin BioScience Licenses a Novel Anti-Cancer Therapy for Hematological Malignancies and Solid Tumors from Columbia University and Memorial Sloan Kettering Cancer Center

      Lin BioScience Licenses a Novel Anti-Cancer Therapy for Hematological Malignancies and Solid Tumors from Columbia University and Memorial Sloan Kettering Cancer Center

      SAN DIEGO, March 3, 2017 /PRNewswire/ -- Lin BioScience has licensed the intellectual property portfolio for a novel inhibitor of CDC7 kinase. Under this worldwide exclusive licensing agreement with Columbia University and Memorial Sloan Kettering Cancer Center, Lin BioScience plans to...

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    13. Heparin-binding epidermal growth factor-like growth factor promotes neuroblastoma differentiation.

      Heparin-binding epidermal growth factor-like growth factor promotes neuroblastoma differentiation.

      FASEB J. 2017 Feb 07;:

      Authors: Gaviglio AL, Knelson EH, Blobe GC

      Abstract High-risk neuroblastoma is characterized by undifferentiated neuroblasts and low Schwannian stroma content. The tumor stroma contributes to the suppression of tumor growth by releasing soluble factors that promote neuroblast differentiation.

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    14. Targeting Neuroblastoma Cell Surface Proteins: Recommendations for Homology Modeling of hNET, ALK, and TrkB.

      Targeting Neuroblastoma Cell Surface Proteins: Recommendations for Homology Modeling of hNET, ALK, and TrkB.

      Front Mol Neurosci. 2017;10:7

      Authors: Haddad Y, Heger Z, Adam V

      Abstract Targeted therapy is a promising approach for treatment of neuroblastoma as evident from the large number of targeting agents employed in clinical practice today.

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      Mentions: Treatment ALK
    15. Aurora A kinase inhibition enhances oncolytic herpes virotherapy through cytotoxic synergy and innate cellular immune modulation.

      Aurora A kinase inhibition enhances oncolytic herpes virotherapy through cytotoxic synergy and innate cellular immune modulation.

      Oncotarget. 2017 Jan 28;:

      Authors: Currier MA, Sprague L, Rizvi TA, Nartker B, Chen CY, Wang PY, Hutzen BJ, Franczek MR, Patel AV, Chaney KE, Streby KA, Ecsedy JA, Conner J, Ratner N, Cripe TP

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    16. A Metastatic Mouse Model Identifies Genes That Regulate Neuroblastoma Metastasis

      Metastatic relapse is the major cause of death in pediatric neuroblastoma, where there remains a lack of therapies to target this stage of disease. To understand the molecular mechanisms mediating neuroblastoma metastasis, we developed a mouse model using intracardiac injection and in vivo selection to isolate malignant cell subpopulations with a higher propensity for metastasis to bone and the central nervous system.

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      Mentions: Relapse Metastasis
    17. Transfer of Allogeneic CD4+ T Cells Rescues CD8+ T Cells in Anti-PD-L1-Resistant Tumors Leading to Tumor Eradication

      Adoptively transferred CD8+ T cells can stabilize the size of solid tumors over long periods of time by exclusively recognizing antigen cross-presented on tumor stroma. However, these tumors eventually escape T-cell–mediated growth control. The aim of this study was to eradicate such persistent cancers. In our model, the SIYRYYGL antigen is expressed by cancer cells that lack the MHC-I molecule Kb needed for direct presentation, but the antigen is picked up and cross-presented by tumor stroma.

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      Mentions: PD-1
    18. Dual ALK and CDK4/6 inhibition demonstrates on-target synergy against neuroblastoma.

      "The combination of Ribociclib, a dual inhibitor of cyclin-dependent kinase (CDK) 4 and 6, and the ALK inhibitor Ceritinib demonstrated higher cytotoxicity (p=0.008) and synergy scores (p=0.006) in cell lines with ALK mutations as compared to cell lines lacking mutations or alterations in ALK. Compared to either drug alone, combination therapy enhanced growth inhibition, cell cycle arrest, and caspase-independent cell death. Combination therapy achieved complete regressions in neuroblastoma xenografts with ALK-F1174L and F1245C de novo resistance mutations, and prevented the emergence of resistance. Murine Ribociclib and Ceritinib plasma concentrations were unaltered by combination therapy.  This preclinical ...

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      Mentions: ALK
    19. Bromodomain and extraterminal protein inhibitors in pediatrics: A review of the literature

      "The last few years have seen the identification of pharmacologic approaches to target bromodomain and extraterminal (BET) proteins for cancer treatment. These proteins have an essential role in gene transcription regulation by binding acetylated lysine residues on histone tails, activating gene transcription. BET inhibitors have been tested in preclinical models including pediatric malignancies and several adult clinical trials are ongoing."

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      Mentions: Treatment
    20. The BET bromodomain inhibitor exerts the most potent synergistic anticancer effects with quinone-containing compounds and anti-microtubule drugs.

      "Treatment with JQ1 blocked the recruitment of Nrf2 to the antioxidant responsive elements at Nrf2 target gene promoters, and JQ1 exerted synergistic anticancer effects with nanaomycin by blocking the Nrf2-antioxidant signaling pathway. JQ1 and vincristine synergistically induced neuroblastoma cell cycle arrest at the G2/M phase, aberrant mitotic spindle assembly formation and apoptosis, but showed no effect on cell survival in normal non-malignant cells. Importantly, co-treatment with JQ1 and vincristine synergistically suppressed tumor progression in neuroblastoma-bearing mice. These results strongly suggest that patients treated with BET bromodomain inhibitors in clinical trials should be co-treated with vincristine."

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      Mentions: Treatment
    21. Efficient Killing of High Risk Neuroblastoma Using Natural Killer Cells Activated by Plasmacytoid Dendritic Cells.

      "Here, we developed a novel approach to improve the current anti-GD2 immunotherapy based on NK cell stimulation using toll-like receptor (TLR)-activated plasmacytoid dendritic cells (pDCs). We demonstrated that this strategy led to the efficient killing of NB cells. When the expression of GD2 was heterogeneous on NB cells, the combination of pDC-mediated NK-cell activation and anti-GD2 treatment significantly increased the cytotoxicity of NK cells against NB cells. Activation by pDCs led to a unique NK-cell phenotype characterized by increased surface expression of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), with increased expression of CD69 on CD56dim cytotoxic cells, and strong ...

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      Mentions: Antibody Treatment
    1-24 of 518 1 2 3 4 ... 20 21 22 »
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