Therapy and progression – induced O6‑methylguanine‑DNA methyltransferase and mismatch repair alterations in recurrent glioblastoma multiforme.
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Date
2015-10
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Abstract
Despite multimodality treatment protocol including surgical resection, radiotherapy, and chemotherapy in patients with glioblastoma multiforme (GBM),
most suffer from treatment failure and tumor recurrence within a few months of initial surgery. The effectiveness of temozolomide (TMZ), the most
commonly used chemotherapeutic agent, is largely dependent on the methylation status of the promoter of the gene O6‑methylguanine‑DNA
methyltransferase (MGMT) and the integrity of the mismatch repair (MMR) system. Changes in these regulatory mechanisms at the time of recurrence
may influence response to therapy. Deciphering the molecular mechanisms of resistance to these drugs may in future lead to improvised patient
management. In this article, we provide an update of the spectrum of molecular changes that occur in recurrent GBMs, and thus may have an
impact on patient survival and treatment response. For review, electronic search for the keywords “Recurrent GBM”, “Recurrent GBM AND MGMT”
“Recurrent glioma AND MGMT”, “Recurrent GBM AND MMR” and “Recurrent glioma AND MMR”, “Recurrent GBM AND MMR” and “Recurrent
glioma AND MMR” was done on PubMed and relevant citations were screened including cross‑references.
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Keywords
Glioblastoma, mismatch repair, molecular, recurrent gliomas, O6‑ Methylguanine-DNA methyltransferase
Citation
Agarwal S, Suri V, Sharma M C, Sarkar C. Therapy and progression – induced O6‑methylguanine‑DNA methyltransferase and mismatch repair alterations in recurrent glioblastoma multiforme. Indian Journal of Cancer. 2015 Oct-Dec; 52(4): 568-573.