2018
DOI: 10.1016/j.wneu.2018.08.019
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Towards Molecular Classification of Meningioma: Evolving Treatment and Diagnostic Paradigms

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Cited by 52 publications
(54 citation statements)
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“…The E17K mutation in AKT1 leads to constitutive activation of its gene product, protein kinase B, and stimulates downstream mTOR signaling (12,19,26). Known to be oncogenic in many other cancer types (27), this mutation is found in 7-12% of grade I meningiomas (3,11,12,19), is enriched in the meningothelial subtype (11), and is predictive of decreased progression free survival in olfactory groove tumors (28). Altering the same signaling pathway PIK3CA mutations are also found in ∼7% of non-NF2 tumors, and are mutually exclusive with AKT1 mutation (26).…”
Section: Non-nf2 Meningiomamentioning
confidence: 99%
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“…The E17K mutation in AKT1 leads to constitutive activation of its gene product, protein kinase B, and stimulates downstream mTOR signaling (12,19,26). Known to be oncogenic in many other cancer types (27), this mutation is found in 7-12% of grade I meningiomas (3,11,12,19), is enriched in the meningothelial subtype (11), and is predictive of decreased progression free survival in olfactory groove tumors (28). Altering the same signaling pathway PIK3CA mutations are also found in ∼7% of non-NF2 tumors, and are mutually exclusive with AKT1 mutation (26).…”
Section: Non-nf2 Meningiomamentioning
confidence: 99%
“…Best known for its role in pluripotency, Klf4 is thought to act as a tumor suppressor in meningioma, being robustly expressed in low grade tumors and downregulated in anaplastic tumors (30). At the genetic level, KLF4 is mutated in ∼12% of grade I meningiomas (3,11), virtually all of which are of the secretory sub-type and also harbor TRAF7 mutations (31). All identified KLF4 mutations result in a K409Q substitution within the DNA binding domain, which likely alters or blocks key protein functions (32).…”
Section: Non-nf2 Meningiomamentioning
confidence: 99%
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