Neoplasms

All Conditions

Heart and Blood Diseases

Rare Diseases

Glioma

Astrocytoma

Oligodendroglioma

Mitral Valve Insufficiency

Neoplasms, Neuroepithelial

Neuroectodermal Tumors

Neuroectodermal Tumors, Primitive

Neoplasms, Germ Cell and Embryonal

Neoplasms by Histologic Type

Neoplasms, Glandular and Epithelial

Neoplasms, Nerve Tissue

Neuroepithelioma

3 Tesla Scanning: MRI/MRS of glioma and non-glioma patients.

Approximately 38 brain tumor patients with IDH mutated gliomas and 50 patients with non-glioma disease will be scanned.

3 Tesla scanning

Changho Choi, PhD

The Investigators will examine the disease specificity of 2-hydroxyglutarate in non-glioma brain lesions, and the clinical utility of 2-hydroxyglutarate, glycine and citrate in IDH mutated gliomas and IDH wild type gliomas.

Malignant gliomas represent the majority of primary brain tumors in adults and are among the most intractable tumors. Cancers reprogram their metabolism to meet the needs of rapid cell growth. Alterations in metabolite abundance may serve as biomarkers of malignancy, and the capability to monitor the changes non-invasively would have significant clinical utility in cancer. Gliomas often contain a specific metabolic activity that is predictive of the genotype and has predictive value with respect to tumor stage and patient survival. A high fraction of gliomas contain mutations in the metabolic enzymes, isocitrate dehydrogenase (IDH) 1 and 2. These heterozygous mutations are confined to the active site of the enzyme and result in a neomorphic activity that causes the mutant enzyme to produce an "oncometabolite", 2-hydroxyglutarate (2HG). Non-invasive identification of this onco-metabolite by MRS is therefore a major breakthrough in cancer research. Beyond simple detection of 2HG, our preliminary data show that 2HG is a remarkably sensitive biomarker for monitoring tumor progression and response to treatment in IDH mutated gliomas. Glycine (Gly) is a biomarker of tumor malignancy, as indicated in prior studies. Our data also indicate that citrate (Cit) is elevated in gliomas.

Over the course of this preliminary study, there has been crucial need for 3D evaluation of these onco-metabolites within the tumor mass. The Investigators will examine the clinical utility of 2HG, Gly and Cit, in a large cohort of subjects using multi-slice 2D MRSI at 3T. The specific aims include, first, an in-vivo MRS study for the disease specificity of 2HG (Aim 1). The Investigators will examine clinically proven non-glioma lesions that mimic glioma in clinical MRI. To increase the clinical applicability of the result, the Investigators will select non-enhancing brain diseases, given that IDH mutation occurs largely in grade-2 and -3 gliomas, which are often non-enhancing. Second, the Investigators will examine the clinical utility of 2HG, Gly, Cit and other metabolites in patients with IDH mutated gliomas (Aim 2). Third, the Investigators will examine the clinical utility of Gly, Cit and other metabolites in patients with IDH wild type gliomas (Aim 3). In Aim 2 and 3, the patients will undergo MRSI scans at multiple time points, and the Investigators will monitor the metabolic changes with tumor progression and in response to treatment. The Investigators anticipate our study will provide significant value in many aspects of management of gliomas. 3D evaluation of the cancer biomarkers using MRSI will provide biological insights for making the diagnosis of gliomas, tracking of infiltrative cells during follow up, and determining response to treatment. Success of the 2HG specificity study in non-glioma neurological diseases will provide an experimental evidence for use of non-invasive 2HG imaging as a triaging tool in the workup of a new brain mass.

Clinical Development of Cancer-Specific MRS Biomarkers in Malignant Gliomas

The investigators anticipate the study will provide significant value in many aspects of management of gliomas. 3D evaluation of the cancer biomarkers using MRSI will provide biological insights for making the diagnosis of gliomas, tracking of infiltrative cells during follow up, and determining response to treatment.

National Institutes of Health (NIH)

National Cancer Institute (NCI)

University of Texas Southwestern Medical Center

Nervous System Diseases

Brain Neoplasms

Meningioma

Central Nervous System Neoplasms

Nervous System Neoplasms

Brain Diseases

Central Nervous System Diseases

Neoplasms, Vascular Tissue

Meningeal Neoplasms

Coagulants

All Drugs and Chemicals

Tranexamic Acid

Antifibrinolytic Agents

Hemostatics

15 mg/Kg Tranexamic Acid IV after anesthesic induction,and continues with a dose of 1mg/kg/h intraoperatory

15 mg/Kg of Saline IV after anesthesic induction,and continues with a dose of 1mg/kg/h intraoperatory

Placebo: Saline

Randy Guerra, MD

Fredy Diaz, MD

Randy O Guerra, MD

The purpose of this study is to determine whether Tranexamic Acid is effective or not in the reduction of intraoperative bleeding loss in brain tumors resections.

Brain tumor resection has been associated with increased blood loss and a significant increase in the incidence of Intravascular disseminated coagulopathy. The development of coagulopathy in the context of tumor resection is associated with poor results. Transfusion decision during the course of neurosurgical surgery offers benefits such as increased oxygen carrying capacity but may increase the risk associated with transfusions such as blood infections, hemolysis, lung injury and immunosuppression. The information available on tranexamic acid used in neurosurgery is little, therefore this opens up new alternatives in the techniques of reducing intraoperative bleeding.

Tranexamic acid is an antifibrinolytic agent that blocks the binding of plasminogen to the fibrin surface. It has been used to reduce blood loss during coronary revascularization, liver resection, obstetrics and orthopedic procedures. Tranexamic acid intraoperatively has been shown to reduce blood loss up to 45%. The primary concern when administering an antifibrinolytic drug is the potential increased incidence of thromboembolic events. There is no actual data on the utility of tranexamic acid to reduce blood loss in brain tumors resection surgery.

We want to compare Tranexamic Acid to Saline solution(Placebo) to see whether Tranexamic ACid Administration will reduce blood loss during brain tumor resection. Reduction in transfusion requirements will lead to reduced costs and possible reduction in complications of blood transfusion and perioperative incidents.

Efficacy of Tranexamic Acid in Brain Tumor Resections

PHASE 3 STUDY OF EFFICACY OF TRANEXAMIC ACID IN BRAIN TUMORS RESECTIONS

(Measured with Hemoglobin/Hematocrit, PT, PTT, Plackets: pre-surgery, 6 hrs after surgery and 24 hours after.)

Colombian Foundation for Epilepsy and Neurological Disease

Oligoastrocytoma

Antineoplastic Agents

Temozolomide

Antineoplastic Agents, Alkylating

Alkylating Agents

Total resected LGGs treated with early radiation

Total resected LGGs treated without radiation

Residual LGGs treated with early radiation

Radiation therapy

Zhongping Chen, M.D., Ph.D.

Although the prognosis of patients with low-grade glioma (LGG) is generally good, recurrence seems unavoidable in some patients because of the infiltrative growth of the tumors. How to treat LGGs is still under controversy. The role of radiation therapy and chemotherapy in the treatment of LGG need to be further investigated. The purpose of this study is the following:

1. to investigate the role of early radiation therapy in MRI-determined total resected LGGs;
2. to compare the efficacy of early radiation therapy and that of initial chemotherapy in the LGGs without total resection.

Treatment Strategy for Low-grade Gliomas

Sun Yat-sen University

Zhongping CHEN

Symptoms and General Pathology

Recurrence

Ependymoma

Pharmaceutical Solutions

Immunotoxins

All subjects are enrolled onto this arm. All subjects will receive MR1-1.

Based on preclinical toxicity studies, the starting total drug dose will be 0.5μg (500ng) which represents 1/20th of the MTD in rats. The infusion flow rate will be fixed at 0.5 mL/h from each of two catheters. A total of 96 mLs of drug solution will be delivered over 96 hours. MR1-1KDEL dose escalation will be accomplished by increasing drug concentration allowing flow rate and infusion volume to remain unchanged. Drug dose will be doubled in successive cohorts so long as DLTs are not observed as follows: 25 ng/mL (2.4 μg)(starting dose); 50ng/mL (4.8μg); 100 ng/mL (9.6μg); 200ng/mL (19.2μg); 400 ng/mL (38.4μg); 800 ng/mL (76.8μg); and 1600 ng/mL (153.6μg).

MR1-1

Annick Desjardins, MD

Purpose of the study:

Primary Objective: Determine the maximum tolerated dose (MTD) and dose limiting toxicity (DLT) of MR1-1KDEL when delivered intracerebrally by convection-enhanced delivery (CED) in patients with supratentorial malignant brain tumors.

Secondary Objective: Document any radiographic responses associated with intracerebral CED of MR1-1KDEL.

Hypothesis: The investigators believe that MR1-1KDEL will be an effective anti-tumor agent for patients with supratentorial malignant brain tumors when delivered by CED.

Design \& procedures: This protocol is designed primarily to determine the MTD and DLT of a novel, tumor-specific immunotoxin, MR1-1KDEL. MR1-1KDEL will be delivered intracerebrally by CED using 2 intracerebral catheters with at least one catheter placed within the enhancing portion of the tumor. 124I-labeled albumin will be co-infused with gadolinium and PET and MRI images will be obtained at the conclusion of the infusion to monitor volume of drug distribution and leakage into the CSF space.

Based on preclinical toxicity studies, the starting total drug dose will be 0.5μg (500ng) which represents 1/20th of the MTD in rats. The infusion flow rate will be fixed at 0.5 mL/h from each of two to four catheters. A total of 144 mLs of drug solution will be delivered over 72 hours. MR1-1KDEL dose escalation will be accomplished by increasing drug concentration allowing flow rate and infusion volume to remain unchanged. Drug dose will be doubled in successive cohorts so long as DLTs are not observed as follows: 25 ng/mL (2.4 μg)(starting dose); 50ng/mL (4.8μg); 100 ng/mL (9.6μg); 200ng/mL (19.2μg); 400 ng/mL (38.4μg); 800 ng/mL (76.8μg); and 1600 ng/mL (153.6μg). At least 3 patients will be enrolled in each cohort. All patients in a given cohort will be observed for at least two weeks following infusion of the study drug before patients in the next cohort are treated. If no patients in a given cohort experience a DLT, the dose will be escalated in the next cohort. If 1 out of 3 patients in a given cohort experience DLT, 3 additional patients will be entered in that cohort. If 2 patients develop a DLT in any cohort of 3 or 6 patients, the previous dose will be declared the MTD. Patients will be followed at 1, 3, 6, 9, 12 month intervals for toxicity and adverse events, radiographic response, and survival. Patients will be off study when progressive disease is documented.

Risk/benefit assessment: This is an experimental study and unforeseeable or unexpected risks may be involved.

Study of Immunotoxin, MR1-1

Phase I Study of Immunotoxin, MR1-1

National Institute of Neurological Disorders and Stroke (NINDS)

Darell D. Bigner, MD, PhD

Director, The Preston Robert Tisch Brain Tumor Center at Duke

Nutritional and Metabolic Diseases

Glioblastoma

Ketosis

Hypoglycemic Agents

Metformin

Insulin

Insulin, Globin Zinc

Biguanides

Partial brain re-irradiation combined with metabolic intervention (low carbohydrate diet and/or metformin treatment)

Partial brain re-irradiation to a dose of 30-35Gy delivered over 2 weeks (10 fractions).

Partial brain re-irradiation.

Different cohorts will receive no, low dose or higher dose metformin.

Under close supervision of a dietician, patients will receive a low carbohydrate diet, enriched as necessary with medium chain triglyceride (MCT) supplements.

low carbohydrate diet

Yaacov R Lawrence, MBBS MA MRCP

Hila Gnessin, Bsc

Yaacov R Lawrence, MA MBBS MRCP

Recurrent brain tumours are extremely aggressive and despite optimal treatment, median survival is less than two years. One of the standard treatment options in this situation is radiation therapy. Currently there is intense scientific interest concerning the abnormal energy metabolism in cancer cells. All cells require energy in order to function, obtaining 'fuel' molecules such as glucose and fatty acids from the blood stream. Brain tumours exhibit "metabolic reprogramming", meaning that their energy requirements and utilization of fuel molecules are quite different from normal cells. Brain tumour cells are exquisitely dependant on glucose as a source of energy. Animal studies have shown that when these tumours are deprived of glucose they are very sensitive to radiation therapy.

In this clinical trial the investigators combine radiation therapy with a low-carbohydrate diet, in patients with recurrent brain tumours. In addition, subjects will receive medication with metformin, a drug usually used to treat diabetes. Metformin inhibits glucose metabolism within cancer cells, and additionally has reported intrinsic anti-cancer activity. Subjects will undergo advanced imaging and hormonal studies before, during and after the trial in order to obtain maximal translational-scientific impact.

The hypothesis:

The metabolic changes induced by the combination of a moderately-low carbohydrate diet combined with supplementary MCT and metformin therapy will selectively starve tumor cells. While normal brain cells are capable of deriving energy from ketone bodies during glucose restriction, tumor cells remain largely glucose-dependent for energy due to oncogene induced down-regulation of oxidative phosphorylation. While the tumor cells are in this 'vulnerable' state they will be less able to repair the damage induced by ionizing radiation.

Short-term implementation of the metabolic intervention (i.e. combined diet and metformin therapy) prior to, during, and after hypofractionated (2 week) radiation therapy is expected to increase tolerability, increase compliance and avoid the chronic metabolic complications associated with extreme carbohydrate restriction diets.

Treatment of Recurrent Brain Tumors: Metabolic Manipulation Combined With Radiotherapy

Improving the Response of Recurrent Glioma to Radiation Therapy Through Metabolic Intervention

The investigators will track adverse events in order to determine the safety of the intervention.

We will track patient compliance in order to determine the tolerability of the intervention.

We will assess plasma levels of glucose, insulin and other relevant hormones before, during and after the intervention.

Study title	NCT ID	Conditions	Interventions	Eligibility	Organization
Clinical Development of Cancer-Specific MRS Biomarkers in Malignant Gliomas	NCT02388659	Malignant Gliom... Oligodendroglio... Astrocytomas	3 Tesla scannin...	18 Years -	University of Texas Southwestern Medical Center
Efficacy of Tranexamic Acid in Brain Tumor Resections	NCT01655927	Brain Tumors Neoplasms Gliomas Astrocytomas Meningiomas	Tranexamic Acid Placebo: Saline	18 Years - 65 Years	Colombian Foundation for Epilepsy and Neurological Disease
Treatment Strategy for Low-grade Gliomas	NCT00897377	Astrocytomas Oligodendroglio... Oligoastrocytom...	Radiation thera... Temozolomide	18 Years - 60 Years	Sun Yat-sen University
Study of Immunotoxin, MR1-1	NCT01009866	Supratentorial ...	MR1-1	18 Years -	Duke University
Clinical Development of Cancer-Specific MRS Biomarkers in Malignant Gliomas	NCT02388659	Malignant Gliom... Oligodendroglio... Astrocytomas	3 Tesla scannin...	18 Years -	University of Texas Southwestern Medical Center
Efficacy of Tranexamic Acid in Brain Tumor Resections	NCT01655927	Brain Tumors Neoplasms Gliomas Astrocytomas Meningiomas	Tranexamic Acid Placebo: Saline	18 Years - 65 Years	Colombian Foundation for Epilepsy and Neurological Disease
Study of Immunotoxin, MR1-1	NCT01009866	Supratentorial ...	MR1-1	18 Years -	Duke University
Treatment of Recurrent Brain Tumors: Metabolic Manipulation Combined With Radiotherapy	NCT02149459	Brain Neoplasms	Partial brain r... Metformin low carbohydrat...	18 Years -	Sheba Medical Center

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