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.
Not exact matches
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 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.
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.
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.
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 cel
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 cel
glioblastoma cells that were associated with a more differentiated
cell of origin.
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 cell
By treating
glioblastoma cells with decitabine, we found that we can unmask targets on the tumor
cell that can be recognized
by killer T cell
by killer T
cells.
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.
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.
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 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.
Integrated Genomic Analysis Identifies Clinically Relevant Subtypes of
Glioblastoma Characterized
by Abnormalities in PDGFRA, IDH1, EGFR, and NF1 Cancer
Cell, 17 (1), 98 - 110 DOI: 10.1016 / j.ccr.2009.12.020
BAI1 is produced
by brain
cells naturally, but is often silenced epigenetically in
glioblastoma cells.