salicylate/breast neoplasms

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The aspirin metabolite, salicylate, inhibits 7,12-dimethylbenz[a]anthracene-DNA adduct formation in breast cancer cells.

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There is evidence that aspirin and other non-steroidal anti-inflammatory drugs may be protective agents against cancer in the gastrointestinal tract. These effects are particularly well documented for the colon and rectum. Some epidemiological and experimental studies have suggested that aspirin

The aspirin metabolite salicylate inhibits breast cancer cells growth and their synthesis of the osteolytic cytokines interleukins-6 and -11.

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Some epidemiological studies have suggested that aspirin could be a chemopreventive agent against breast cancer. We tested the effects of the aspirin metabolite salicylate (SA) on four (Hs578T, MCF-7, MDA-MB-231, and T-47D) breast cancer cell (BCC) lines in vitro. Two features were studied: the

Oestrogenic activity of benzyl salicylate, benzyl benzoate and butylphenylmethylpropional (Lilial) in MCF7 human breast cancer cells in vitro.

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Benzyl salicylate, benzyl benzoate and butylphenylmethylpropional (Lilial) are added to bodycare cosmetics used around the human breast. We report here that all three compounds possess oestrogenic activity in assays using the oestrogen-responsive MCF7 human breast cancer cell line. At 3 000 000-fold

Salicylate •Phenanthroline copper (II) complex induces apoptosis in triple-negative breast cancer cells.

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In this study, we investigated anti-tumor activity and associated molecular mechanism of action of Salicylate ●Phenanthroline Copper (II) Complex in triple-negative breast cancer. Salicylate ●Phenanthroline Copper (II) Complex inhibited the growth of four breast cancer cell lines (MCF-7, T47D,

Interaction of Salicylates and the Other Nonsteroidal Anti-Inflammatory Agents With Breast Cancer Endocrine Treatment: Systematic Review.

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Despite advances in breast cancer treatment, mortality from breast cancer is still high. Undoubtedly, novel treatment strategies are needed for chemoprevention of high-risk women and for the treatment of receptor-negative breast cancer. An appealing strategy would be the combination of breast

Sodium Salicylate Inhibits Urokinase Activity in MDA MB-231 Breast Cancer Cells.

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Sodium salicylate (NaS) is a derivate of acetylsalicylic acid or aspirin, used as a nonsteroidal anti-inflammatory drug for centuries, for its analgesic and anti-inflammatory effects. It was found to modulate different signaling pathways, in a cell-specific way. Here, we explore the effect of NaS on

Sodium salicylate activates caspases and induces apoptosis of myeloid leukemia cell lines.

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Nonsteroidal antiinflammatory agents (NSAIA) have been shown to exert potent chemopreventive activity against colon, lung, and breast cancers. In this study, we show that at pharmacological concentrations (1 to 3 mmol/L) sodium salicylate (Na-Sal) can potently induce programmed cell death in several

Sodium salicylate is a novel catalytic inhibitor of human DNA topoisomerase II alpha.

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We have previously reported that pretreatment of human lymphoblastoid cells with the hydroxyl radical scavenger, N-acetyl cysteine, attenuates doxorubicin-induced DNA damage signalling through the ATM protein kinase. We sought to extend these studies to examine the effects of other hydroxyl radical

Salicylate enhances necrosis and apoptosis mediated by the mitochondrial permeability transition.

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Onset of the mitochondrial permeability transition (MPT) causes both necrotic and apoptotic cell death in cultured hepatocytes. Salicylate lowers the threshold for onset of the MPT. In this study, our aim was to determine whether nontoxic concentrations of salicylate potentiate MPT-mediated cell

Synergistic interaction between a novel mixed ligand copper(II) chelate complex and a panel of anticancer agents in T47D human breast cancer cells in vitro.

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OBJECTIVE We have developed a novel copper(II) chelate complex with a tridentate ONN-Schiff base ligand and the anion of salicylate, which presented a potent cytotoxic activity against a panel of human and murine cancer cell lines. In this experiment we explored the combined effect between

Synergistic interaction between a mixed ligand copper (II) chelate complex and two anticancer agents in T47D human breast cancer cells in vitro.

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OBJECTIVE We have developed a copper(II) chelate complex with a tridentate ONN-Schiff ligand and the anion of salicylate, showing a potent cytotoxic activity against a panel of human and murine cancer cell lines. In this experiment we have explored the combination effect between

Aspirin and NSAIDs for breast cancer chemoprevention.

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Novel treatment strategies are needed for breast cancer chemoprevention. Tamoxifen is the only drug approved for the chemoprevention of estrogen receptor-positive breast cancer. However, to date, no treatment exists for the chemoprevention of estrogen receptor-negative breast cancer. NSAID use is

Salicylate protects hearing and kidney function from cisplatin toxicity without compromising its oncolytic action.

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Salicylate has recently been demonstrated to protect against the auditory and vestibular side effects of aminoglycoside antibiotics. Similarities in the toxic mechanisms suggest salicylate as a treatment strategy to prevent the ototoxic side effects of cisplatin (CDDP). We first tested protection of

ytotoxic Constituents of Mallotus microcarpus.

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A new 3-methoxybenzensulfonic acid 4-0-0-D-glucopyranoside (1), and ten known compounds (2-11) were isolated from the methanolic extract of the stems of Mallotus microcarpus. The cytotoxicity of the isolated compounds was evaluated by the MTT method. 3-Methoxybenzensulfonic acid 4-Ο-β-D-

β-Lapachone and Paclitaxel Combination Micelles with Improved Drug Encapsulation and Therapeutic Synergy as Novel Nanotherapeutics for NQO1-Targeted Cancer Therapy.

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β-Lapachone (LPC) is a novel cytotoxic agent that is bioactivated by NADP(H): quinone oxidoreductase 1 (NQO1), an enzyme elevated in a variety of tumors, such as non-small cell lung cancer (NSCLC), pancreatic cancer, liver cancer, and breast cancer. Despite its unique mechanism of action, its

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