The Transcription Factor ZFX Is Required for Maintaining the Tumorigenic Potential of
Glioblastoma Stem Cells.
Nigericin and grisorixin methyl ester from the Algerian soil - living Streptomyces youssoufiensis SF10 strain: a computational study on their epimeric structures and evaluation of
glioblastoma stem cells growth inhibition — Nassima Leulmi — Natural Product Research
Molecular Targeting of TRF2 Suppresses the Growth and Tumorigenesis of
Glioblastoma Stem Cells.
Figure 2: Abnormal accumulation of the FGFR - TACC fusion protein (red) in
glioblastoma stem cells isolated from a primary human glioblastoma with fused FGFR - TACC genes.
tumors from neural stem cells also contained more
glioblastoma stem cells, cells that are believed to give rise to tumor recurrence after therapy,» says Lene Uhrbom, senior lecturer at the Department of Immunology, Genetics and Pathology and lead author of the study.
Zika virus has oncolytic activity against
glioblastoma stem cells.
«We have identified a code of «molecular switches» that control a very aggressive subpopulation of brain cancer cells, so - called
glioblastoma stem cells,» says Mario Suvà, MD, PhD, of the MGH Department of Pathology and Center for Cancer Research, co-lead author of the Cell article.
«Transcription factors distinguishing
glioblastoma stem cells identified.»
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.»
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.
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 cells.
The current study was designed to clarify the cellular hierarchy underlying glioblastoma, to identify epigenetic factors that distinguish
glioblastoma stem cells from more differentiated tumor cells and to suggest potential therapies targeting those factors.
Several studies have used cell - surface markers — proteins found on the outer membranes of tumor cells — to identify
glioblastoma stem cells; but the specific markers used have been controversial and can not reflect molecular processes going on within tumor cells.
Not exact matches
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 alone.
Small populations of adult
stem cells with somewhat limited developmental potential are responsible for the body's ability to heal injuries and replace worn out cells and tissues, and evidence is growing that rare cancer
stem cells are responsible for the uncontrolled growth of some malignant tumors, including
glioblastoma.
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.
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.
The physician scientists sought to identify
glioblastoma subtype - specific cancer
stem cells.
Inhibiting ALDH1A3 - mediated pathways slows the growth of mesenchymal glioma
stem cells and might provide a promising therapeutic approach for
glioblastomas with a mesenchymal signature.
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 nothing
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 nothing
glioblastomas but which, lacking tumor
stem cells, were nothing of the kind.
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.
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.
«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 paper.
«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.
VIRUS VICTORY Zika virus (green) infects and kills
stem cells (red) in human
glioblastoma tissue, without infecting healthy brain 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 diagnosis.
«Areas of
glioblastoma tumors correlate with separate subtypes of glioma
stem cells.»
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.
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.
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.
The findings may even have implications for studying
glioblastoma, a common brain cancer whose ability to grow, migrate and hack into the brain's blood supply appears to rely on a pattern of gene activity similar to that now identified in these neural
stem cells.
We initially focused on drilling down into the genetic differences between
glioblastoma tumour
stem cells and normal neural
stem cells.
«These findings show that our cancer model will not only allow us to start understanding the biology of
glioblastoma but will also allow us to answer many questions surrounding cancer
stem cells,» says Verma.
His team is using innovative cell culture models to advance our understanding of brain
stem cells and their potential role in
glioblastoma.
The â $ œcancer
stem cellâ $ hypothesis has invigorated the neuro - oncology field with a breath of fresh thinking that may end up shaking the foundation of old dogmas, such as the widely held belief that
glioblastoma tumors are incurable because of infiltrative disease.
Frisco, TX About Blog Beloved and gentle husband, daddy, son, brother, friend, co-worker and neighbor who battled brain cancer - a
glioblastoma in the brain
stem that we call Spot.