View clinical trials related to Brain Neoplasms.
Filter by:This clinical trial studies positron emission tomography (PET) imaging utilizing 18F-(2S,4R)4-fluoroglutamine, a glutamic acid derivative, to image patients with malignant tumor. [18F]Fluoroglutamine PET may provide additional information that help diagnose and stage cancer patients.
The aim of this study was to investigate the effect of cerebral oxygenation on postoperative compilation in intracranial surgery.
The purpose of this study is to evaluate the safety of BBB disruption using the ExAblate 4000-system Type 2 in patients with Her-2 positive breast cancer metastases in the brain.
Phase III trial comparing local control and side effects after fractionated stereotactic radiotherapy and single session radiosurgery in patients with larger brain metastases (2-4 cm)
This prospective 2-stage, non-randomized Phase 2 trial evaluates the safety and efficacy of FSRT for the management of hemorrhagic brain metastases
MRI-based sequences can provide non-invasive quantification of intratumoral 2-hydroxyglutarate (2HG) distribution and tumor cellularity in human gliomas and help guide the development of novel glioma therapies.
This Phase I dose-escalation trial is designed to determine the safety and feasibility of rapidly generated tumor multi-antigen associated specific cytotoxic T lymphocytes (TAA-T) in patients with newly diagnosed diffuse intrinsic pontine gliomas DIPGs (Group A) or recurrent, progressive, or refractory non-brainstem CNS malignancies (Group B). Pediatric and adult patients who have high-risk CNS tumors known to typically have positivity for one or more Tumor Antigen Associated (TAA) (WT1, PRAME and/or Survivin) will be eligible. TAA-T will all be generated from patient peripheral blood mononuclear cells (PBMC). Group A patients (DIPG): The first TAA-T dose will be infused any time 14 days or more after completion of radiotherapy. Group B patients (other recurrent/progressive/refractory CNS tumors): The first TAA-T dose will be infused any time 14 days or more after completing most recent course of conventional (non-investigational) therapy for their disease AND after appropriate washout periods as detailed in eligibility criteria.
This phase II trial studies how well ¹⁸F- fluoromisonidazole (FMISO) works with positron emission tomography (PET)/magnetic resonance imaging (MRI) in assessing participants with malignant (cancerous) brain tumors. FMISO provides information about the oxygen levels in a tumor, which may affect how the tumor behaves. PET/MRI imaging produces images of the brain and how the body functions. FMISO PET/MRI may help investigators see how much oxygen is getting in the brain tumors.
In order to come as close as possible to the correct diagnosis of CNS tumors, MRI is the long-standing accepted method of choice that can in some cases be supported by the use of CT to demonstrate calcification or bone destruction. In individual cases MRI spectroscopy can be helpful for the differentiation between neoplasms and inflammatory lesions or surveillance of tumor therapy, just as perfusion
The HuR protein binds to AU-rich elements in the untranslated 3' region of messenger RNA, thus allowing their stabilization. Its targets include multiple cell cycle regulating proteins, cytokines and growth factors. In some cancers, its overall expression level but especially its cytoplasmic expression are correlated to a higher grade and constitute a poor prognostic factor. To date, HuR's deregulation mechanisms remain poorly understood. A few experimental studies have shown the role of certain microARNS, or of post-translational modifications. In brain tumours, HuR expression, its prognostic value and its deregulation mechanisms have been little studied to date. The first part of the project will be a monocentric retrospective study of human brain tumour samples collected during biopsies or surgical removal. We will first evaluate HuR expression in 140 brain tumors, including 40 meningiomas and 100 gliomas of increasing grade, and look for a correlation with histological grade and survival. We will then apprehend the consequences of its deregulation by analyzing different factors involved in the cell cycle and stress response markers. Finally, we will study the mechanisms of HuR deregulation by analyzing the expression level of several microRNAs (miR16, miR519) and the methylation state of HuR. The second part of the project will focus on cell lines from human brain tumours. We will first attempt to confirm the interactions between HuR and markers involved in the cell cycle and stress response, then the regulation of HuR by its methylation and by microRNAs (miR16 and miR519). We would also like to study the consequences of HuR inhibition and overexpression on cell proliferation, under various conditions of induced stress (pharmacological agents, physical stress). Finally, we will study the consequences of an experimental vitamin B12 deficiency on HuR expression and tumor cell adaptation to stress.