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Vishal Ranjan

Researcher at Central Drug Research Institute

Publications -  5
Citations -  185

Vishal Ranjan is an academic researcher from Central Drug Research Institute. The author has contributed to research in topics: MCF-7 & Apoptosis. The author has an hindex of 5, co-authored 5 publications receiving 174 citations. Previous affiliations of Vishal Ranjan include Allahabad University & Council of Scientific and Industrial Research.

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Journal ArticleDOI

Centchroman induces G0/G1 arrest and caspase-dependent apoptosis involving mitochondrial membrane depolarization in MCF-7 and MDA MB-231 human breast cancer cells.

TL;DR: Results demonstrate that CC induces caspase-dependent apoptosis in MCF-7 and MDA MB-231 cells irrespective of ER status similar to TAM in terms of anti-neoplastic activity.
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Caspase Mediated Enhanced Apoptotic Action of Cyclophosphamide- and Resveratrol-Treated MCF-7 Cells

TL;DR: It is found that RES significantly enhances the caspase-mediated cytotoxic activity of CPA on MCF-7 cells in vitro, suggesting the possibility of a new combination chemotherapeutic regimen leading to improvements in the treatment of breast cancer.
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Resveratrol as an adjunct therapy in cyclophosphamide‐treated MCF‐7 cells and breast tumor explants

TL;DR: The molecular basis of 5’mM CPA and 50’μM RES as a combination on cell‐cycle progression, apoptosis and oxidative stress in MCF‐7 breast cancer cells is explored and co‐treatment superiority in histologically validated ER positive breast cancer explants suggests that this combination may be a worthy future clinical anti‐neoplastic regimen.
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Centchroman mediated apoptosis involves cross-talk between extrinsic/intrinsic pathways and oxidative regulation.

TL;DR: Results confirm that the antineoplasticity of CC in MCF-7 and MDA MB-231 cells involves the extrinsic and intrinsic pathways of apoptosis along with oxidative stress.
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Insulin catalyzes the curcumin-induced wound healing: an in vitro model for gingival repair.

TL;DR: The in vitro model for gingival wound healing establishes that insulin significantly enhanced wound filling faster than CUR-treated hGF cells over 48 h, which reinforces the pivotal role of insulin in supporting C UR-mediated wound repair.