ribonuclease/cancer mamar

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[Value of plasma ribonuclease as a marker for gynecologic tumors and breast tumors].

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In 151 patients the plasma-ribonuclease-activity was measured. The results of a control group of 47 patients were compared to the pretherapeutic values of 21 cases with cervical intraepithelial neoplasia, 83 cases with gynecologic cancer and 47 cases with breast cancer. The upper limit of the normal

Induction of 2'-5' oligoadenylate synthetase and activation of ribonuclease in tamoxifen treated human breast cancer cell lines.

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In the present study the intracellular activity of oligoadenylate synthetase and ribonuclease have been evaluated in two human breast cancer cell lines treated with tamoxifen, a well known antiestrogenic drug. Increased levels of oligoadenylate synthetase and enhanced ribonuclease activity have been

Transcriptional targeting of gene expression in breast cancer by the promoters of protein regulator of cytokinesis 1 and ribonuclease reductase 2.

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For cancer gene therapy, cancer-specific over- expression of a therapeutic gene is required to reduce side effects derived from expression of the gene in normal cells. To develop such an expression vector, we searched for genes over-expressed and/or specifically expressed in cancer cells using

[Analysis of gene expression of ribonuclease inhibitor in human breast cancer tissue].

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OBJECTIVE Ribonuclease inhibitor (RI), which is rich in human placenta, is a multi-functional acidic glycoprotein. Our previous studies showed that the growth of some solid tumors (S180 sarcoma, Ca761 breast cancer, and H22 hepatoma) could be significantly inhibited by RI extracted and purified from

A Novel Ribonuclease from Rana Chensinensis and Its Potential for the Treatment of Human Breast Cancer.

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Onconase, a member of the pancreatic RNAase A superfamily of ribonucleases, is a chemotherapeutic agent, which has demonstrated selective antitumor activity in a variety of human malignancies. However, little is known about the mechanisms of it's action on human breast cancer cells. To investigate a

Ribonuclease H2 Subunit A impacts invasiveness and chemoresistance resulting in poor survivability of breast cancer in ER dependent manner

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Ribonuclease H2 subunit A (RNASEH2A), a member of the RNase HII family, acts in DNA replication by mediating removal of lagging-strand Okazaki fragment RNA primers. We explored the roles of RNASEH2A in the prognosis of breast cancer, specifically in relation to proliferation, invasiveness, and

Hypoxia-sensitive supramolecular nanogels for the cytosolic delivery of ribonuclease A as a breast cancer therapeutic.

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As the most common malignancy in women, breast cancer causes >40,000 deaths annually. Ribonuclease A (RNase), a new anti-cancer agent, has attracted intense interest due to its high efficacy and specificity. However, RNase suffers from instability, a short half-life in the circulation and poor

RNase MC2: a new Momordica charantia ribonuclease that induces apoptosis in breast cancer cells associated with activation of MAPKs and induction of caspase pathways.

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Ribonucleases (RNases) are ubiquitously distributed nucleases that cleave RNA into smaller pieces. They are promising drugs for different cancers based on their concrete antitumor activities in vitro and in vivo. Here we report for the first time purification and characterization of a 14-kDa RNase,

Effective stimulation of growth in MCF-7 human breast cancer cells by inhibition of syntaxin18 by external guide sequence and ribonuclease P.

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Syntaxin18 (Stx18) is an endoplasmic reticulum (ER)-membrane bound SNARE protein involved in membrane trafficking between the ER and Golgi as well as in phagocytosis. Stx18 has also been shown to physically interact with proteins involved in the cell cycle and apoptosis. These findings suggest the

[Effects of ribonuclease inhibitor on apoptosis and invasion of human breast cancer MDA-MB-231 cells].

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OBJECTIVE RI gene is transfected into human breast cell line MDA-MB-231 which is relatively hypo-expression RI gene. To investigate how RI gene affect the cell apoptosis and invasion of MDA-MB-231. METHODS (1) A recombinate pLNCX-RI and an empty pLNCX were transferred into MDA-MB-231 cells by using

Regulation of retinoblastoma gene expression in hormone-dependent breast cancer.

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Studies have shown an increased risk for breast cancer in the mothers of children suffering from retinoblastoma and osteosarcoma, suggesting a role for the retinoblastoma susceptibility (Rb) gene product in breast cancer. We now show that estradiol decreases the expression of Rb at the level of

In Vitro Assessment of the Inflammatory Breast Cancer Cell Line SUM 149: Discovery of 2 Single Nucleotide Polymorphisms in the RNase L Gene.

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BACKGROUND Inflammatory breast cancer (IBC) is a rare, highly aggressive form of breast cancer. The mechanism of IBC carcinogenesis remains unknown. We sought to evaluate potential genetic risk factors for IBC and whether or not the IBC cell lines SUM149 and SUM190 demonstrated evidence of viral

Expression profile of agonistic Smads in human breast cancer cells: absence of regulation by estrogens.

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Transforming growth factor-beta1 (TGF-beta1) is a cytokine expressed by mammary cells. While TGF-beta1 can inhibit the proliferation of human breast cancer cells, many cell lines are unresponsive to it. To shed light on the mechanisms underlying resistance to TGF-beta1, we examined expression of the

Regulation of insulin-like growth factor-binding protein (IGFBP) expression by breast cancer cells: use of IGFBP-1 as an inhibitor of insulin-like growth factor action.

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BACKGROUND The insulin-like growth factors (IGFs) play an important role in normal growth and development. Evidence suggests they may also regulate the growth of several cancer cell types. This regulation is mediated by interactions between the receptors and ligands. There is now ample evidence to

A metastatic breast tumor cell line, GI-101A, is estrogen receptor positive and responsive to estrogen but resistant to tamoxifen.

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The progression of human breast cancer is often associated with a loss of estrogen dependence for growth, a resistance to estrogen antagonists such as tamoxifen, and the metastatic spread of the disease to secondary sites. Cell lines developed from such advanced breast tumors are often metastatic in

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