Sentences with phrase «glioblastoma by»

The company's lead candidate, GLN - 1001, is a first - in - class, orally available oncolytic small molecule, currently being developed as a potentially disease modifying therapy for glioblastoma by targeting specific vulnerabilities in tumor cells.

The other study showed how using a combination of drugs at increased potency could prove an effective therapy against glioblastoma by inhibiting the PI3K and MAPK cellular pathways.

While the virus is unlikely to lengthen the lives of people with glioblastoma by much, the small chance of benefit is worth investigating, says Bulstrode.

«Drug could limit spread of deadly brain tumors: Study shows PPF could help treat glioblastomas by sensitizing tumors to chemotherapy, radiation treatments.»

Not exact matches

Now, a high - fat, low - carbohydrate version of the ketogenic diet has been shown to slow glioblastoma tumors by cutting back on the energy supply they need to thrive, said Brent Reynolds, Ph.D., a professor in the Lillian S. Wells Department of Neurosurgery.

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 researchers.

Using human - derived glioblastoma cells in a mouse models, researchers found that the modified high - fat, low - carbohydrate diet increased life expectancy by 50 percent while also reducing tumor progression by a similar amount.

By combining this strategy with cancer cell - targeting materials, we should be able to develop a therapy for glioblastoma and other challenging cancers in the future.»

A glioblastoma tumor requires large amounts of energy as it grows, and the dietary intervention works by drastically limiting the tumor's supply of glucose, Reynolds said.

The latest findings build on previous work by Dr. Habib's lab showing that the same combination of drugs was successful in a mouse model of glioblastoma, a deadly type of brain cancer.

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) has identified an abnormal metabolic pathway that drives cancer - cell growth in a particular glioblastoma subtype.

In a study published in the Journal of NeuroOncology, TGen researchers report that PPF works to limit the spread of glioblastoma multiforme, or GBM — the most common primary tumor of the brain and central nervous system — by targeting a protein called TROY.

A neuro - oncology research team at Dartmouth's Norris Cotton Cancer Center, led by the Director Mark A. Israel, MD with first author Gilbert J. Rahme, PhD, recently identified the transcription factor Id4 as a suppressor of tumor cell invasion in glioblastoma.

Their paper, «Id4 suppresses MMP2 - mediated invasion of glioblastoma - derived cells by direct inactivation of Twist1 function,» was recently published in Oncogene.

Glioblastoma is the most lethal form of primary brain tumor and leads to death in patients by invading the brain tissue in a process that allows single cells to move through normal brain tissue, which makes complete surgical removal of the tumor impossible.

In a model of glioblastoma, a brain cancer that does not metastasize outside of the brain, they could readily see that the length of circulating tumor DNA was smaller than healthy DNA by 20 - 50 base pairs.

Shah next plans to rationally combine the toxin - secreting stem cells with a number of different therapeutic stem cells developed by his team to further enhance their positive results in mouse models of glioblastoma, the most common brain tumor in human adults.

Based on recent information on the mechanisms of chemotherapy, a team of researchers of the McGill University Health Centre (MUHC) developed a new clinical approach to increase the efficiency of treatment in glioblastomas that increased the median survival to 22 months — bringing much needed hope to those affected by this aggressive disease.

Through a mouse model of glioblastoma developed by Lionel Chow, MD, PhD, a pediatric hematologist - oncologist at Cincinnati Children's Hospital, Chen's team was able to confirm this hypothesis.

To identify the main compounds (metabolites) produced by glioblastoma cells during infection by Zika, the researchers analyzed the cells using matrix - assisted laser desorption / ionization mass spectrometry imaging (MALDI - MSI).

Because digoxin and other cardiac glycosides have been shown to induce cancer cell death, the researchers concluded that infection by Zika triggered synthesis of the molecule in glioblastoma cells and that this phenomenon is probably one of the factors that lead to neuronal cell death.

Glioblastoma cells from patients that could be linked by the gene signature analysis with an immature origin generally showed a higher sensitivity to cancer drugs than glioblastoma cells that were associated with a more differentiated celGlioblastoma cells from patients that could be linked by the gene signature analysis with an immature origin generally showed a higher sensitivity to cancer drugs than glioblastoma cells that were associated with a more differentiated celglioblastoma cells that were associated with a more differentiated cell of origin.

Patients with recurrent glioblastoma multiforme (GBM) treated with an experimental vaccine made from the patient's own resected tumor tissue showed an improved survival compared with historical patients who received the standard of care alone, according to an analysis of a phase 2 trial of this vaccine that was recently published in the journal Neuro - Oncology and accompanied by an editorial highlighting the importance of the trial.

A new study published in the Oct. 9 issue of the journal Nature Medicine demonstrates, for the first time, that glioblastoma (GBM), the most common and most lethal brain tumor, is driven by two distinct subsets of cancer stem cells.

«By treating glioblastoma cells with decitabine, we found that we can unmask targets on the tumor cell that can be recognized by killer T cellBy treating glioblastoma cells with decitabine, we found that we can unmask targets on the tumor cell that can be recognized by killer T cellby killer T cells.

On the other hand, aberrant expression of miR - 7 was observed in glioblastomas, and it has been characterized as a putative tumor suppressor by targeting EGFR and AKT (23, 24).

Glioblastoma is typically treated with surgery, followed by radiation and chemotherapy.

In their previous study, the researchers found that drugs that inhibit FGFR3 kinase, an enzyme that helps the protein produced by this fusion gene do its work, increased survival when tested in mice with glioblastoma.

Surgery, radiation and chemotherapy do prolong survival by several months, but targeted therapies, which have been effective with other forms of cancer, have not lengthened survival in patients fighting glioblastoma.

A research team led by Christine Brown, Ph.D., and a clinical team headed by Behnam Badie, M.D., has received a $ 12.8 million grant from the CIRM to fund a phase 1 chimeric antigen receptor (CAR) T cell trial targeting an aggressive brain cancer called malignant glioma, which includes glioblastoma.

With the development of new immunotherapies and targeted personalized medicine therapies, the glioblastoma treatment market is in rapid expansion and estimated to reach nearly $ 3.3 billion by 2024, with a fivefold increase in 10 years.

Since astrocytes reproduce quickly and are supported by a large network of blood vessels, glioblastomas are usually highly malignant.

This technology is based on differential expression of key gene transcript variants (isoform - level gene expression) and was originally tested on a vast collection of glioblastoma samples made available by the University of Pennsylvania.

The study also found that drugs that target the protein produced by this genetic aberration can dramatically slow the growth of glioblastomas in mice.

Dr. Iavarone and his colleagues suspected that glioblastomas might be addicted to proteins produced by gene fusions.

In another experiment, mice with this form of glioblastoma were given a drug that inhibits FGFR kinase, an enzyme essential for the protein produced by FGRF - TACC to do its work.

«ISOMA intends to help change how glioblastoma is treated by changing how the cancer is diagnosed.

These drugs are now being tested in patients with recurrent glioblastoma that contains the gene fusion by one of the paper's co-authors, Marc Sanson, MD, of Pitié Salpêtrière Hospital in Paris.

In a 2012 study published in Science, the CUMC team found that some cases of glioblastoma, the most common and aggressive form of primary brain cancer, are caused by the fusion of two genes, FGFR3 and TACC3.

Brazilians show that the infection by Zika virus kills glioblastoma, one of the most common and aggressive kinds of malignant brain tumour in adults.

«First we looked at pieces of the glioblastoma genome from several samples, and then we extended the analysis to a large set of glioblastomas from the Cancer Genome Atlas project, sponsored by the National Cancer Institute.»

Inhibition of the self - renewal in CD133 - positive glioblastoma TICs by PPAM was attributed to inhibition of stem cell regulatory pathways [67].

Analysis of glioblastoma tumor coverage by oncolytic virus - loaded neural stem cells using MRI - based tracking and histological reconstruction.

Identification of novel small - molecule inhibitors of glioblastoma cell growth and invasion by high - throughput screening.

There is another report by Bai et al which showed the role of TRF2 in maintenance of neurospheres in glioblastoma multiforme (GBM)[18].

The TRPC channel blocker SKF 96365 Inhibits Glioblastoma Cell Growth by Enhancing Reverse Mode of the Na + / Ca2 + Exchanger and Increasing Intracellular Ca2 +.

Glioblastoma angiogenesis and tumor cell invasiveness are differentially regulated by β8 integrin.

Regulation of Glioblastoma Tumor - Propagating Cells by the Integrin Partner Tetraspanin CD151.

The information gained by his experiments have the potential to improve the clinical management of patients with glioblastoma

The study, run by Washington University and the University of California San Diego, used 33 lab mice with glioblastoma, an aggressive form of brain cancer.