Premium
Meningeal hemangiopericytomas: A clinicopathological study with emphasis on MGMT ( O 6 ‐methylguanine‐ DNA methyltransferase) promoter methylation status
Author(s) -
Kakkar Aanchal,
Kumar Anupam,
Jha Prerana,
Goyal Nishant,
Mallick Supriya,
Sharma Mehar Chand,
Suri Ashish,
Singh Manmohan,
Kale Shashank S,
Julka Pramod Kumar,
Sarkar Chitra,
Suri Vaishali
Publication year - 2014
Publication title -
neuropathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.701
H-Index - 61
eISSN - 1440-1789
pISSN - 0919-6544
DOI - 10.1111/neup.12107
Subject(s) - temozolomide , methylation , methyltransferase , dna methylation , o 6 methylguanine dna methyltransferase , immunohistochemistry , cancer research , epigenetics , carcinogenesis , promoter , medicine , biology , cancer , glioblastoma , dna , gene expression , gene , genetics
Meningeal hemangiopericytomas ( HPC s) are aggressive dural‐based tumors, for which no prognostic or predictive marker has been identified. Gross total resection is treatment of choice, but not easily achieved; hence, alkylating agents like temozolomide ( TMZ ) are now being tried. O 6 ‐methylguanine‐ DNA methyltransferase ( MGMT ) promoter methylation has proven prognostic and predictive value in glioblastomas. This study evaluates MGMT promoter methylation in meningeal HPC s to determine its role in HPC oncogenesis and its association with patient outcome. Meningeal HPC s diagnosed between 2002 and 2011 were retrieved and clinicopathological features reviewed. MGMT promoter methylation status was assessed by methylation‐specific polymerase chain reaction ( MSP ) and immunohistochemistry ( IHC ) for MGMT protein. HPC s accounted for 1.1% of all CNS tumors. Forty cases were analyzed; the majority were adults (mean age = 41.4 years). Seventy percent were primary and 30% were recurrent tumors; 60% were grade II and 40% were grade III . MGMT promoter methylation was identified in 45% of cases, including Grade II (54.2%) and Grade III (31.3%) ( P = 0.203). Promoter methylation was significantly ( P = 0.035) more frequent in primary (57.1%) than in recurrent (16.7%) tumors. No correlation was noted between MGMT promoter methylation by MSP and MGMT protein expression by IHC , or with progression‐free survival. Thus, a significant proportion of HPC s demonstrate MGMT promoter methylation, suggesting possible susceptibility to TMZ . As promoter methylation is more frequent in primary tumors, TMZ may serve as a therapeutic option in residual primary tumors. Epigenetic inactivation of MGMT in HPC s necessitates the assessment of prognostic and predictive value of MGMT promoter methylation in HPC s in larger clinical trials.