Sentences with phrase «in breast cancer cell growth»

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In 2010, researchers from the University of Michigan Comprehensive Cancer Center published a study in the journal Clinical Cancer Research showing that sulforaphane had the ability to kill breast cancer stem cells in mice and in lab cultures, and it also prevented the growth of new tumor cellIn 2010, researchers from the University of Michigan Comprehensive Cancer Center published a study in the journal Clinical Cancer Research showing that sulforaphane had the ability to kill breast cancer stem cells in mice and in lab cultures, and it also prevented the growth of new tumor Cancer Center published a study in the journal Clinical Cancer Research showing that sulforaphane had the ability to kill breast cancer stem cells in mice and in lab cultures, and it also prevented the growth of new tumor cellin the journal Clinical Cancer Research showing that sulforaphane had the ability to kill breast cancer stem cells in mice and in lab cultures, and it also prevented the growth of new tumor Cancer Research showing that sulforaphane had the ability to kill breast cancer stem cells in mice and in lab cultures, and it also prevented the growth of new tumor cancer stem cells in mice and in lab cultures, and it also prevented the growth of new tumor cellin mice and in lab cultures, and it also prevented the growth of new tumor cellin lab cultures, and it also prevented the growth of new tumor cells.

Cancer: Flaxseed may protect against breast cancer, prostate cancer, and colon cancer by inhibiting tumor growth and blocking enzymes that are involved in the spread of tumor Cancer: Flaxseed may protect against breast cancer, prostate cancer, and colon cancer by inhibiting tumor growth and blocking enzymes that are involved in the spread of tumor cancer, prostate cancer, and colon cancer by inhibiting tumor growth and blocking enzymes that are involved in the spread of tumor cancer, and colon cancer by inhibiting tumor growth and blocking enzymes that are involved in the spread of tumor cancer by inhibiting tumor growth and blocking enzymes that are involved in the spread of tumor cells.

Breast cancer is the uncontrollable growth of malignant cells in the breasts.

For example, in experiments, they have been found to stimulate the growth of breast cancer cells and feminize male fish.

The researchers observed the effect of the synthetically produced molecule, JK - 31, on the growth and proliferation of a model human breast cancer cell line and found that it effectively blocked the protein cyclin - dependent kinase 1 (CDK1), which plays a key part in the process of the division of cancer cells, and therefore inhibited the proliferation of the cells.

They found that atypical protein kinase c lambda / iota, which is known to influence cell growth, was highly expressed and phosphorylated in metastatic breast cancers.

Isoflavones have been shown to slow the growth of breast cancer cells in laboratory studies, and epidemiological analyses in East Asian women with breast cancer found links between higher isoflavone intake and reduced mortality.

Moreover, epalrestat, a drug that inhibits AKR1B1 and is approved in Japan to treat peripheral neuropathies associated with diabetes, was similarly able to block the growth and metastasis of human basal - like breast cancer cells.

The substance vigorously inhibited the growth of cultured tumor cells from colon, lung, and breast cancers, the team reports in the 20 January issue of Angewandte Chemie.

Overexpression of ZMYND11 in an osteosarcoma cell line and a triple - negative breast cancer cell line inhibited tumor growth.

Through these effects, the PERY peptide reduced the proliferation of several (but not all) cancer cell lines in culture and inhibited the growth of a human breast cancer xenograft in mice.

Until now, little was known in preclinical models about the mechanisms that allow breast cancer cells to leave the latent state and even less is known in patients,» explains Roger Gomis, head of the Growth Control and Cancer Metastasicancer cells to leave the latent state and even less is known in patients,» explains Roger Gomis, head of the Growth Control and Cancer MetastasiCancer Metastasis Lab.

In animal and cell culture studies, the drug inhibited growth both in estrogen - dependent breast cancer cells and in cells that had developed resistance to the anti-estrogen tamoxifen and / or to the aromatase inhibitors, two of the most widely used types of drugs to prevent and treat estrogen - dependent breast canceIn animal and cell culture studies, the drug inhibited growth both in estrogen - dependent breast cancer cells and in cells that had developed resistance to the anti-estrogen tamoxifen and / or to the aromatase inhibitors, two of the most widely used types of drugs to prevent and treat estrogen - dependent breast cancein estrogen - dependent breast cancer cells and in cells that had developed resistance to the anti-estrogen tamoxifen and / or to the aromatase inhibitors, two of the most widely used types of drugs to prevent and treat estrogen - dependent breast cancein cells that had developed resistance to the anti-estrogen tamoxifen and / or to the aromatase inhibitors, two of the most widely used types of drugs to prevent and treat estrogen - dependent breast cancer.

«Both the natural and the synthetic substances inhibit the growth and spread of cancer stem cells in breast cancer cell lines.

A drug approved in Europe to treat osteoporosis has now been shown to stop the growth of breast cancer cells, even in cancers that have become resistant to current targeted therapies, according to a Duke Cancer Institute cancer cells, even in cancers that have become resistant to current targeted therapies, according to a Duke Cancer Institute Cancer Institute study.

«Osteoporosis drug stops growth of breast cancer cells, even in resistant tumors, study suggests.»

However, when the tips of these blood cells begin to sprout, the thrombospondin - 1 proteins give way to TGF - beta 1 and periostin proteins in the neovasculature, turning it into a metastatic niche that not only permits but accelerates the growth of breast cancer cells.

To determine whether endothelial cells — the cells that line the interior surface of blood vessels — directly influence breast cancer cell growth, they then created unique organotypic models of lung and bone marrow microvascular niches, in which endothelial cells formed blood vessel - like structures in culture as they would in the original organ.

By performing a genome - wide screen in breast cancer cells, Dr. Oesterreich and her colleagues identified a gene called HOXC10 as one that the cancer seems to modify to allow continued tumor growth in patients whose cancer becomes resistant to traditional therapies.

Other studies have found that nutrients in dark, leafy greens may inhibit the growth of tumor cells in breast, skin, lung and stomach cancers and that green tea may thwart cancer development in colon, liver, breast and prostate cells.

«In lab tests, the antimicrobial ingredient triclosan spurs growth of breast cancer cells.»

Their study, published in the ACS journal Chemical Research in Toxicology, found that triclosan, as well as another commercial substance called octylphenol, promoted the growth of human breast cancer cells in lab dishes and breast cancer tumors in mice.

In tests on human breast cancer cells and in special immunodeficient mice with tissue grafts, the scientists found that both agents interfered with genes involved with breast cancer cell growth, resulting in more cancer cellIn tests on human breast cancer cells and in special immunodeficient mice with tissue grafts, the scientists found that both agents interfered with genes involved with breast cancer cell growth, resulting in more cancer cellin special immunodeficient mice with tissue grafts, the scientists found that both agents interfered with genes involved with breast cancer cell growth, resulting in more cancer cellin more cancer cells.

Now, results of a new study by Johns Hopkins Kimmel Cancer Center scientists suggests a powerful role for the protein in normal breast cells, acting as a tumor suppressor that halts abnormal cell growth.

In a development that could lead to a new generation of drugs to precisely treat a range of diseases, scientists from the Florida campus of The Scripps Research Institute (TSRI) have for the first time designed a drug candidate that decreases the growth of tumor cells in animal models in one of the hardest to treat cancers — triple negative breast canceIn a development that could lead to a new generation of drugs to precisely treat a range of diseases, scientists from the Florida campus of The Scripps Research Institute (TSRI) have for the first time designed a drug candidate that decreases the growth of tumor cells in animal models in one of the hardest to treat cancers — triple negative breast cancein animal models in one of the hardest to treat cancers — triple negative breast cancein one of the hardest to treat cancers — triple negative breast cancer.

Across multiple triple - negative breast cancer subtypes, inhibiting the androgen receptor greatly increased apoptosis (programmed cell death), inhibited growth and increased necrosis by 60 percent in animal models.

The growth rate of the cells exploded, and they quickly became disorganized masses characteristic of early stage, aggressive breast cancer, the team reports in the 7 February issue of the Journal of Experimental Medicine.

When a chemical that inhibits entosis was applied to a line of breast cancer cells, colony formation — an indicator of tumor growth in vitro — increased 10-fold.

Based on analyses of over 600 drug and breast cancer cell pairings, researchers showed that, for some cells, drug exposure can cause significant changes in gene expression — indicating the successful action of a drug on its target — without affecting cell growth or survival.

Additionally, overexpression of POSTN in human mammary epithelial and breast cancer cells resulted in enhanced tumor growth and metastasis (Wang et al., 2013), which is similar to a colon cancer cell model where overexpression of POSTN resulted in an increase in the number and size of liver metastases (Bao et al., 2004).

Biologically, hypermethylation often silences genes that keep runaway cell growth in check, and its appearance in the DNA code of breast cancer - related genes shed into the blood may indicate that a patient's cancer growth is increasing and the disease has worsened.

In this way they were able to reactivate the senescence program and stop the growth of the breast cancer cells.

Now Javier Menendez at the Northwestern University Feinberg School of Medicine in Chicago and his team have shown that oleic acid, the major fatty acid component of olive oil, blocks the production of a protein that boosts the growth of breast cancer cells.

Mutations in the gene increase rat susceptibility to mammary cancer and FRY reduced the growth of highly aggressive human breast cancer cells.

The current study shows that NUDT5 is operates in the nucleus of hormone - driven breast cancer cells, to produce energy for the expression of genes important for cancer growth.

Now, in Stem Cells Translation Medicine, the group of Shu Wang at the National University of Singapore describe the derivation of EPCs from human iPSCs, their therapeutic modification, and their ability to inhibit tumor growth in a mouse breast cancer model [4].

Many breast cancers use hormones, such as oestrogen, to drive their growth and current treatment options aim to block the hormonal activity in order to halt the growth of the breast cancer cells.

They demonstrated that this new molecule can stop the growth of breast cancer cells in laboratory experiments.

Injections of iPSC - EPCs did not however have significant effect on tumor growth or on overall survival, but transducing cells with a baculovirus expressing CD40L, a member of the TNF gene family which can induce apoptosis [6, 7], and injection into the breast cancer lung metastasis, increased levels of pro-apoptotic cytokines in lung tissues, indicating the induction of apoptosis by CD40L carried by the EPCs (See figure).

Zhu Q, Jin L, Casero RA, Davidson NE, Huang Y. Role of ornithine decarboxylase in regulation of estrogen receptor alpha expression and growth in human breast cancer cells.

The Salk scientists are now characterizing the stem - like cells in certain forms of breast cancer to arrest their growth.

Through its various targets, MMP1 promotes not only tumor invasion but also breast cancer colonization to bone by mechanisms that include the release of membrane - bound EGF - like growth factors from tumor cells, leading to activation of EGF receptor signaling and suppression of OPG expression in osteoblasts, which in turn promotes the differentiation and activation of osteoclasts required for bone destruction and enhanced tumor growth in the bone microenvironment (32).

-- discovery awarded international science prize Researcher Allison Cleary has, for the first time, demonstrated that different types of tumor cells cooperate in the development and growth of breast cancer.

The recently discovered protein NUDT5 is now presented as a candidate target for development of breast cancer treatment after being demonstrated to stop breast tumor cell growth in laboratory experiments.

When breast cancer cells invade the bone microenvironment, they produce molecules that activate osteoclastic bone resorption, leading to the release of growth factors stored in the bone matrix to promote tumor growth.

He has over 250 publications in the areas of signaling by growth factor receptors and oncogenes in breast tumor cells, development of targeted therapies and biomarkers of drug action and resistance, and investigator - initiated clinical trials in breast cancer.

Depletion of ABL kinases in breast cancer cells also decreased the abundance of MMP1, a protease that cleaves fibrillar collagens and promotes the proteolytic release of bound growth factors (32).

Researcher Allison Cleary has, for the first time, demonstrated that different types of tumor cells cooperate in the development and growth of breast cancer.

The effect of a novel antagonist of growth hormone releasing hormone on cell proliferation and on the key cell signaling pathways in nine different breast cancer cell lines.

We also found that the EphB4 receptor expressed on the surface of breast cancer cells can promote tumor xenograft growth by enhancing blood vessel formation through interactions with its preferred ligand, ephrin - B2, present in tumor endothelial cells.