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Open AccessJournal ArticleDOI

Curcumin selectively induces apoptosis in deregulated cyclin D1-expressed cells at G2 phase of cell cycle in a p53-dependent manner.

Tathagata Choudhuri, +3 more
- 20 May 2005 - 
- Vol. 280, Iss: 20, pp 20059-20068
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TLDR
Curcumin selectively increases p53 expression at G2 phase of carcinoma cells and releases cytochrome c from mitochondria, which is an essential requirement for apoptosis, suggesting that curcumin may have a possible therapeutic potential in breast cancer patients.
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This article is published in Journal of Biological Chemistry.The article was published on 2005-05-20 and is currently open access. It has received 319 citations till now. The article focuses on the topics: Cyclin A & Cyclin D.

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Journal ArticleDOI

Molecular targets of dietary agents for prevention and therapy of cancer

TL;DR: Evidence is presented that numerous agents identified from fruits and vegetables can interfere with several cell-signaling pathways and the active principle identified in fruit and vegetables and the molecular targets modulated may be the basis for how these dietary agents not only prevent but also treat cancer and other diseases.
Journal ArticleDOI

Curcumin: From ancient medicine to current clinical trials

TL;DR: Curcumin exhibits great promise as a therapeutic agent, and is currently in human clinical trials for a variety of conditions, including multiple myeloma, pancreatic cancer, myelodysplastic syndromes, colon cancer, psoriasis and Alzheimer’s disease.
Journal ArticleDOI

Toxicity of lead: A review with recent updates.

TL;DR: A comprehensive account of recent updates describing health effects of lead exposure, relevant biomarkers and mechanisms involved in lead toxicity, and updates the readers about recent advances in chelation therapy and newer therapeutic strategies, like nanoencapsulation, to treat lead induced toxic manifestations are provided.
Book ChapterDOI

Curcumin: The Indian solid gold

TL;DR: Curcumin has been shown to exhibit antioxidant, anti-inflammatory, antiviral, antibacterial, antifungal, and anticancer activities and thus has a potential against various malignant diseases, diabetes, allergies, arthritis, Alzheimer's disease, and other chronic illnesses.
Journal ArticleDOI

Polymeric nanoparticle-encapsulated curcumin ("nanocurcumin"): a novel strategy for human cancer therapy

TL;DR: Nanocurcumin provides an opportunity to expand the clinical repertoire of this efficacious agent by enabling ready aqueous dispersion and demonstrating comparable in vitro therapeutic efficacy to free curcumin against a panel of human pancreatic cancer cell lines.
References
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Journal ArticleDOI

Cancer Cell Cycles

TL;DR: Genetic alterations affecting p16INK4a and cyclin D1, proteins that govern phosphorylation of the retinoblastoma protein and control exit from the G1 phase of the cell cycle, are so frequent in human cancers that inactivation of this pathway may well be necessary for tumor development.
Journal ArticleDOI

Induction of apoptotic program in cell-free extracts : requirement for datp and cytochrome c

TL;DR: Cells undergoing apoptosis in vivo showed increased release of cy tochrome c to their cytosol, suggesting that mitochondria may function in apoptosis by releasing cytochrome c.
Journal ArticleDOI

Tumor suppressor p53 is a direct transcriptional activator of the human bax gene

TL;DR: The bax gene promoter region contains four motifs with homology to consensus p53-binding sites and wild-type but not mutant p53 protein bound to oligonucleotides corresponding to this region of the bax promoter, suggesting that bax is a p53 primary-response gene, presumably involved in a p 53-regulated pathway for induction of apoptosis.
Journal ArticleDOI

Induction of apoptosis in fibroblasts by c-myc protein

TL;DR: It is demonstrated that deregulated c-myc expression induces apoptosis in cells growth arrested by a variety of means and at various points in the cell cycle.
Journal ArticleDOI

Cell cycle control and cancer

TL;DR: New insights in understanding of the cell cycle reveal how fidelity is normally achieved by the coordinated activity of cyclin-dependent kinases, checkpoint controls, and repair pathways and how this fidelity can be abrogated by specific genetic changes.
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