valproic acid/neoplasms

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Antineoplastic effects of the DNA methylation inhibitor hydralazine and the histone deacetylase inhibitor valproic acid in cancer cell lines.

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BACKGROUND Among the epigenetic alterations occurring in cancer, DNA hypermethylation and histone hypoacetylation are the focus of intense research because their pharmacological inhibition has shown to produce antineoplastic activity in a variety of experimental models. The objective of this study

The Combination of Metformin and Valproic Acid Has a Greater Anti-tumoral Effect on Prostate Cancer Growth In Vivo than Either Drug Alone.

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The hypoglycemic drug metformin (MET) and the anti-epileptic drug valproic acid (VPA) have individually shown anti-tumor effects in prostate cancer in vitro. The present study intended to investigate the efficacy of the combination of MET and VPA in prostate cancer treatment in a

N-(2-hydroxyphenyl)-2-propylpentanamide, a valproic acid aryl derivative designed in silico with improved anti-proliferative activity in HeLa, rhabdomyosarcoma and breast cancer cells.

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Epigenetic alterations are associated with cancer and their targeting is a promising approach for treatment of this disease. Among current epigenetic drugs, histone deacetylase (HDAC) inhibitors induce changes in gene expression that can lead to cell death in tumors. Valproic acid (VPA) is a HDAC

Valproic acid induces apoptosis and cell cycle arrest in poorly differentiated thyroid cancer cells.

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Poorly differentiated thyroid carcinoma is an aggressive human cancer that is resistant to conventional therapy. Histone deacetylase inhibitors are a promising class of drugs, acting as antiproliferative agents by promoting differentiation, as well as inducing apoptosis and cell cycle arrest.

Long-term use of valproic acid and the prevalence of cancers in bipolar disorder patients in a Taiwanese population: An association analysis using the National Health Insurance Research Database (NHIRD).

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Epigenetic events play a major role in the carcinogenesis of many cancers. A retrospective cohort study had been performed to evaluate the effects of exposure to the anticonvulsant agent valproic acid (VPA), a histone deacetylase inhibitor, on the risk of developing cancers. The study was based on

Expressional changes after histone deacetylase inhibition by valproic acid in LNCaP human prostate cancer cells.

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Pathogenesis of prostate cancer is paralleled by aberrant transcriptional regulation which involves gene silencing by histone deacetylases. In cancer cells, inhibitors of histone deacetylases such as valproic acid can act as differentiation agents which relieve pro-apoptotic factors from

Induction of apoptosis and autophagy in metastatic thyroid cancer cells by valproic acid (VPA).

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The present study investigated the effect of valproic acid (VPA) on the inhibition of RET signaling and induction of apoptosis in human thyroid carcinoma cells. VPA inhibited the viability of ARO and WRO cells and also inhibited cyclin D1 and caused caspase-3 cleavage. VPA decreased the level of RET

Valproic acid induces the expression of the Na+/I- symporter and iodine uptake in poorly differentiated thyroid cancer cells.

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In poorly differentiated thyroid cancer, molecular characteristics are reported to be lost such as to cause insensitivity of the tumor to radiometabolic therapy. Considerable work is in progress to identify compounds that redifferentiate thyroid cancer cells. The present study evaluates the action

Phospho-valproic acid inhibits pancreatic cancer growth in mice: enhanced efficacy by its formulation in poly-(L)-lactic acid-poly(ethylene glycol) nanoparticles.

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Pancreatic cancer (PC) is one of the most difficult cancers to treat. Since the current chemotherapy is inadequate and various biological approaches have failed, the need for agents that have a potential to treat PC is pressing. Phospho-valproic acid (P-V), a novel anticancer agent, is efficacious

Valproic acid resensitizes cisplatin-resistant ovarian cancer cells.

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Although certain inhibitors of histone deacetylases have been shown to induce cytotoxicity alone or in combination with chemotherapeutic agents in cancer cells, the molecular mechanism is not clear. The goal of the present study was to determine whether the antiseizure drug valproic acid

A Phase II Clinical Trial of Oral Valproic Acid in Patients with Castration-Resistant Prostate Cancers Using an Intensive Biomarker Sampling Strategy.

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Oral valproic acid (VPA), which is a histone deacetylase inhibitor, was used in a phase II trial to treat patients with castration-resistant prostate cancer (CRPC). Ten patients with CRPC were treated with oral VPA. Oral VPA was not well tolerated in this patient population at a dose targeted to a

Valproic Acid Enhances the Anti-tumor Effect of (-)-gossypol to Burkitt Lymphoma Namalwa Cells.

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Burkitt lymphoma is a highly aggressive B-cell neoplasm. New therapeutic methods are needed to overcome the adverse effect of intensive chemotherapy regimens. Valproic acid and (-)-gossypol are two kinds of chemical compounds used as new anti-tumor drugs in recent years. To investigate the

Valproic acid enhances the efficacy of chemotherapy in EBV-positive tumors by increasing lytic viral gene expression.

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EBV infection in tumor cells is generally restricted to the latent forms of viral infection. Switching the latent form of viral infection into the lytic form may induce tumor cell death. We have previously reported that certain chemotherapy agents can increase the amount of lytic viral gene

Valproic acid inhibits human hepatocellular cancer cells growth in vitro and in vivo.

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BACKGROUND Valproic acid (VPA) a histone deacetylase inhibitor has been shown to inhibit the growth of a variety of cancer cells. We examined the effect of VPA in human hepatocellular cancer cells (HuH7) in vitro and in vivo. We hypothesized that VPA may be able to modulate Notch-1 signaling in

Valproic acid suppresses cervical cancer tumor progression possibly via activating Notch1 signaling and enhances receptor-targeted cancer chemotherapeutic via activating somatostatin receptor type II.

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OBJECTIVE We investigated the effects of the anti-epilepsy drug valproic acid (VPA) alone and in combination in treating cervical cancer. METHODS VPA was investigated for its effects on cervical cancer Hela cell proliferation and tumor growth via in vitro and in vivo assays. RESULTS VPA induce cell

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