Sentences with phrase «modeling cell growth»

Not exact matches

«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.

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.

The compound then was tested in an experimental model for melanoma and found to significantly inhibit tumor cell growth without appreciable toxicities.

Because of the strong association between hippocampal cell growth and exercise in models, previous work on exercise and the brain has not focused on the entorhinal cortex, despite its critical role in learning and memory until now.

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.

«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.

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.

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 Metastasis Lab.

When the researchers reduced the amount of IL13RA2 expression in the cancer cells, they found that the tumor growth was significantly slower in models.

The cancer stem cell model differs from the traditional idea that tumor growth is equal opportunity — that is, any and all cancerous cells can divide and cause the tumor to grow and spread.

The stem cell model says that tumor growth is more hierarchical, mainly driven by a subset of cells that can make new copies of themselves and give rise to the other cell types the tumor contains.

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.

Morris says vaccination with modified tumor cells producing IL - 15 and IL - 15Rα slowed tumor growth and led to increased survival for animal models.

The study, called «Molecular Determinants of Drug - Specific Sensitivity for Epidermal Growth Factor Receptor (EGFR) Exon 19 and 20 Mutants in Non-Small Cell Lung Cancer,» and published online in the journal Oncotarget, demonstrates how computer modeling of EGFR mutations found in lung cancer can elucidate their molecular mechanism of action and consequently optimize the selection of therapeutic agents to treat patients.

As a result, the researchers were able to prevent the growth and malignant spread of the cancer in the animal model and human melanoma cells.

They found that, by using math models to understand the complex dynamics within cancers, they could use small changes in the environment to promote the growth of cells that are less aggressive and thereby decrease tumor growth.

«Mathematical modeling can identify ways to limit aggressive tumor cell growth.»

The study revealed that in the model system chosen by Opitz and colleagues the winning side becomes apparent at a very early stage in the growth of the population, when the numbers of cells are still relatively small.

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 cancer.

Researchers at University of California San Diego School of Medicine, with colleagues at the National Institute of Diabetes and Digestive and Kidney Diseases, the University of Manitoba and St. Boniface Hospital Albrechtsen Research Centre in Canada, have identified a molecular signaling pathway that, when blocked, promotes sensory neuron growth and prevents or reverses peripheral neuropathy in cell and rodent models of type 1 and 2 diabetes, chemotherapy - induced neuropathy and HIV.

Using a three - dimensional model of mammary cell development created by Dr. Sentil Muthuswamy, formerly of CSHL and now at the University of Toronto, the team tested to see if abnormal growth initiated by HER2 signaling would be either enhanced or reduced if any of the 37 PTPs was experimentally «knocked down.»

The study also presents a new model that explains how growth promoting genes could be epigenetically turned on and growth inhibiting genes could be epigenetically turned off in cancer cell formation.

«We have identified a number of pharmaceutical compounds that selectively inhibit — in different experimental models — the mitochondrial enzyme responsible for the tumour growth, thus limiting fat synthesis and without harming normal cells.»

In a paper published online May 17, 2016 in the journal Nature Communications, de Jong and co-first author Koji Taniguchi, MD, PhD, and colleagues, report that treating both ERK1 / 2 and the compensatory pathway, ERK5, concurrently with a combination of drug inhibitors halted colorectal cancer growth more effectively in both mouse models and human colorectal cancer cell lines.

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.

These inhibitors effectively targeted and blocked Msi expressing cells, resulting in halted tumor growth in animal models as well as in patient - derived cancer cells, which harbor more complex mutations and are uniformly drug - resistant.

The combination was significantly toxic to pancreatic cancer cells and disrupted tumor growth and extended survival in several types of advanced pancreatic cancer mouse models.

The test drug slowed the growth of kidney cysts in two mouse models and in cell cultures of human kidney cysts, the study showed.

By means of their mouse model, the hormone researchers from Ulm could prove that dexamethasone — mediated through the dimer function of GR — leads to the release of sphingosine -1-phosphate in the macrophages, a tissue hormone that fosters growth, migration and division of cells and has a stabilization effect on inner vessel walls.

A truly multidisciplinary subject, tissue engineering requires the skills of chemists and materials engineers to design and build organ scaffolds, physicists and mathematicians to model tissue growth, and biologists to monitor and control cell growth.

Mathematical models employed by the researchers suggest that the key is a molecule that inhibits branching, namely, a protein called transforming growth factor - β (TGF - β), which is produced by mammary cells and which is known to stop branching in developing tissues.

In the study, the compound caused human melanoma cells to die and inhibited tumor growth by about 69 percent in a mouse model.

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).

Using animal models and cells, Counter and colleagues found that when they experimentally inhibited copper uptake by tumors with the BRAF mutation, they could curb tumor growth.

In a previous study, Lonard and co-senior study author Bert O'Malley of Baylor College of Medicine screened a large number of compounds to identify SRC - inhibiting molecules that kill a wide variety of cancer cells and inhibit tumor growth in animal models.

Kinetic Modeling of Virus Growth in Cells — John Yin — Microbiology and Molecular Biology Reviews

«We have identified the genes and growth factors involved and, thanks to a collaboration with Microsoft Research, we can now computationally model the control circuitry in mouse cells.

Drew Pardoll, Glenn Dranoff, Elizabeth Jaffee, Hyam Levitsky, and colleagues conduct preclinical studies showing that a vaccine composed of tumor cells irradiated and genetically modified to produce immune system growth factor GM - CSF (granulocyte - macrophage colony - stimulating factor)-- which would become known as the therapeutic cancer vaccine GVAX — could induce potent, specific, and long - lasting anti-tumor immunity in multiple mouse tumor models.

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].

Their results, published in Emerging Infectious Diseases, demonstrate that the highly differentiated 3 - D cell culture model can support the natural growth of human noroviruses, whereas previous attempts using differentiated monolayer cultures failed.

The anthelmintic drug mebendazole inhibits growth, migration and invasion in gastric cancer cell model.

In the paper, the authors use several animal models to show that the progenitor cells could contribute to the formation of new lymph ducts, both by becoming part of the lymph ducts and by stimulating the growth of nearby cells.

Nakano S, Nagasawa T, Ijiro T, Inada Y, Tamura T, Maruyama K, Kuroda J, Yamazaki Y, Kusama H, Shibata N. Bezafibrate prevents hepatic stellate cell activation and fibrogenesis in a murine steatohepatitis model, and suppresses fibrogenic response induced by transforming growth factor - beta1 in a cultured stellate cell line.

Biocellion is being used to model a variety of biological system behaviors, such as biofilm formation and wrinkling, microbial growth dynamics in complex soil structure, brain tumor growth and invasion, formation of complex bacterial colonies, and changes in blood vessels and skin cells.

Over the last 3 years, the partnership between the Salk Institute and Ipsen has delivered significant scientific advances in the cancer field such as the development of biological models mimicking human cancerous processes as well as identification of specific cells driving tumor growth.

Many studies in tumor models have forcibly provided 4 - 1BB signals, injecting either agonist antibodies to 4 - 1BB, or transfecting 4 - 1BBL into the tumor cells, also highlighting the stimulatory capability of 4 - 1BB in driving suppression of tumor growth largely through augmenting CTL and NK responses.

Six ovarian factors (BDNF, IGF - I, estradiol, GDNF, leptin and FGF2) were further studied based upon the expression of their receptors in oocytes and cumulus cells described above, as well as the availability of growth factor concentration information from previous animal model studies [1], [20], [21], [22], [23].

To investigate which mechanism drives cells to stop elongating and become fully differentiated mature cells, we first constructed a computational model for stationary root growth dynamics in the EZ and DZ.

In a xenograft KMT2D - mutated T - lymphoma model, dual treatment with chidamide and decitabine significantly retarded tumor growth and induced cell apoptosis through modulation of the KMT2D / H3K4me axis.