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MeSH Review

Brain Neoplasms

 
 
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Disease relevance of Brain Neoplasms

 

Psychiatry related information on Brain Neoplasms

 

High impact information on Brain Neoplasms

  • Reduced levels of N-acetylaspartate in malignant brain tumors [11].
  • In brat or prospero mutants, both daughter cells grow and behave like neuroblasts leading to the formation of larval brain tumors [12].
  • These findings provide evidence that alterations in the NF2 transcript occur not only in the hereditary brain neoplasms typically associated with NF2, but also as somatic mutations in their sporadic counterparts and in seemingly unrelated tumour types [13].
  • Children under 36 months of age with biopsy-proved malignant brain tumors were treated postoperatively with two 28-day cycles of cyclophosphamide plus vincristine, followed by one 28-day cycle of cisplatin plus etoposide [14].
  • It has been hypothesized that a high dietary intake of nitrosamines and their precursors, nitrites and nitrates, is a risk factor for brain tumors [15].
 

Chemical compound and disease context of Brain Neoplasms

 

Biological context of Brain Neoplasms

 

Anatomical context of Brain Neoplasms

 

Gene context of Brain Neoplasms

  • In addition, we found that the transcriptional repressor protein, lethal (3) malignant brain tumor protein, L(3)MBT, and the histone deacetylase, Rpd3, associated with the Myb-MuvB complex [29].
  • We report here that in 55% (64/117) of cases, histologically normal brain tissue adjacent to primary human brain tumors lacked detectable MGMT activity [methyl excision repair-defective (Mer-) status] [30].
  • A small-molecule antagonist of CXCR4 inhibits intracranial growth of primary brain tumors [31].
  • Ptc+/- p53-/- mice provide a useful model for investigation of the molecular bases of medulloblastoma and for evaluation of the efficacy of therapeutic intervention strategies in a spontaneously arising endogenous brain tumor [32].
  • Notch1 and notch2 have opposite effects on embryonal brain tumor growth [33].
  • Our results suggest that common variants in the SOD2, SOD3, and CAT genes may influence brain tumor risk [34].
  • 61% of the malignant brain tumors expressed programmed death ligand-1 (PD-L1), while the inhibitory PD-1 receptor was expressed on CD4+ effector cells present in 26% of tumors [35].
 

Analytical, diagnostic and therapeutic context of Brain Neoplasms

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