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eRAM

encyclopedia of Rare Disease Annotation for Precision Medicine




Disease li-fraumeni syndrome
Comorbidity C0017636|glioblastoma
Sentences 4
PubMedID- 24156637 Of interest in this regard is the recent identification, in glioblastoma multiforme, of a mir/tp53 feedback autoregulatory circuit involving expression of p53, e2f1 and myc to regulate expression of mir-25, which in turn controls p53 accumulation [65], most likely via direct targeting of the 3′utr region of tp53 [97].
PubMedID- 22870228 Etienne and colleagues demonstrated that older patients, who often have the de novo (primary) form of gbm, have egfr overexpression which is responsible for increased angiogenesis, edema, and invasion and might account for the decrease in survival in elderly patients [24]; younger patients more often exhibit a secondary form of glioblastoma that is associated with tp53 mutation [24].
PubMedID- 21665183 glioblastoma specimens with tp53 mutations do not show egfrviii amplification.
PubMedID- 26008975 Gx15-070 is unique in that it suppressed bag3 and usp9x levels simultaneously in glioblastoma cells independently of their tp53 status, which most likely further enhanced gx15-070 mediated susceptibility to bh3-mimetics.

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