• Corpus ID: 82393976

WITHAFERIN A: A NOVEL THERAPEUTIC APPROACH FOR MALIGANT BRAIN TUMORS

@inproceedings{Grogan2014WITHAFERINAA,
  title={WITHAFERIN A: A NOVEL THERAPEUTIC APPROACH FOR MALIGANT BRAIN TUMORS},
  author={Patrick T. Grogan},
  year={2014}
}
Glioblastoma Stem Cells and Withaferin A, A Review
  • L. Helson
  • Medicine
    Biomedical Journal of Scientific & Technical Research
  • 2019
Glioblastoma multiforme is characterized by tumor cell heterogeneity, and by recurrent invasive tumors following conventional radiation, cytotoxic drugs, and limited ablative surgery [1-5]...
Treatment of adult and pediatric high-grade gliomas with Withaferin A: antitumor mechanisms and future perspectives
TLDR
Withaferin A (WA), utilized in Ayurvedic medicine for centuries, is attracting attention for its antitumor capabilities and is relatively nontoxic and has shown potential in crossing the blood–brain barrier.
Withaferin A and its potential role in glioblastoma (GBM)
TLDR
This review focuses on the use of Withaferin A alone, or in combination with other treatments, as a newer option for therapy against the most aggressive variant of brain tumors, Glioblastoma.

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MGMT methylation predicts the clinical response of primary gliomas to first-line chemotherapy with the alkylating agent temozolomide, and may open up possibilities for more customized treatments of human brain tumors.
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Inhibition of DNA repair is further indicated in a significant decrease in surviving fraction of DT40 cells by post-irradiation incubation with WA, suggesting that WA enhances radiosensitivity by interfering with homologous repair, the major pathway of DSB repair in these cells.
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Withaferin A induces apoptosis by activating p38 mitogen-activated protein kinase signaling cascade in leukemic cells of lymphoid and myeloid origin through mitochondrial death cascade
TLDR
Findings suggest that p38MAPK in leukemic cells promotes WA-induced apoptosis, and therefore WA holds promise as a new, alternative, inexpensive chemotherapeutic agent for the treatment of patients with leukemia of both lymphoid and myeloid origin.
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