Sentences with phrase «in tumor cell growth»

The fat stored in your body can produce estrogen (which can also lead to breast cancer) or proteins that cause inflammation and insulin resistance, resulting in tumor cell growth.
TKM - 080301 targets a specific gene called polo - like kinase 1 (PLK1), which codes for a protein involved in tumor cell growth.

Not exact matches

So even if a tumor is surgically removed, it is difficult to extract every cancerous cell; any left behind will result in the growth of a new tumor.
Mogroside V has been found in research to have the ability to inhibit tumor growth in pancreatic cancer by interfering with the rapid dividing of cancer cells, preventing angiogenesis (blood flow to the tumor), and even promoting cancer cell death (10).
Cauliflower is high in sulforaphane, a sulphur compound that has been shown to kill cancer stem cells, thereby slowing tumor growth and support liver detoxification pathways.
Sulforaphane (a sulphur compound) is a key compound in broccoli which has the ability to kill cancer stem cells, which slows tumor growth.
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 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 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 cells.
After EZH2 enzymes rise, their levels taper off, and then, the scientists found two to three-fold increases in a protein called DNMT1, which maintains DNA methylation in the «start» location of a variety of tumor suppressor genes that normally suppress cell growth.
«To my great surprise, even injecting 10 million activated T cells specific to the P1A antigen did not affect tumor growth in this induced tumor model,» says Van den Eynde.
Scientists at the Rosalind Franklin University of Medicine and Science in Chicago found a «remarkable similarity» between the cells that support the growth and development in placentas and in tumors.
Also limiting the use of therapeutic stem cells to date, self - renewal, a quality so vital to a fast - growing fetus, can also be a source of cancer risk when haphazard, unlimited cell multiplication results in the abnormal tissue growth seen in tumors.
«Our work strongly supports that cancer stem cells are the main source of growth in these tumors and, as such, should be considered promising targets for treatment,» says Mario Suvà, MD, PhD, of the MGH Department of Pathology, co-senior author of the Nature paper.
In addition to diminishing the tumor's energy supply, the diet slows the growth of glioblastoma cells by altering a cellular - signaling pathway that commonly occurs in cancers, according to the researcherIn addition to diminishing the tumor's energy supply, the diet slows the growth of glioblastoma cells by altering a cellular - signaling pathway that commonly occurs in cancers, according to the researcherin cancers, according to the researchers.
An experimental drug in early development for aggressive brain tumors can cross the blood - brain tumor barrier, kill tumor cells and block the growth of tumor blood vessels, according to a study led by researchers at the Ohio State University Comprehensive Cancer Center — Arthur G. James Cancer Hospital and Richard J. Solove Research Institute (OSUCCC — James).
Nagoya University - led research team shows in mice the potential of a special immune cell that targets a key protein in tumor growth that helps stop brain cancer.
They cross the blood - brain / blood - tumor barrier, and accumulate within brain tumor sites, where they target oncogenes, regulate cell growth and differentiation, reduce tumor burden and prolong survival in our mouse models.»
The researchers took this discovery and, in an animal model, identified a drug that is able to re-activate those immune cells and reduce brain tumor growth, thereby increasing the lifespan of mice two to three times.
Dr. Massagué is particularly interested in the ability of tumor cells to hug blood vessels, as he suspects this behavior may be essential for the survival of metastatic cancer cells not only in the brain but also in other parts of the body where metastatic tumor growth can occur.
These findings also have implications for treatment of cancer and other disorders, such as obesity, in which M2 macrophage cells play a regulatory role in tumor growth and fat deposition.
The compound then was tested in an experimental model for melanoma and found to significantly inhibit tumor cell growth without appreciable toxicities.
In mice, the Runx2 knock - in myeloma cells produced greater tumor growth and a wider spread of disease compared with the original myeloma cells; conversely, the Runx2 knock - down cells had less tumor growth and disease spreaIn mice, the Runx2 knock - in myeloma cells produced greater tumor growth and a wider spread of disease compared with the original myeloma cells; conversely, the Runx2 knock - down cells had less tumor growth and disease spreain myeloma cells produced greater tumor growth and a wider spread of disease compared with the original myeloma cells; conversely, the Runx2 knock - down cells had less tumor growth and disease spread.
«Taken together, these results support the hypothesis that multiple myeloma cells express bone - related genes in a Runx2 - dependent fashion that mimics bone marrow resident cells and likely contributes to tumor survival and growth in the bone microenvironment,» Yang and colleagues wrote in the paper.
In the last few years, a bulk of data pointing to a small population of cells in tumors that maintain tumor growth, are particularly resistant to chemotherapy, are responsible for relapses, and develop metastaseIn the last few years, a bulk of data pointing to a small population of cells in tumors that maintain tumor growth, are particularly resistant to chemotherapy, are responsible for relapses, and develop metastasein tumors that maintain tumor growth, are particularly resistant to chemotherapy, are responsible for relapses, and develop metastases.
Researchers at the Bellvitge Biomedical Research Institute of Bellvitge, the Catalan Institute of Oncology and the University Hospital of Bellvitge have participated in an international study published in the journal Cancer Cell that describes how exosomes secreted by tumor cells contain protein and microRNA molecules capable of transform neighboring cells into tumoral cells promoting tumor growth.
The Campàs lab is studying several of these questions, including how limbs are built and how mechanical changes in tumors affect the behavior of malignant cells and the growth of the tumor.
The researchers also tested a Runx2 knock - down variant of a human multiple myeloma cell line and found that it produced significantly less tumor growth in immunodeficient mice than the original human multiple myeloma cells.
With these in vitro test methods, the KU researchers have shown that anti-CD44s antibody can reduce pancreatic cancer cell growth, metastasis and ability of the tumors to recur after radiation therapy.
«Despite the low infection levels of mouse cells with oHSV, we were able to cause a delay in tumor growth in one of the cancer models and even cure many of the mice in a second model,» said first author Jennifer Leddon, who conducted much of the laboratory work during a research experience in the Center for Childhood Cancer and Blood Diseases.
In cancer, these switches inappropriately activate or silence important genes, such as those that regulate cell growth and life cycle, ultimately leading to tumors.
In pancreatic cancer, their activity boosts tumor growth and spread, and may also help suppress T cells and other immune elements that would otherwise attack the tumor.
«Tumor cells produce larger quantities of H2O2 and use oxidative signals at higher levels than normal cells in order to drive their own growth,» says Mirko Sobotta, first author of the publication.
In this study, we found that chloroquine not only has an effect on the growth of the cancer cells, but also makes the tumor environment less aggressive by normalizing the abnormal blood vessels in the tumor,» says Patrizia AgostiniIn this study, we found that chloroquine not only has an effect on the growth of the cancer cells, but also makes the tumor environment less aggressive by normalizing the abnormal blood vessels in the tumor,» says Patrizia Agostiniin the tumor,» says Patrizia Agostinis.
«About five percent of people have some kind of cartilage tumor in their bones, and in most cases it's because the growth - plate cartilage cells weren't fully replaced by bone tissue,» Alman said.
When present in tumors, both abnormal myc and abnormal mTOR are known to be able to rev up protein production and to foster cell growth.
Scientists now know that what matters most in determining the behavior of a particular cancer (and its response to specific therapy) are the molecular pathways that drive malignant cell growth instead of where the tumor begins in the body.
However, cancer cells may instead be coaxed to turn back into normal tissue simply by reactivating a single gene, according to a study that found that restoring normal levels of a human colorectal cancer gene in mice stopped tumor growth and re-established normal intestinal function within only 4 days.
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.
Multiple myeloma is a cancer of plasma cells in the blood that causes tumor growths in bone marrow.
Bacteria had to be in direct contact with tumor cells to speed growth, but exactly how the bacteria do that isn't yet known.
Damage occurs when metastatic tumor cells recruit pre-osteoclast cells to the bone and then induce their differentiation into mature bone - degrading cells, which results in the release of proteins from the bone matrix that promote tumor cell growth.
«In drug development, it's easier to turn that growth function off than it is to switch on the cell's defective tumor suppression mechanism.»
The researchers identified a genetic mutation in the tumor cells that plays a role in both the growth and the death of a cell.
Terbinafine, a U.S. Food and Drug Administration — approved antifungal drug targeting SQLE, markedly inhibited SQLE - induced NAFLD - HCC cell growth in NAFLD - HCC and HCC cells and attenuated tumor development in xenograft models and in Sqle transgenic mice.
«We demonstrated that alpha - KGDH interacts with Gcn5 in the cell nucleus and found that tumor cell proliferation and tumor growth were inhibited when alpha - KGDH was blocked from entering the cell nucleus or by disruption of Gcn5's binding to succinyl - coenzyme A,» said Lu.
The idea has been controversial, but three papers published today report evidence that in certain brain, skin, and intestinal tumors, cancer stem cells are the source of tumor growth.
He and his colleagues report online in Nature that in mouse papilloma tumors, a precursor to skin cancer, most of the tumor growth came from a few cells, which in some ways resembled the stem cells that maintain healthy skin.
For several years already, it is well known that tumor growth can be reduced by suppressing autophagy in cancer cells.
Epidermal growth factor receptor (EGFR) mutations found in the circulating free tumor DNA (ctDNA) from the plasma of advanced non-small cell lung cancer (NSCLC) patients correlates well with the EGFR mutations from patient - matched tumor tissue DNA.
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