Sentences with phrase «how glioblastomas»

During a conversation this month in his office at Weill Cornell Medicine in New York City, Fine rattled off more dismal stats, like the many failed clinical trials of experimental drugs for glioblastoma; like the paltry increase in life expectancy for people with glioblastoma from 12 months in 1990 to 15 today; like the stupid (in hindsight) assumptions about how glioblastomas grow and how to study them in mice.

Although there have been great advances made in the treatment of leukemias and other cancers, little is known about how Glioblastomas are formed and how these tumors infiltrate the brain tissue.

«The results of both studies help us continue to paint a more defined picture of how glioblastoma starts, evolves and kills, and how we might find a way to slow it down and eventually stop it,» said TGen Professor and Deputy Director Dr. Michael Berens, one of the study's authors.

But itâ $ ™ s difficult not to think in terms of purpose or intent when looking at what cancers do. For example, Winship Cancer Institute scientists Abdessamad (Samad) Zerrouqi, Beata Pyrzynska, Dan Brat and Erwin Van Meir have a recent paper in Cancer Research examining how glioblastoma cells regulate the process of blood clotting.

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

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.

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.

The study — Genomic profiles of low - grade murine gliomas evolve during progression to glioblastoma — published April 7, shows how these tumors continue to rapidly evolve, becoming ever more genetically diverse, as they become malignant and progress.

The other study — Combination therapy with potent PI3K and MAPK inhibitors overcomes adaptive kinome resistance to single agents in preclinical models of glioblastoma — published March 30, shows how drugs targeting PI3K and MAPK could represent promising candidates for glioblastoma therapy.

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.

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.

Clearly a lot more work needs to be done to understand the precise cause of glioblastoma recurrence after surgery and chemotherapy and how to prevent it.

Massachusetts General Hospital pathologist Bradley Bernstein has studied how alterations to chromatin drive glioblastomas, the most common form of brain tumor.