{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,27]],"date-time":"2026-08-27T16:21:07Z","timestamp":1787847667730,"version":"build-2784847793"},"reference-count":30,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"1","content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2021,1]]},"abstract":"\n Background:<\/jats:title>\n \n Telomerase reverse transcriptase promoter<\/jats:italic>\n (\n pTERT)<\/jats:italic>\n mutation is a dominant altered telomere maintenance mechanism in primary glioblastomas (GBMs).\n <\/jats:p>\n <\/jats:sec>\n \n Objective:<\/jats:title>\n \n The aim of this study was to correlate\n pTERT<\/jats:italic>\n mutations with clinico-histological features and other molecular markers (p53 protein-expression,\n ATRX<\/jats:italic>\n protein-expression,\n IDH<\/jats:italic>\n mutations,\n EGFR<\/jats:italic>\n gene amplification and\n MGMT<\/jats:italic>\n methylation) in adult GBMs.\n <\/jats:p>\n <\/jats:sec>\n \n Materials and Methods:<\/jats:title>\n \n Evaluated for histological patterns, p53 and\n ATRX<\/jats:italic>\n protein expression by immunohistochemistry (IHC),\n IDH<\/jats:italic>\n mutations by IHC followed by sequencing in IHC negative cases,\n EGFR<\/jats:italic>\n gene amplification by fluorescence\n in situ<\/jats:italic>\n hybridization,\n MGMT<\/jats:italic>\n promoter methylation by methylation-specific PCR and\n pTERT<\/jats:italic>\n mutation by sequencing.\n <\/jats:p>\n <\/jats:sec>\n \n Results:<\/jats:title>\n \n A total of 155 adult supratentorial GBMs [age-range 20-80 years] formed study cohort. 15.6% were\n IDH1R132<\/jats:italic>\n mutated, none were\n IDH2R172<\/jats:italic>\n mutated and 27% were\n EGFR<\/jats:italic>\n amplified. 43% were MGMT methylated and were more common with\n IDH-<\/jats:italic>\n mutation (\n mIDH<\/jats:italic>\n ) than\n EGFR<\/jats:italic>\n amplification. 90% of\n mIDH<\/jats:italic>\n (but no\n EGFR<\/jats:italic>\n amplified) cases showed ATRX-loss. 43.5% were\n pTERT<\/jats:italic>\n mutated (C228T was the commonest type) and were mutually exclusive with ATRX-loss. 14% of\n mIDH<\/jats:italic>\n and 42% of\n EGFR<\/jats:italic>\n amplified cases showed\n pTERT<\/jats:italic>\n mutation, the latter was more commonly\n pMGMT<\/jats:italic>\n unmethylated (63.6%).\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions:<\/jats:title>\n \n 43.5% of the GBMs showed\n pTERT<\/jats:italic>\n mutation (C228T was commonest; 72%).\n pTERT<\/jats:italic>\n mutations were mutually exclusive with\n ATRX<\/jats:italic>\n protein loss, more commonly associated with\n IDH<\/jats:italic>\n wild type and\n EGFR<\/jats:italic>\n amplified GBMs.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.4103\/0028-3886.310096","type":"journal-article","created":{"date-parts":[[2021,4,26]],"date-time":"2021-04-26T01:22:00Z","timestamp":1619400120000},"page":"126-134","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":5,"title":["TERT Promoter Mutation in Adult Glioblastomas: It's Correlation with Other Relevant Molecular Markers"],"prefix":"10.4103","volume":"69","author":[{"given":"Mukesh","family":"Barange","sequence":"first","affiliation":[{"name":"Department of Pathology (Including Division of Molecular Pathology), Tata Memorial Hospital and ACTREC, Tata Memorial Centre, Homi Bhabha National Institute, Parel, Mumbai, Maharashtra, India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sridhar","family":"Epari","sequence":"additional","affiliation":[{"name":"Department of Pathology (Including Division of Molecular Pathology), Tata Memorial Hospital and ACTREC, Tata Memorial Centre, Homi Bhabha National Institute, Parel, Mumbai, Maharashtra, India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mamta","family":"Gurav","sequence":"additional","affiliation":[{"name":"Department of Pathology (Including Division of Molecular Pathology), Tata Memorial Hospital and ACTREC, Tata Memorial Centre, Homi Bhabha National Institute, Parel, Mumbai, Maharashtra, India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Omshree","family":"Shetty","sequence":"additional","affiliation":[{"name":"Department of Pathology (Including Division of Molecular Pathology), Tata Memorial Hospital and ACTREC, Tata Memorial Centre, Homi Bhabha National Institute, Parel, Mumbai, Maharashtra, India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ayushi","family":"Sahay","sequence":"additional","affiliation":[{"name":"Department of Pathology (Including Division of Molecular Pathology), Tata Memorial Hospital and ACTREC, Tata Memorial Centre, Homi Bhabha National Institute, Parel, Mumbai, Maharashtra, India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Prakash","family":"Shetty","sequence":"additional","affiliation":[{"name":"Department of Neurosurgical division of Surgical Oncology, Tata Memorial Hospital and ACTREC, Tata Memorial Centre, Homi Bhabha National Institute, Parel, Mumbai, Maharashtra, India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jayantsastri","family":"Goda","sequence":"additional","affiliation":[{"name":"Department of Radiation Oncology, Tata Memorial Hospital and ACTREC, Tata Memorial Centre, Homi Bhabha National Institute, Parel, Mumbai, Maharashtra, India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aliasagar","family":"Moyiadi","sequence":"additional","affiliation":[{"name":"Department of Neurosurgical division of Surgical Oncology, Tata Memorial Hospital and ACTREC, Tata Memorial Centre, Homi Bhabha National Institute, Parel, Mumbai, 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