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Arman Jahangiri

Researcher at University of California, San Francisco

Publications -  58
Citations -  3261

Arman Jahangiri is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: Tumor microenvironment & Angiogenesis. The author has an hindex of 25, co-authored 56 publications receiving 2506 citations. Previous affiliations of Arman Jahangiri include University of California & Emory University Hospital.

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Hypoxia-Induced Autophagy Promotes Tumor Cell Survival and Adaptation to Antiangiogenic Treatment in Glioblastoma

TL;DR: The hypothesis that hypoxia caused by antiangiogenic therapy induces tumor cell autophagy as a cytoprotective adaptive response, thereby promoting treatment resistance is explored, and a novel mechanism of resistance to antiangIogenic therapy in which Hypoxia-mediatedautophagy promotes tumor cell survival is elucidated.
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Association of Maximal Extent of Resection of Contrast-Enhanced and Non-Contrast-Enhanced Tumor With Survival Within Molecular Subgroups of Patients With Newly Diagnosed Glioblastoma.

TL;DR: An association between maximal resection of CE tumor and OS in patients with glioblastoma is confirmed across all subgroups and was associated with longer OS in younger patients, regardless of IDH status, and among patients with IDH-wild-type gliOBlastoma regardless of the methylation status of the promoter region of the DNA repair enzyme O6-methylguanine-DNA methyltransferase.
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Prognostic value of medulloblastoma extent of resection after accounting for molecular subgroup: a retrospective integrated clinical and molecular analysis

Eric M. Thompson, +111 more
- 01 Apr 2016 - 
TL;DR: A re-evaluation of the long-term implications of intensified craniospinal irradiation in children with small residual portions of medulloblastoma is suggested as the marked benefit of EOR in the overall cohort was greatly attenuated after including molecular subgroup in the multivariable analysis.
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Gene Expression Profile Identifies Tyrosine Kinase c-Met as a Targetable Mediator of Antiangiogenic Therapy Resistance

TL;DR: Findings support the role of c-Met in survival in hypoxia and invasion, features associated with antiangiogenic therapy resistance, and growth and therapeutic resistance of xenografts resistant to antiangIogenic therapy.
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Tumor cell autophagy as an adaptive response mediating resistance to treatments such as antiangiogenic therapy.

TL;DR: Efforts to understand and modulate the autophagy pathway will be crucial to maximize the full therapeutic potential of cancer therapies that are currently hindered by tumor cell Autophagy as a resistance mechanism.