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Aamir Ahmad

Researcher at University of Alabama at Birmingham

Publications -  257
Citations -  15418

Aamir Ahmad is an academic researcher from University of Alabama at Birmingham. The author has contributed to research in topics: Cancer & Cancer stem cell. The author has an hindex of 63, co-authored 251 publications receiving 13404 citations. Previous affiliations of Aamir Ahmad include Aligarh Muslim University & Hamad Medical Corporation.

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Down‐regulation of uPA and uPAR by 3,3′‐diindolylmethane contributes to the inhibition of cell growth and migration of breast cancer cells

TL;DR: The results suggest that B‐DIM down‐regulates uPA‐uPAR in aggressive breast cancers but in the absence of uPA•uPAR, B‐ DIM can directly inhibit VEGF and MMP‐9 leading to the inhibition of cell growth and migration of breast cancer cells.
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Flavonoids-induced redox cycling of copper ions leads to generation of reactive oxygen species: A potential role in cancer chemoprevention.

TL;DR: A copper dependent pro-oxidant cytotoxic mechanism better explains the anticancer activity and preferential cytotoxicity of dietary phytochemicals against cancer cells.
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Induction of cancer cell death by isoflavone: the role of multiple signaling pathways.

TL;DR: The knowledge gained will provide a comprehensive view on the molecular mechanism(s) by which soy isoflavones may exert their effects on the prevention of tumor progression and/or treatment of human malignancies, which would also aid in stimulating further in-depth mechanistic research and foster the initiation of novel clinical trials.
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Oxidative DNA damage by capsaicin and dihydrocapsaicin in the presence of Cu(II)

TL;DR: It is shown that capsaicin is capable of causing strand scission in calf thymus and plasmid DNA in the presence of Cu(II) and that this breakage is mediated by reactive oxygen species, especially the hydroxyl radical.
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Impact of sex differences and gender specificity on behavioral characteristics and pathophysiology of neurodegenerative disorders.

TL;DR: Understanding the sex as a biological variable in the etiology of the neurodegenerative diseases may advance the status of the pathophysiology and treatment strategies while improving the associated decline in cognitive and functional abilities.