1. Articles in category: Oncogenesis

    1-5 of 5
    1. Metabolic Adaptation in High-Risk Neuroblastoma Lacking p53

      Neuroblastoma is the most common childhood extracranial solid tumor. In high-risk cases, many of which are characterized by amplification of MYCN, outcome remains poor. Mutations in the p53 (TP53) tumor suppressor are rare at diagnosis, but evidence suggests that p53 function is often impaired in relapsed, treatment-resistant disease.

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      Mentions: Relapse
    2. Gene regulatory mutation linked to rare childhood cancer

      Gene regulatory mutation linked to rare childhood cancer

      ( University of Wisconsin-Madison ) A single defect in a gene that codes for a histone -- a 'spool' that wraps idle DNA -- is linked to pediatric cancers in a study published today in the journal Science. 'Unlike most cancers that require multiple hits, we found that this particular mutation can form a tumor all by itself,' says Peter W. Lewis, an assistant professor of biomolecular chemistry in the School of Medicine and Public Health at the University of Wisconsin-Madison.

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    3. Cell Proliferation in Neuroblastoma.

      Cell Proliferation in Neuroblastoma.

      Cancers (Basel). 2016;8(1)

      Authors: Stafman LL, Beierle EA

      Abstract Neuroblastoma, the most common extracranial solid tumor of childhood, continues to carry a dismal prognosis for children diagnosed with advanced stage or relapsed disease. This review focuses upon factors responsible for cell proliferation in neuroblastoma including transcription factors, kinases, and regulators of the cell cycle.

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    4. Cancer-driving signals cause high-risk neuroblastoma

      Cancer-driving signals cause high-risk neuroblastoma

      "They showed that variants in the LIN28B gene generate abnormal signals that regulate another gene called RAN. The RAN gene, in turn, becomes overactive and produces higher levels of the RAN protein, causing cells to grow out of control in tumours. Acting in both direct and indirect ways, LIN28B also blocks tumour suppressor genes that normally put the brakes on cancer. The research suggests that signals originating in LIN28B ultimately promote another gene called AURKA, already known to play key roles in neuroblastoma and other cancers. All three genes, LIN28B, RAN, and AURKA , function as oncogenes--genes known to drive cancer ...

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    1-5 of 5
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