Sentences with phrase «tumor models for»

Using tumor models for both astrocytoma and oligodendroglioma, which are very similar to human tumors, they could show that one and the same cell type, called oligodendrocyte precursor cells, could give rise to both tumor forms.

Not exact matches

«We're trying to build models that describe how tumors grow and respond to therapy,» said Yankeelov, director of the Center for Computational Oncology at The University of Texas at Austin (UT Austin) and director of Cancer Imaging Research in the LIVESTRONG Cancer Institutes of the Dell Medical School.

According to ICES Director J. Tinsley Oden, mathematical models of the invasion and growth of tumors in living tissue have been «smoldering in the literature for a decade,» and in the last few years, significant advances have been made.

They implemented this principle through the development and application of something they call the «Occam Plausibility Algorithm,» which selects the most plausible model for a given dataset and determines if the model is a valid tool for predicting tumor growth and morphology.

«Particularly in such patients with underlying CKD, our modeling results support the integration of renal tumor anatomic features at cross-sectional imaging into decision making for treatment of small renal masses and may be used to provide a patient - centered framework for selection of optimal candidates for ablative therapy,» Kang said.

Traditional genetic approaches together with the new wealth of genomic information for both human and model organisms open up strategies by which drugs can be profiled for their ability to selectively kill cells in a molecular context that matches those found in tumors.

«We know that 70 - 75 percent of glioblastoma patients undergo surgery for tumor debulking, and we have previously shown that MSCs encapsulated in biocompatible gels can be used as therapeutic agents in a mouse model that mimics this debulking,» he continued.

For this study, Guttridge, first author David J. Wang, who developed many of the study's concepts, and their colleagues monitored NF - kB activity during tumor development using mouse embryonic fibroblasts and two mouse models.

Testing each of these factors for their ability to return differentiated tumor cells to a stem - like state, identified a combination of four — POU3F2, SOX2, SALL2 and OLIG2 — that was able to reprogram differentiated tumor cells back into glioblastoma stem cells, both in vitro and in an animal model.

This treatment prevented the formation of polyps, showing that bacteria are essential for early tumor development in this model.

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

The next step for the researchers is to demonstrate the viability of this approach to the production and delivery of an anticancer molecule in a whole tumor model system.

BPTES has been used in animal models for a variety of cancers but has not substantially reduced tumor sizes, probably because the drug concentration in tumor tissue is not high enough when using conventional drug formulation methods, say the scientists.

«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 a mouse model of triple - negative breast cancer, mice injected with cancer cells that over-express ZMYND11 had tumor volumes of less than 50 cubic millimeters while control mice and those injected with cells expressing ZMYND11 deficient for binding to the methyl group had tumor volumes ranging from 150 to 400 cubic millimeters at eight weeks.

Daley and Urbach's team found that they could reverse Lin28's tumor - causing effects in their transgenic model by forcing expression of Let - 7, suggesting that treatments targeting Lin28 hold promise for treating Wilms tumors.

«And while the tumor model we're now studying doesn't present targets for new drugs, if we can discover the mechanism controlling that model, it may yield therapeutic drug targets.»

A study combining tumor cells from patients with breast cancer with a laboratory model of blood vessel lining provides the most compelling evidence so far that a specific trio of cells is required for the spread of breast cancer.

This group's achievement shows the possibility to clarify the mechanism of human tumor formation, especially the molecular mechanism responsible for in the initial stage of cell cancerization due to DNA damaged by radiation in the initial stage, by using the model of budding yeast, a primitive eukaryote.

Combining their strategy with an existing immunotherapy treatment that works by releasing the «brakes» on immune cells, they found they could shrink melanoma tumors, and prolong survival in preclinical models for melanoma.

«In the future, our models should provide robust tools to screen for therapies that impact tumor dormancy and metastasis, and should also provide a platform to solve other biological mysteries that underlie dormancy.»

We created a mouse xenograft model in which SiHa cervical cancer cells were injected into mice subcutaneously, and the resultant tumors were treated with PAL three times a week for 6 weeks.

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

In their report that has received advance online publication in Nature Nanotechnology, a research team based at the Wellman Center for Photomedicine at Massachusetts General Hospital (MGH) describes how a nanomedicine that combines photodynamic therapy — the use of light to trigger a chemical reaction — with a molecular therapy drug targeted against common treatment resistance pathways reduced a thousand-fold the dosage of the molecular therapy drug required to suppress tumor progression and metastatic outgrowth in an animal model.

Human tumor tissue or cell lines can be coengrafted into these mouse models, providing a powerful tool for studying the interactions between human immune cells and human cancers.

It has been known for decades that warfarin, the most widely used anticoagulant worldwide, reduces tumor metastasis in model systems.

For example, in colorectal cancer lab models, where a mutation in the beta - catenin gene drives MYC to cancerous levels, eliminating PVT1 from these cells made the tumors nearly disappear.

With the help of various mouse models for pancreatic cancer, they have succeeded in elucidating the molecular pathways of tumor development in detail and have gained a better understanding of how various characteristics of the disease arise.

Meng and Nel also collaborated with Dr. Timothy Donahue, chief of gastrointestinal and pancreatic surgery and a Jonsson Comprehensive Cancer Center member, to demonstrate that treatment with the iRGD peptide can enhance tumor cell killing for patient - derived pancreatic cancers, growing subcutaneously in a mouse model.

It's remarkably difficult to model for a solid tumor,» said Shen.

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.

Ongoing studies from the Discher lab are focused on finding that sweet spot with additional tumor models, as well as on how to engineer macrophages for longer - lasting effect.

They further investigated this phenotype in a skin tumor model system, provided by Maria Sibilia from the Institute for Cancer Research of the Medical University of Vienna, and found that deactivating HDAC1 actually accelerates tumor development, while HDAC2 deactivation has no effect.

Researchers gave animal models an oral supplement of spermidine and found that they lived longer and were less likely than untreated individuals to have liver fibrosis and cancerous liver tumors, even when predisposed for those conditions.

In the new treatment model, medical oncologists and palliative care physicians partnered in a «co-rounding» format to deliver cancer care for patients admitted to Duke University Hospital's solid tumor unit.

Sanford Research scientists are published in Nature Cell Biology for their work developing a model to explore therapies for a pediatric brain tumor known as choroid plexus carcinoma.

«Animal model for pediatric brain tumor created.»

«Novel imaging model helps reveal new therapeutic target for pancreatic cancer: Antisense treatment in preclinical models shows effectiveness against deadly tumors.»

In a previous study, investigators at the Cancer Institute showed that using a vaccine treatment for bladder and breast cancer tumors in laboratory models resulted in a reversal of the traditional immune blockade, as well as the development of tumor specific immunity throughout the body.

For the new study, they added a component to the model that simulates the tumor's response to drugs that target VEGF and inhibit its activity.

In their search for novel, tumor - specific therapies that could target multiple brain metastases without damaging adjacent tissues, the research team first developed a mouse model that more closely mimics what is seen in patients.

«This model, when combined with a rare genetic disease, revealed for the first time how a protein known to prevent tumor growth in most cases, p53, may instead drive bone cancer when genetic changes cause too much of it to be made in the wrong place.»

An extension of this model, however, proposes that EMT forms a key mechanistic basis for the progression of malignant tumors (reviewed by Nieto MA [1]-RRB-.

In a 1988 paper summarizing his findings, Fiebig concluded that xenograft mice were wonderful models for broadly testing new drugs against human tumors, but they «can not be used as a clinical routine method» for predicting patient treatment.1 The idea of using xenograft mice as personal avatars for cancer patients was discarded.

The goal, for now, is to prove that the drug predictions from the computer model successfully treat their corresponding mouse tumors.

In addition to developing the new genetically engineered mouse model for the form of cancer called glioblastoma multiforme, the researchers made a key discovery about brain tumor biology via the mice.

First, the team sequences DNA and RNA from tumor biopsies and inputs that information into a computer model that identifies a handful of dysregulated proteins necessary for survival of the tumor cell, what Califano calls the «master regulators.»

The data allowed the researchers to generate personalized genome - scale metabolic models for cancer patients to identify key genes involved in tumor growth.

Due to the high efficiency of establishing organoid models from different tissues and diseases, such as cancer, organoid technology allows the generation of large living biobanks of tumor organoids that are amenable for middle - throughput drug screens and may allow personalized therapy design, as a complement to cell line and xenograft - based drug studies (7,19).

Unlike previous MRI studies of tumors in mice, the researchers were able to detect very small naturally occurring cancers, which were excellent models for human breast cancer; the tumors the mice developed were «realistic models of the most frequently detected human cancers,» the authors wrote.