Research News

Published research supported by the PBTF 

• Amifostine Protects Against Cisplatin-Induced Ototoxicity in Children with Average-Risk Medulloblastoma (Journal of Clinical Oncology. 2008 August 1; 26(22): 3749–3755)
  
• IDH1 and IDH2 Mutations in Gliomas (New England Journal of Medicine 360:765-73, Feb. 19, 2009)
  
• Identification of CD15 as a Marker for Tumor-Propagating Cells in a Mouse Model of Medulloblastoma (Cancer Cell 15:135–147, Feb. 3, 2009)
  
• N-myc alters the fate of preneoplastic cells in a mouse model of medulloblastoma (Genes & Development 23:157–170, Jan. 31, 2009)
  
• Medulloblastoma Can Be Initiated by Deletion of Patched in Lineage-Restricted Progenitors or Stem Cells (Cancer Cell 14:135–145, Aug. 12, 2008)
  
• Even Cancers Want Commitment: Lineage Identity and Medulloblastoma Formation (Cancer Cell 14, Aug. 12, 2008)
  
• Acquisition of Granule Neuron Precursor Identity Is a Critical Determinant of Progenitor Cell Competence to Form Shh-Induced Medulloblastoma (Cancer Cell 14:123–134, Aug. 12, 2008)
  
• Researchers Uncover Errors in Immature Brain Cells in Lab and Animal Studies that May Promote the Growth of Some Brain Tumors (NCI News, Jan. 7, 2008)
  
• Medulloblastoma: Encouraging Data for Reduced RT Dose in Children with Average-Risk Disease (Oncology Times, Nov. 10, 2006, PDF)
  
• PBTF-funded researcher Jeremy Rich, Ph.D. published in AACR (Cancer Research Journal, PDF)
  
• Brain Cancer Cells of Orgin Discovered to Survive Radiation Treatment - Research by Dr. Jeremy Rich, Ph.D., Pediatric Brain Tumor Foundation Institute at Duke researchers published in Nature.  

Articles published in Nature and the National Cancer Institute Bulletin on October 24, 2006, reported on another research project by Dr. Jeremy Rich in which he has isolated from brain tumor tissues "cells of origin" that can survive radiation. He found that these cells could deal with DNA damage from both chemotherapy and radiation more readily than other cells. When these cancer cells were implanted in mice they formed tumors that resembled the original tumors, even after being irradiated.  His team used protein CD133 to distinguish these "cells of origin" from other cells. "Knowing that DNA repair was important, the researchers blocked the DNA-repair response in mice as a potential strategy for overcoming resistance," the article reported. The NCI article went on to say that "the study offers insights into the biology of the tumor that could be relevant to treating patients."  

• PBTF-funded researcher Dr. Erwin Van Meir at Emory University has done a pioneering study that looks at p53's role in tumor-stroma interactions. according to the online version of Oncogene on Oct. 9, 2006.