Spandana Kotian

Abstract Telomerase counteracts telomere shortening, enabling human embryonic stem cells (hESC) to undergo long-term proliferation. MAPK signaling plays a major role in regulating the self-renewal of hESC, and previous studies in induced pluripotent stem cells (iPSC) suggested that expression of TERT, the gene encoding the catalytic subunit of telomerase, relies on MAPK signaling. We examined whether MEK-ERK signaling regulated TERT transcription in a model of normal hESC.

1. Introduction Glioblastoma (GBM) is the most common malignant primary brain tumor in patients [1]. The current standard of care is surgical resection of the tumor followed by radiation and chemotherapy with the DNA alkylating agent temozolomide (TMZ) [2,3]. Even with this treatment, approximately 90% of patients undergo recurrence within five years post-diagnosis [4]. There is a pressing need to develop new therapeutic approaches for GBM.

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