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Viveka Nand Yadav

Researcher at University of Michigan

Publications -  33
Citations -  709

Viveka Nand Yadav is an academic researcher from University of Michigan. The author has contributed to research in topics: Glioma & Complement control protein. The author has an hindex of 11, co-authored 29 publications receiving 500 citations. Previous affiliations of Viveka Nand Yadav include Savitribai Phule Pune University.

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Mechanisms of Glioma Formation: Iterative Perivascular Glioma Growth and Invasion Leads to Tumor Progression, VEGF-Independent Vascularization, and Resistance to Antiangiogenic Therapy

TL;DR: Agent-based computational modeling recapitulated biological perivascular glioma growth without the need for neoangiogenesis, providing compelling experimental evidence in support of the recently described failure of clinically used antiangiogenics to extend the overall survival of human GBM patients.
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Integrated Metabolic and Epigenomic Reprograming by H3K27M Mutations in Diffuse Intrinsic Pontine Gliomas.

TL;DR: Overall, it is demonstrated that H3.3K27M and mIDH1 hijack a conserved and critical metabolic pathway in opposing ways to maintain their preferred epigenetic state, and interruption of this metabolic/epigenetic pathway showed potent efficacy in preclinical models, suggesting key therapeutic targets for much needed treatments.
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CXCR4 increases in-vivo glioma perivascular invasion, and reduces radiation induced apoptosis: A genetic knockdown study

TL;DR: The data suggest that CXCR4 signaling is critical for perivascular invasion of GBM cells and targeting this receptor makes tumors less invasive and more sensitive to radiation therapy.
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Natural killer cells eradicate galectin-1-deficient glioma in the absence of adaptive immunity.

TL;DR: It is shown that malignant glioma cells suppress NK immune surveillance by overexpressing the β-galactoside-binding lectin galectin-1, suggesting that galectIn-1 suppression in humanglioma could improve patient survival by restoring NK immune Surveillance that can eradicate gli cancer cells.
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Survival and proliferation of neural progenitor derived glioblastomas under hypoxic stress is controlled by a CXCL12/CXCR4 autocrine positive feedback mechanism.

TL;DR: This study demonstrates that the CXCL12/CXCR4 axis operates in glioblastoma cells under hypoxic stress via an autocrine-positive feedback mechanism, which promotes survival and cell-cycle progression.