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Robert L. Martuza

Researcher at Harvard University

Publications -  264
Citations -  30135

Robert L. Martuza is an academic researcher from Harvard University. The author has contributed to research in topics: Oncolytic virus & Herpes simplex virus. The author has an hindex of 79, co-authored 263 publications receiving 27228 citations. Previous affiliations of Robert L. Martuza include Georgetown University Medical Center & House Ear Institute.

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Journal Article

Treatment of Malignant Gliomas Using Ganciclovir-hypersensitive, Ribonucleotide Reductase-deficient Herpes Simplex Viral Mutant'

TL;DR: It is demonstrated that attenuated mutants of herpes simplex virus (HSV) have therapeutic potential for malignant brain tumors and drug sensitivity assays demonstrated that HSV-RR- mutant hrR3 is hypersensitive to the antiherpetic agent ganciclovir.
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An aberrant transcription factor network essential for Wnt signaling and stem cell maintenance in glioblastoma

TL;DR: A comparative analysis of chromatin state in GBM CSCs is presented that reveals widespread activation of genes normally held in check by Polycomb repressors, and demonstrates regulatory connections among ASCL1, Wnt signaling, and collaborating TFs that are essential for the maintenance and tumorigenicity of GBMCSCs.
Journal Article

Selective killing of glioma cells in culture and in vivo by retrovirus transfer of the herpes simplex virus thymidine kinase gene.

TL;DR: The effectiveness of the thymidine kinase expressed by the HSV-1 ks gene in sensitizing brain tumor cells to the toxic effects of nucleoside analogs is demonstrated.
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Common pathogenetic mechanism for three tumor types in bilateral acoustic neurofibromatosis

TL;DR: Specific loss of alleles from chromosome 22 was detected with polymorphic DNA markers in two acoustic neuromas, two neurofibromas, and one meningioma from BANF patients, indicating a common pathogenetic mechanism for all three tumor types.
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Association of epidermal growth factor receptor gene amplification with loss of chromosome 10 in human glioblastoma multiforme.

TL;DR: The presence of 15 cases of glioblastoma with loss of chromosome 10 but without EGFR gene amplification may imply that the loss of a tumor suppressor gene (or genes) on chromosome 10 precedes EG FR gene amplification in gliOBlastoma tumorigenesis.