1. Articles in category: Small Molecules

    1-16 of 16
    1. 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
    2. 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
    3. PARP inhibitors enhance replication stress and cause mitotic catastrophe in MYCN-dependent neuroblastoma.

      PARP inhibitors enhance replication stress and cause mitotic catastrophe in MYCN-dependent neuroblastoma.

      Oncogene. 2017 Apr 10;:

      Authors: Colicchia V, Petroni M, Guarguaglini G, Sardina F, Sahún-Roncero M, Carbonari M, Ricci B, Heil C, Capalbo C, Belardinilli F, Coppa A, Peruzzi G, Screpanti I, Lavia P, Gulino A, Giannini G

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      Mentions: MYCN
    4. 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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    5. A Phase I/II, Multicenter, OPEN-LABEL, DOSE-ESCALATION Study Of The Safety And Pharmacokinetics Ofcobimetinib In Pediatric And Young Adult Patients With Previously Treated Solid Tumors

      EudraCT Number: 2014-004685-25Sponsor Protocol Number: GO29665Sponsor Name: F. Hoffmann-La Roche LtdStart Date: 2016-04-28Medical condition: Solid TumorsDisease: Version: 19.0SOC Term: 100000004864Classification Code: 10065252Term: Solid tumorLevel: LLTPopulation Age: Children, Adolescents, Under 18, AdultsGender: Male, FemaleTrial Protocol: DE (Ongoing)

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    6. Many Targeted Cancer Therapies Suppress T Cell Immune Responses

      PHILADELPHIA--(March 22, 2016)--In many cases, targeted therapies for cancer are preferred as treatments over chemotherapy and surgery because they attack and kill cancer cells with specific tumor-promoting mutations while sparing healthy, normal cells that do not express these mutations. In clinical trials, a heavy emphasis on the effects of targeted therapies on tumor cells has been explored, but the effects they have on the immune system have not been thoroughly investigated.

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    7. Advances in the translational genomics of neuroblastoma: From improving risk stratification and revealing novel biology to identifying actionable genomic alterations.

      "However, the clonally acquired, oncogenic aberrations in relapsed neuroblastomas are currently being defined and may offer an opportunity to improve patient outcomes with molecularly targeted therapy directed toward aberrantly regulated pathways in relapsed disease. This review summarizes the current state of knowledge about neuroblastoma genetics and genomics, highlighting the improved prognostication and potential therapeutic opportunities that have arisen from recent advances in understanding germline predisposition, recurrent segmental chromosomal alterations, somatic point mutations and translocations, and clonal evolution in relapsed neuroblastoma."

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      Mentions: MYCN Genetics
    8. PDK1-mTOR signaling pathway inhibitors reduce cell proliferation in MK2206 resistant neuroblastoma cells.

      PDK1-mTOR signaling pathway inhibitors reduce cell proliferation in MK2206 resistant neuroblastoma cells.

      Cancer Cell Int. 2015;15:91

      Authors: Qi L, Toyoda H, Xu DQ, Zhou Y, Sakurai N, Amano K, Kihira K, Hori H, Azuma E, Komada Y

      Abstract PURPOSE: AKT plays a pivotal role in the signal transduction of cancer cells. MK2206, an AKT inhibitor, has been shown to be an effective anti-cancer drug to a variety of cancer cell lines.

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    9. PLK1 INHIBITION: PROSPECTIVE ROLE FOR THE TREATMENT OF PEDIATRIC TUMORS.

      PLK1 INHIBITION: PROSPECTIVE ROLE FOR THE TREATMENT OF PEDIATRIC TUMORS.

      Curr Drug Targets. 2015 Aug 25;

      Authors: Pezuk JA, Valera ET, Brassesco MS

      Abstract Over the years, polo-like kinase 1 (PLK1) has garnered great interest as a therapeutic target. The PLK1 is a member of a highly conserved serine/threonine kinase family that plays pivotal roles in mitosis, cytokinesis and DNA damage response in eukaryotic cells.

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    10. PI3K Inhibitor Combined With Chemotherapy Can Enhance the Apoptosis of Neuroblastoma Cells In Vitro and In Vivo.

      1Department of General Surgery, Children's Hospital of Zhengzhou, Henan, China. 2Division of Surgery, Hospital of Chinese Medicine, Zhangqiu, Shandong, China. 3Department of Neurosurgery, People's Hospital of Weifang, Shandong, China xinghongshun@163.com. Activation of the phosphoinositide 3-kinase (PI3K)/Akt signaling pathway is a novel poor prognostic indicator of neuroblastoma (NB), and the positive effects of chemotherapy on NB have been confirmed.

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    11. GD2 ganglioside specific antibody treatment downregulates PI3K/Akt/mTOR signaling network in human neuroblastoma cell lines.

      Mechanisms leading to inhibitory effects of an anti-GD2 ganglioside (GD2) 14G2a mouse monoclonal antibody (mAb) and PI3K/Akt/mTOR pathway inhibitors on human neuroblastoma cell survival were studied in vitro. We have recently shown on IMR-32, CHP‑134, and LA-N-1 neuroblastoma cells that targeting GD2 with the mAb decreases cell viability of the cell lines. In this study we used cytotoxicity assays, proteomic arrays and immunoblotting to evaluate the response of the three cell lines to the anti‑GD2 14G2a mAb and specific PI3K/Akt/mTOR pathway inhibitors.

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    1-16 of 16
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