Sentences with phrase «in glioblastoma cells»

BAI1 is produced by brain cells naturally, but is often silenced epigenetically in glioblastoma cells.

Researchers have demonstrated that the enzymatic activity of R5 receptor - type protein tyrosine phosphatases is a requisite for the maintenance of stem cell properties and tumorigenicity in glioblastoma cells and could be a promising drug target for treatment.

Fenofibrate - induced nuclear translocation of FoxO3A triggers Bim - mediated apoptosis in glioblastoma cells in vitro.

A chalcone - related small molecule that induces methuosis, a novel form of non-apoptotic cell death, in glioblastoma cells.

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.

Protein expression in these glioblastoma cells more closely mimicked that in real cancer cells than in 2D cultures of cells, indicating that this method could be used to study cancer (Nature Nanotechnology, DOI: 10.1038 / nnano.2010.23).

Not exact matches

«Ultimately, we needed 20 years to learn how to supercharge these cells to deliver anticancer activity,» says Arie Belldegrun, president and CEO of Kite Pharma in Santa Monica, California, which is assessing CAR T cells in six trials for B cell leukemia and lymphomas, and glioblastoma.

In human cells and in mice, the virus infected and killed the stem cells that become a glioblastoma, an aggressive brain tumor, but left healthy brain cells alonIn human cells and in mice, the virus infected and killed the stem cells that become a glioblastoma, an aggressive brain tumor, but left healthy brain cells alonin mice, the virus infected and killed the stem cells that become a glioblastoma, an aggressive brain tumor, but left healthy brain cells alone.

In glioblastoma, the cancer cells resemble those in the developing brain, suggesting that the Zika infection could attack them toIn glioblastoma, the cancer cells resemble those in the developing brain, suggesting that the Zika infection could attack them toin the developing brain, suggesting that the Zika infection could attack them too.

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.

These were released into tumour cells that had been taken from glioblastoma patients and grown in the lab.

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.»

The investigators report that trapping virus - loaded stem cells in a gel and applying them to tumors significantly improved survival in mice with glioblastoma multiforme, the most common brain tumor in human adults and also the most difficult to treat.

The team found that exposing samples of human glioblastoma tumours grown in a dish to the Zika virus destroyed the cancer stem cells.

Shah and his team loaded the herpes virus into human MSCs and injected the cells into glioblastoma tumors developed in mice.

In a series of experiments, the researchers first identified a set of 19 transcription factors that were expressed at significantly greater levels in cultured human glioblastoma stem cells capable of tumor propagation than in differentiated tumor cellIn a series of experiments, the researchers first identified a set of 19 transcription factors that were expressed at significantly greater levels in cultured human glioblastoma stem cells capable of tumor propagation than in differentiated tumor cellin cultured human glioblastoma stem cells capable of tumor propagation than in differentiated tumor cellin differentiated tumor cells.

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.

Identifying the drivers of these different cellular states in glioblastoma stem cells could offer us the best opportunity for treating what remains an extremely difficult - to - treat tumor.»

Several studies have supported a role for cancer stem cells in the aggressive brain tumors called glioblastoma, but those studies involved inducing human tumors to grow in mice, and as such their relevance to cancer in humans has been questioned.

Looking through the microscope: The image illustrates the differences in tumor cells in glioblastoma patients.

From tissue and cell samples from five glioblastoma patients, the scientists obtained 33 individual cancer cells capable of reproduction, which grew into very different tumors in the lab.

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.

Glioblastomas in lab dishes and mouse brains are fakes, little Potemkin villages that everyone thought were faithful replicas of human glioblastomas but which, lacking tumor stem cells, were nothingGlioblastomas in lab dishes and mouse brains are fakes, little Potemkin villages that everyone thought were faithful replicas of human glioblastomas but which, lacking tumor stem cells, were nothingglioblastomas but which, lacking tumor stem cells, were nothing of the kind.

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.

According to his unpublished findings, when he puts glioblastoma cells from patients into lab dishes with brain organoids, the cells attach to the surface of the organoids, burrow into them, and within 24 to 48 hours grow into a mass that eventually «looks exactly like what happened in the patient's own brain,» Fine said.

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.

Researchers have identified a group of immune system genes that may play a role in how long people can live after developing a common type of brain cancer called glioblastoma multiforme, a tumor of the glial cells in the brain.

Invasion assays using Glioblastoma (GBM) cells on the left lacking Id4, in comparison to the same cells being genetically engineered to express Id4 on the right.

Another is that the transplanted bits of tumor act nothing like cancers in actual human brains, Fine and colleagues reported in 2006: Real - life glioblastomas grow and spread and resist treatment because they contain what are called tumor stem cells, but tumor stem cells don't grow well in the lab, so they don't get transplanted into those mouse brains.

«This finding suggests a novel therapeutic target to decrease invasion of tumor cells in patients and may also provide a novel biomarker that could help predict survival of patients with glioblastoma,» explained Israel.

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.

These findings provide further evidence of ONC201 as an inhibitor of cancer stem cells and support ongoing clinical trials in prostate cancer and glioblastoma that have shown evidence of tumor shrinkage.

The results suggest the simultaneous activation of certain molecular pathways — actions among molecules in a cell that can lead to change — in particular the MAPK and PI3K cellular pathways, triggered tumor initiation and produced increasingly dense low - grade gliomas that quickly progressed to glioblastoma multiforme (GBM).

«Combining CAR T cells with existing immunotherapies may overcome resistance in glioblastomas.»

«In principle, both these features make GA11 an attractive drug candidate to target glioma stem - like cells in glioblastoma multiforme tumors,» said Ichiro Nakano, M.D., Ph.D., and colleagues in the papeIn principle, both these features make GA11 an attractive drug candidate to target glioma stem - like cells in glioblastoma multiforme tumors,» said Ichiro Nakano, M.D., Ph.D., and colleagues in the papein glioblastoma multiforme tumors,» said Ichiro Nakano, M.D., Ph.D., and colleagues in the papein the paper.

«This trial showed that there is a need to target additional antigens in glioblastoma, as well as overcome the immunosuppressive environment that the CAR T cells encountered in the tumor,» Maus said.

«This is an important paper because it illustrates the potentially significant capabilities of CAR T cells in glioblastoma,» O'Rourke said.

Genetically modified «hunter» T cells successfully migrated to and penetrated a deadly type of brain tumor known as glioblastoma (GBM) in a clinical trial of the new therapy, but the cells triggered an immunosuppressive tumor microenvironment and faced a complex mutational landscape that will need to be overcome to better treat this aggressive cancer, Penn Medicine researchers report in a new study this week in Science Translational Medicine.

«Our study suggests that if a cancer - causing mutation occurs in the neural stem cell population in the SVZ, it gives rise to the proneural or the neural glioblastoma subtype.

The results of the analysis showed that the glioblastoma cells displayed moderate cytopathic effects 24 hours after infection, such as rounded, swollen cell bodies and formation of syncytia, masses of cytoplasm in which the membrane contains several nuclei.

VIRUS VICTORY Zika virus (green) infects and kills stem cells (red) in human glioblastoma tissue, without infecting healthy brain cells.

«Zika virus, which has become a threat to health in the Americas, could be genetically modified to destroy glioblastoma cells,» said Rodrigo Ramos Catharino, a professor at FCF - UNICAMP and head of the institution's Innovare Biomarker Laboratory.

In light of these findings, the researchers at FCF - UNICAMP set out to investigate the effects of Zika virus when it infects glioblastoma cells.

In collaboration with co-senior authors Diamond and Milan G. Chheda, MD, of Washington University School of Medicine, and Jeremy N. Rich, MD, of UC San Diego, Zhu tested whether the virus could kill stem cells in glioblastomas removed from patients at diagnosiIn collaboration with co-senior authors Diamond and Milan G. Chheda, MD, of Washington University School of Medicine, and Jeremy N. Rich, MD, of UC San Diego, Zhu tested whether the virus could kill stem cells in glioblastomas removed from patients at diagnosiin glioblastomas removed from patients at diagnosis.

The team's next steps are to test coibamide A in a mouse model for triple negative breast cancer and in a mouse model for brain cancer in which the glioblastoma cells are grown in the brain instead of the flank.

The screening revealed coibamide A to be capable of killing many types of cancer cells, but Ishmael decided to focus subsequent studies on two types in particular — brain tumors, or glioblastomas, and a breast cancer subtype known as triple negative breast cancer.

«When we compared the gene signature activity of glioblastoma cells from around 60 patients we found that a large number of patients could be divided into subgroups that showed a correlation between gene activity, tumor cell characteristics and cell of origin similar to the one we had seen in the mouse study.

This visual abstract depicts how Wei et al. utilize single - cell phosphoproteomic analysis of patient derived glioblastoma models to identify shifts in signaling coordination following short - term treatment with kinase inhibitors, which facilitates the design of combination therapy approaches with reduced resistance and improved efficacy.