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Stimulation of differentiated functions in human melanoma cells by tumor-promoting agents and dimethyl sulfoxide.

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Treatment of cultured human HO melanoma cells with the mouse skin tumor promoter phorbol-12-myristate-13-acetate (PMA) at 5 x 10(-10) to 5 x 10(-7) M resulted in a dose-related inhibition of growth and a stimulation of differentiated functions. These included melanin synthesis and formation of

Regulation of hepatocyte epidermal growth factor receptors by n-butyrate and dimethyl sulfoxide: sensitivity to modulation by the tumor promoter TPA.

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n-Butyrate and dimethyl sulfoxide (DMSO) are known to promote differentiated characteristics in certain cells, including hepatocytes. We have previously reported that butyrate up-regulates the surface expression of hepatocyte epidermal growth factor (EGF) receptors and preserves a high-affinity

Inhibition and enhancement of skin tumors in mice by dimethyl sulfoxide depending on method of application.

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The role of dimethyl sulfoxide [(DMSO) CAS: 67-68-5] in experimental tumorigenesis was investigated because of conflicting reports in the literature ranging from inhibition to no effect to enhancement. With the use of numbers of skin tumors produced on the back of the mouse following topical

Magnetic resonance imaging assays for dimethyl sulfoxide effect on cancer vasculature.

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OBJECTIVE To evaluate the potential of quantitative assays of vascular characteristics based on dynamic contrast-enhanced magnetic resonance imaging (MRI) using a macromolecular contrast medium (MMCM) to search for and measure effects of dimethyl sulfoxide (DMSO) on cancer vasculature with

The effects of dimethyl sulfoxide and retinoic acid on the cell growth and the phenotype of ovarian cancer cells.

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We have compared the in vitro effects of the differentiation inducers dimethyl sulfoxide (DMSO) and retinoic acid (RA) on a polyclonal human ovarian cancer cell line (HOC-7). Density gradient fractionation of untreated cells reveals that a proportion of rapidly growing, polygonal cells with medium

Synergistic cytotoxicity between dimethyl sulfoxide and antineoplastic agents against ovarian cancer in vitro.

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Dimethyl sulfoxide is a well-known differentiating agent that has been shown to inhibit tumor growth in vitro. We hypothesized that antineoplastic agents might show synergistic cytotoxicity when combined with 10% dimethyl sulfoxide. Twenty-four malignant ovarian tumors were removed and used in tests

Dimethyl sulfoxide promotes the multiple functions of the tumor suppressor HLJ1 through activator protein-1 activation in NSCLC cells.

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BACKGROUND Dimethyl sulfoxide (DMSO) is an amphipathic molecule that displays a diversity of antitumor activities. Previous studies have demonstrated that DMSO can modulate AP-1 activity and lead to cell cycle arrest at the G1 phase. HLJ1 is a newly identified tumor and invasion suppressor that

Regional chemotherapy for bladder neoplasms using continuous intravesical infusion of doxorubicin: impact of concomitant administration of dimethyl sulfoxide on drug absorption and antitumor activity.

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BACKGROUND One objective of regional chemotherapy is to achieve the therapeutic drug levels in local tissues and primary nodal drainage fields, while minimizing systemic drug toxicity. The composition of the drug-delivery vehicle may influence local drug absorption and thereby modulate both tissue

Dimethyl sulfoxide (DMSO) as a potential contrast agent for brain tumors.

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Dimethyl sulfoxide (DMSO) is commonly used in preclinical studies of animal models of high-grade glioma as a solvent for chemotherapeutic agents. A strong DMSO signal was detected by single-voxel MRS in the brain of three C57BL/6 control mice during a pilot study of DMSO tolerance after intragastric

Dimethyl sulfoxide as an excitatory modulator and its possible role in cancer pain management.

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Intractable and untreatable pain from cancer remains a challenge for both patients and clinicians. The pain may be related to the disease itself or the consequences of treatment, such as surgery, chemotherapy or radiation therapy. Cancer pain is intense and has a major impact on patients' quality of

[Local application of dimethyl sulfoxide at different concentrations to the prevention of radiation-induced damages in patient with cancer of the cervix uteri].

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OBJECTIVE to study the efficacy of dimethyl sulfoxide ((DMSO) at different concentrations in preventing radiation-induced rectal and urinary bladder damages in patients with cervix uteri cancer (CUC). METHODS combined radiation therapy (RT) was performed in 807 patients with CUC. In the control

Dimethyl Sulfoxide Suppresses Mouse 4T1 Breast Cancer Growth by Modulating Tumor-Associated Macrophage Differentiation.

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OBJECTIVE The universal organic solvent dimethyl sulfoxide (DMSO) can be used as a differentiation inducer of many cancer cells and has been widely used as a solvent in laboratories. However, its effects on breast cancer cells are not well understood. The aim of this study is to investigate the

Dimethyl Sulfoxide Extract of Dianthus carmelitarum Induces S Phase Arrest and Apoptosis in Human Colon Cancer Cells.

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Although several studies have investigated the cytotoxic effects of different Dianthus species, there has been only limited research into the cytotoxic effect of Dianthus carmelitarum. The purpose of this research was to evaluate the phenolic characterization and the cytotoxic effect

Inability of dimethyl sulfoxide to increase brain uptake of water-soluble compounds: implications to chemotherapy for brain tumors.

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There is conflicting evidence as to whether dimethyl sulfoxide (DMSO) can reversibly open the blood-brain barrier and augment brain uptake of water-soluble compounds, including anticancer agents. To investigate this, 125I-human serum albumin, horseradish peroxidase, or the anticancer drug melphalan

Cytotoxicity of dimethyl sulfoxide and antineoplastic combinations against human tumors.

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Five human tumor reference cell lines were tested in vitro against 0 percent, 5 percent, and 10 percent DMSO; four antineoplastic agents; and combinations of 5 percent or 10 percent DMSO plus each antineoplastic agent. Synergistic cytotoxicity between DMSO and antineoplastic agents against each cell

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