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Nader Sanai on Muck Rack

Nader Sanai

United States
As seen in: Nature, Science Magazine, HemOnc Today, ONCOLOGY journal, Techonomy, OncLive, Neurosurgery Blog
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Articles

Acquired genetic and cell-state changes in IDH-mutant glioma progression

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By Kevin Johnson, Avishay Spitzer, Frederick S. Varn, Masashi Nomura, Luciano Garofano, Tamrin Chowdhury, Anuja Lipsa, Linbin Zhang, Ester Calvo Fernández, Tanyeri Barak, Samirkumar B. Amin, Emre Kocakavuk, Dacheng Zhao, Fulvio D’Angelo, Simona Migliozzi, Lillian Bussema, Simon Gritsch, Sun Ha Paek, Franck Bielle, Alice Laurenge, Bertrand Mathon, Alberto Picca, Marc Sanson, Ann-Christin Hau, Frank Hertel, Kamil Grzyb, Zheng Zhao, Qianghu Wang, Tao Jiang, Julie Miller, Hiroaki Wakimoto, Daniel Cahill, Jennifer Moliterno, Murat Gunel, Beth Hermes, Nader Sanai, Anna Golebiewska, Simone P Niclou, Jason T. Huse, W. K. Alfred Yung, Anna Lasorella, Mario L. Suvà, Antonio Iavarone, Itay Tirosh, Roel G. W. Verhaak, A. Gulhan Ercan-Sencicek, Ayse Buket Peksen, C. Mircea S. Tesileanu, Hyo-Eun Moon
| Nature Verified
Abstract Gliomas with mutant isocitrate dehydrogenase (IDH) are malignant brain tumours that typically arise in early to mid-adulthood and nearly always recur following treatment1,2. However, the genetic and cellular-state changes that drive IDH-mutant glioma progression under treatment remain incompletely understood.
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An early clinical trial of 5-ALA sonodynamic therapy in recurrent high-grade glioma

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By Nader Sanai, Artak Tovmasyan, An-Chi Tien, Yu-Wei Chang
| Science Magazine Verified
Editor’s summary Sonodynamic therapy (SDT) pairs 5-aminolevulinic acid (5-ALA), which is metabolized to protoporphyrin IX in glioma cells, with noninvasive, image-guided focused ultrasound to trigger tumor-selective oxidative injury. In an early clinical study of nine patients with recurrent high-grade glioma, Sanai et al. show that increasing ultrasound doses produced no drug-related or device-related toxicities in the patients.
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Base editing of β0-thalassemia mutations as a therapeutic strategy for severe β-hemoglobinopathies

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By Philipp Gobrecht, Nader Sanai, Megan O’Driscoll, Giulia Hardouin
| Science Magazine Verified
Editor’s summary β-thalassemias are caused by mutations in the HBB gene and are potentially amenable to correction through gene editing. Here, Hardouin and colleagues developed and optimized adenine base editing approaches to correct two of the most severe β-thalassemia mutations, CD39 and IVS2-1, in patient hematopoietic stem and progenitor cells (HSPCs).
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