Articles tagged with Gliomas
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A recent study discovered a connection between glioma cells expressing the protein TAU and better patient outcomes. The presence of TAU helped regulate blood vessel formation, contributing to tumor aggression. Researchers suggest TAU levels could serve as a biomarker for tumor progression in IDH1/2 mutant gliomas.
A recent study by the Glioma Longitudinal Analysis (GLASS) Consortium discovered highly variable and patient-specific genomic alterations in diffuse gliomas over time. The research team characterized initial and recurrence samples from 222 patients, revealing that gliomas do not evolve consistently under cancer therapies.
Researchers at Stanford University School of Medicine discovered that severe brain cancers form synapses with healthy neurons, hijacking electrical signals to drive their own growth. The study found that interrupting these signals with an anti-epilepsy drug greatly reduced tumor growth in human tumors in mice.
Researchers at Cleveland Clinic have identified FGF2 as a novel druggable target for glioblastoma, the most common primary malignant brain tumor. The study reveals that FGF2 is an intermediary in a multi-step pro-cancer signaling loop, suggesting that targeting it may halt the growth and spread of glioblastoma.
A recent analysis of NRG Oncology/RTOG 9802 data suggests that both IDH-mutant subgroups of high-risk low-grade gliomas may benefit from the addition of PCV chemotherapy to radiotherapy. This finding is significant, as it enhances prognostic and predictive clarification of patients with low-grade glioma.
A study published in PLOS Medicine found that a computer-assisted diagnostic procedure can detect the growth of low-grade brain tumors earlier and at smaller volumes than current clinical methods. This could lead to reduced delays in detecting tumor growth and potentially improve patient outcomes.
Researchers found that combining carboplatin and everolimus increased DNA damage and cell death in laboratory models, slowing tumor growth. The treatment showed promise in killing tumor cells and reducing tumor size, especially in tumors with high mTOR expression.
Recent research by Children's Tumor Foundation advances understanding of brain tumors affecting neurofibromatosis patients. Two large-scale studies have identified genetic, epigenetic, and metabolic alterations in NF1 gliomas, paving the way for targeted therapies.
Researchers at Far Eastern Federal University propose using stem cell activation to target glioma tumors. The approach aims to bring cancerous stem cells into an active state, making them vulnerable to chemotherapy. This method has been approved for publishing and is considered promising despite its risks.
Researchers found that many slow-growing NF1 gliomas contain few macrophages and produce proteins that can trigger an immune system attack, making them good candidates for treatment with immunotherapy. Clinical trials are now being planned for these high-immune tumors.
Researchers at Henry Ford Health will explore genetic makeup of gliomas to identify new therapies, building on previous discoveries about DNA methylation and molecular signatures.
Researchers at Brigham and Women's Hospital have developed a rapid molecular diagnostic that can determine if a tumor harbors an IDH1 or IDH2 mutation within 27 minutes. The test is coupled with a sustained release microparticle drug delivery system that provides localized treatment and prolonged survival in a mouse model.
The INTEROCC study found no clear association between occupational exposure to high-frequency electromagnetic fields and risk of glioma or meningioma. However, the researchers suggest that radiofrequency magnetic fields may be associated with increased tumour promotion, warranting further investigation.
A study published in Science Translational Medicine found that acetazolamide increases sensitivity to treatment and enhances survival in mice with glioblastoma. The drug, which is also used to treat altitude sickness, was able to restore the effectiveness of chemotherapy by blocking a protein called BCL-3.
A recent international study has identified three regions in the genome with significant genetic differences between men and women for developing glioma. These differences vary by sex and type of tumor, suggesting a potential path to assessing patient risk for brain cancer through genetic tests.
Using MR spectroscopy imaging, researchers found that a novel IDH1 inhibitor reduced levels of the oncometabolite 2HG in patients with IDH1-mutated gliomas. The study showed a potential metabolic reprogramming of the tumor in response to treatment.
A recent study published in Cell Reports has revealed that mutant Isocitrate dehydrogenase 1 (IDH1) drives glioma development by cooperating with multiple mutations and events in brain tumor cells. This breakthrough discovery provides substantial evidence for the functional role of mutant IDH1 in tumorigenesis.
Research identifies a mechanism by which glioma cells develop resistance to anti-angiogenic treatment, using different strategies to spread through the brain. The study reveals a potential target for combination therapies based on Wnt signaling and vessel co-option pathways.
Researchers have identified seven biomarkers that can predict which glioma patients will progress to a more aggressive form of the disease. A biomarker panel could help physicians decide whether more aggressive treatment is necessary to prevent progression.
Researchers identified epigenetic biomarkers to predict brain tumor recurrence severity, enabling personalized treatment plans. A set of testable DNA-methylation biomarkers may help clinicians assess a patient's disease trajectory.
Scientists have identified a therapeutic approach targeting glioma stem cells, which could lead to improved patient survival. By utilizing drugs that target these cancerous cells, the team aims to increase the effectiveness of chemotherapy agents and prevent recurrences.
Scientists have discovered a novel mechanism that prevents glioblastoma development through the modulation of EFGR expression by RanBP6. The study reveals that silencing of RanBP6 promotes glioma growth by upregulating EGFR expression, while reconstitution of RanBP6 leads to reduction in tumor growth.
Glioblastoma (GBM) is driven by two distinct subsets of cancer stem cells, each with its own transcriptional program and morphological characteristics. Targeting these cell populations using combined BMI1 and EZH2 inhibition achieves modest efficacy in solo treatments but synergistic results when used together.
Researchers at Stanford University School of Medicine found that cutting off access to a signaling molecule can halt the growth of certain aggressive brain tumors. The team's findings suggest that interrupting the neuroligin-3 signal could be a helpful strategy for controlling high-grade gliomas in human patients.
A new study published in Nature found that highly lethal brain tumors stop growing when deprived of a specific molecule naturally produced when brain cells fire. Researchers suggest targeting the protein neuroligin-3 as a potential approach for treating high-grade gliomas.
A new genomic profiling study has identified genetic alterations in 96% of brain tumors in children, including genes that can be targeted with specific treatments. The study found distinct patterns of mutations between low-grade and high-grade gliomas, which could lead to more effective treatment options for these patients.
Researchers discovered a novel molecular mechanism that maintains glioma stem cells, which are responsible for tumorigenesis, treatment resistance, and tumor recurrence in glioblastoma. A small molecule inhibitor CMP3a selectively inhibits NEK2 kinase activity to promote tumor growth and radiation resistance.
Mebendazole, a medication used to treat pinworms, shows promise in treating low-grade glioma brain tumors by crossing the blood-brain barrier more effectively than vincristine. The findings suggest a potential new treatment option that could prolong patient lives without severe side effects.
A massive meta-analysis of brain tumor data has identified 13 new genetic risk factors for glioma, doubling known risk factors. The study provides a better understanding of the disease and may help doctors diagnose high-risk patients early.
Researchers have identified two distinct glioma subtypes associated with specific genetic markers, expanding the understanding of glioma susceptibility. The study found that these genetic markers increase the risk of developing brain tumors, but each marker only provides a modest increase in risk.
A massive study of over 30,000 participants has identified 13 new genetic mutations that significantly increase the risk of developing glioma, the most common form of brain cancer. The research also strengthens evidence for previously known genes linked to glioma and other cancers.
Acquired mutations in IDH enzyme help gliomas evade immune system activation by suppressing T cell recruitment. Inhibition of mutant IDH enhances vaccine-based immunotherapy treatment efficacy in glioma-bearing mice, suggesting potential for combinatorial therapies to counteract mutation effects.
A new biomarker enzyme ALDH1A3 has been identified in mesenchymal glioma stem-like cells, which are responsible for the tumorigenicity of glioblastoma multiforme tumors. The researchers have developed a small molecule inhibitor GA11 that targets this enzyme and has shown potent efficacy in preclinical testing.
Researchers at UT Southwestern Medical Center have identified a new biomarker called SHOX2, which predicts poor survival in intermediate-grade gliomas. The finding has the potential to help doctors choose the best treatment and improve patient outcomes.
Research reveals that childhood brain tumors originating from undifferentiated stem cells are more frequent and aggressive than those from oligodendrocyte precursor cells. Tumor cells from stem cells also show increased susceptibility to cancer drugs, according to a new study published in Cancer Research.
A study at the University of Texas MD Anderson Cancer Center found that the tumor suppressor gene quaking (QKI) plays a major regulator role in cancer stem cells of glioblastoma, the deadliest type of brain tumor. QKI impacts cellular activity called endocytosis, allowing glioma stem cells to thrive in inhospitable sites.
Researchers at Nagoya University developed a micro-sized device that can detect the IDH1-R132H mutation in glioma tumors, enabling real-time identification of tumor margins during surgery. The device takes less than 15 minutes to produce results and requires only small sample sizes.
Researchers found IDH gene mutations to be independently prognostic of overall and progression-free survival in grade II and III gliomas. CIC mutations also showed promise as prognostic markers, although more research is needed to confirm their effectiveness.
Scientists at Newcastle University have made a groundbreaking discovery that brain tumour cells use fats to make energy, not sugars as previously believed. This new understanding has significant implications for developing treatments for glioma, the most common form of primary malignant brain tumour.
A large observational study found that university-educated individuals are more likely to develop certain types of brain tumors, including gliomas and meningiomas. Men with higher education were 19% more likely to develop glioma, while women were 23% more likely.
Researchers at H. Lee Moffitt Cancer Center report a safe and effective treatment regimen for recurrent high-grade glioma brain tumors, with durable disease control in three patients. The combination of pembrolizumab, bevacizumab, and radiation therapy shows promise as a potential new approach to treating these patients.
A recent study by Uppsala University researchers found that genetic analyses in dogs can identify genes linked to human brain tumors, specifically gliomas. The study identified three genes associated with glioma development in dogs, which are also present in humans and show reduced activity in tumor tissue.
A genome-wide association study of 39 dog breeds with gliomas identified three candidate genes associated with the tumor's development. These genes - CAMKK2, P2RX7 and DENR - have also been linked to cancer in humans. Further research into these genes may provide insights for potential treatments of glioma in both species.
A powerful three-way mechanism driving childhood brain cancer growth has been discovered by scientists. The MYB-QKI gene fusion is found in rare pediatric glioma subtype angiocentric glioma and drives tumor formation through abnormal expression, disruption of tumor suppression, and activation via a positive feedback loop.
Researchers created a combined MRI and ultramicroscopy toolkit to study vessel growth in glioma models, providing better understanding of underlying mechanisms and potential novel targets for future drug development. The technique helped assess the effects of existing anti-vascular endothelial growth factor treatments on tumour growth.
A recent study identified the genetic mechanism causing angiocentric gliomas, a rare type of low-grade glioma in children. The discovery revealed an unusual DNA abnormality that triggers three different mechanisms to produce a tumor, leading to the development of a diagnostic test.
Researchers identified new glioma subtypes by analyzing DNA methylation profiles in 1,122 adult glioma samples. These subtypes can help stratify patients more accurately and improve treatment protocols, with some subgroups displaying similarities to pilocytic astrocytomas and better patient survival.
Researchers developed a novel, more accurate classification system for gliomas using molecular profiles of 1122 cells. The study identified seven categories for tumor progression assessment, providing a more precise way to predict patient outcomes and treatment responses.
Researchers discovered a new way to classify gliomas by analyzing their molecular characteristics, specifically DNA methylation levels. This approach predicts which tumors are more likely to grow rapidly and can guide treatment decisions.
A multi-center study identified distinct molecular and clinical features in diffuse glioma patients, shedding light on disease progression. The findings may lead to improved treatment outcomes by enabling precise prediction of tumor growth and response to therapy.
Researchers found that authors from a shared medical training background are more likely to publish articles supporting maximal tumor removal for patient survival. This phenomenon, known as 'medical academic genealogy,' suggests that mentorship and training influence the types of articles published.
A new hypnosis technique called hypnosedation offers a reliable alternative to awake craniotomy for glioma patients. The study found that hypnosis reduced the impact of unpleasant events during surgery and showed little negative psychological impact on patients.
Researchers discovered a novel pathway to cancer that involves the misfolding of the genome and IDH mutations. This disruption allows a potent growth factor gene to be activated by an always-on gene switch, leading to cancer growth.
Researchers at Penn State College of Medicine have developed a new nanotechnology approach using 'smart fat cells' that can pass the blood-brain barrier to detect early-stage brain tumors. This breakthrough could transform gliomas from a death sentence into a treatable condition, enabling patients to receive timely treatment.
A recent study published in Cancer Cell found that a key signaling pathway present in most organisms actually suppresses the formation of specific types of brain tumor, including gliomas. This discovery has significant implications for glioma treatment and diagnosis.
The EORTC trial 26101 found that bevacizumab treatment in progressive glioblastoma patients did not confer a survival advantage despite prolonged progression-free survival. The combination of bevacizumab and lomustine may prolong PFS but does not impact overall survival.
A recent study has discovered five new genetic variants associated with brain cancer, including one that increases the risk of glioblastoma by nearly a quarter. These findings provide important clues for developing new treatments against the disease and offer hope for personalized medicine in the future.
Researchers have discovered that combining tricyclic antidepressants with anticoagulant drugs can slow down glioma tumors in mice by causing excessive autophagy. The study, published in Cancer Cell, found that the combination therapy doubled the lifespan of mice with gliomas.
A study published in Neurosurgery found that complete resection of high-grade brain cancer significantly improves survival rates in children. The study revealed a greater survival benefit for female patients compared to male patients. Gross total resection (GTR) improved the chances of survival free of recurrent or progressive cancer o...
A UBC study suggests targeting healthy cells around tumors to stop brain cancer from spreading. The research team found that glioma cells can hijack astrocytes, regulating their environment to stimulate tumor growth and invasion.