fenofibrate has been researched along with Brain Neoplasms in 6 studies
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Brain Neoplasms: Neoplasms of the intracranial components of the central nervous system, including the cerebral hemispheres, basal ganglia, hypothalamus, thalamus, brain stem, and cerebellum. Brain neoplasms are subdivided into primary (originating from brain tissue) and secondary (i.e., metastatic) forms. Primary neoplasms are subdivided into benign and malignant forms. In general, brain tumors may also be classified by age of onset, histologic type, or presenting location in the brain.
| Excerpt | Relevance | Reference |
|---|---|---|
| " Then, we explored the molecular mechanism by which lncRNA HOTAIR regulates PPARα in cell lines in vitro and in a nude mouse glioma model in vivo and explored the effect of the combined application of HOTAIR knockdown and fenofibrate treatment on glioma invasion." | 8.02 | The lipid-lowering drug fenofibrate combined with si-HOTAIR can effectively inhibit the proliferation of gliomas. ( Dai, X; Huang, B; Ni, S; Nyalali, AMK; Sun, J; Xu, F; Zhang, K; Zhao, H; Zhu, W, 2021) |
| "The effects of fenofibrate on Glioma cell motility, IGF-I receptor (IGF-IR) signaling, PPARalpha activity, reactive oxygen species (ROS) metabolism, mitochondrial potential, and ATP production were analyzed in human glioma cell lines." | 7.76 | ROS accumulation and IGF-IR inhibition contribute to fenofibrate/PPARalpha -mediated inhibition of glioma cell motility in vitro. ( Del Valle, L; Drukala, J; Grabacka, M; Madeja, Z; Reiss, K; Urbanska, K; Wilk, A; Wybieralska, E, 2010) |
| "Fenofibrate (FF) is a common lipid-lowering drug and a potent agonist of the peroxisome proliferator-activated receptor alpha (PPARα)." | 5.42 | Molecular mechanisms of fenofibrate-induced metabolic catastrophe and glioblastoma cell death. ( Culicchia, F; Dean, M; Grabacka, M; Marrero, L; Mullinax, J; Ochoa, A; Parsons, C; Peruzzi, F; Reiss, K; Wilk, A; Wyczechowska, D; Zapata, A, 2015) |
| " Then, we explored the molecular mechanism by which lncRNA HOTAIR regulates PPARα in cell lines in vitro and in a nude mouse glioma model in vivo and explored the effect of the combined application of HOTAIR knockdown and fenofibrate treatment on glioma invasion." | 4.02 | The lipid-lowering drug fenofibrate combined with si-HOTAIR can effectively inhibit the proliferation of gliomas. ( Dai, X; Huang, B; Ni, S; Nyalali, AMK; Sun, J; Xu, F; Zhang, K; Zhao, H; Zhu, W, 2021) |
| "Fenofibrate, a well-known normolipidemic drug, has been shown to exert strong anticancer effects against tumors of neuroectodermal origin including glioblastoma." | 3.81 | Fenofibrate subcellular distribution as a rationale for the intracranial delivery through biodegradable carrier. ( Ayyala, R; Blake, DA; Culicchia, F; Grabacka, M; John, VT; Ponnusamy, T; Reiss, K; Rutkowska, M; Vashistha, H; Waligorski, P; Wilk, A; Wisniewska-Becker, A; Wyczechowska, D; Zapata, A, 2015) |
| "The effects of fenofibrate on Glioma cell motility, IGF-I receptor (IGF-IR) signaling, PPARalpha activity, reactive oxygen species (ROS) metabolism, mitochondrial potential, and ATP production were analyzed in human glioma cell lines." | 3.76 | ROS accumulation and IGF-IR inhibition contribute to fenofibrate/PPARalpha -mediated inhibition of glioma cell motility in vitro. ( Del Valle, L; Drukala, J; Grabacka, M; Madeja, Z; Reiss, K; Urbanska, K; Wilk, A; Wybieralska, E, 2010) |
| "Fenofibrate (FF) is a common lipid-lowering drug and a potent agonist of the peroxisome proliferator-activated receptor alpha (PPARα)." | 1.42 | Molecular mechanisms of fenofibrate-induced metabolic catastrophe and glioblastoma cell death. ( Culicchia, F; Dean, M; Grabacka, M; Marrero, L; Mullinax, J; Ochoa, A; Parsons, C; Peruzzi, F; Reiss, K; Wilk, A; Wyczechowska, D; Zapata, A, 2015) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 0 (0.00) | 29.6817 |
| 2010's | 5 (83.33) | 24.3611 |
| 2020's | 1 (16.67) | 2.80 |
| Authors | Studies |
|---|---|
| Stalinska, J | 1 |
| Houser, L | 1 |
| Rak, M | 1 |
| Colley, SB | 1 |
| Reiss, K | 4 |
| Jursic, BS | 1 |
| Zhu, W | 1 |
| Zhao, H | 1 |
| Xu, F | 1 |
| Huang, B | 1 |
| Dai, X | 1 |
| Sun, J | 1 |
| Nyalali, AMK | 1 |
| Zhang, K | 1 |
| Ni, S | 1 |
| Wilk, A | 3 |
| Wyczechowska, D | 2 |
| Zapata, A | 2 |
| Dean, M | 1 |
| Mullinax, J | 1 |
| Marrero, L | 1 |
| Parsons, C | 1 |
| Peruzzi, F | 1 |
| Culicchia, F | 2 |
| Ochoa, A | 1 |
| Grabacka, M | 3 |
| Waligorski, P | 1 |
| Blake, DA | 1 |
| Rutkowska, M | 1 |
| Vashistha, H | 1 |
| Ayyala, R | 1 |
| Ponnusamy, T | 1 |
| John, VT | 1 |
| Wisniewska-Becker, A | 1 |
| Drukala, J | 1 |
| Urbanska, K | 1 |
| Wybieralska, E | 1 |
| Del Valle, L | 1 |
| Madeja, Z | 1 |
| Greene-Schloesser, D | 1 |
| Moore, E | 1 |
| Robbins, ME | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| Analysis of the Cognitive-behavioral Dysfunctions Profile and the Potential of Neuroplasticity in Patients With Brain Tumors Subjected to Selected Radiotherapy Techniques and the Possibility of Their Compensation by Psycho-physical Training[NCT05192447] | 150 participants (Anticipated) | Interventional | 2021-04-01 | Recruiting | |||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
6 other studies available for fenofibrate and Brain Neoplasms
| Article | Year |
|---|---|
Exploring anticancer activity of structurally modified benzylphenoxyacetamide (BPA); I: Synthesis strategies and computational analyses of substituted BPA variants with high anti-glioblastoma potential.
Topics: Acetamides; Antineoplastic Agents; Blood-Brain Barrier; Brain Neoplasms; Cell Line, Tumor; Cell Surv | 2019 |
The lipid-lowering drug fenofibrate combined with si-HOTAIR can effectively inhibit the proliferation of gliomas.
Topics: Adult; Aged; Animals; Brain; Brain Neoplasms; Cell Line, Tumor; Cell Proliferation; Chromatin Immuno | 2021 |
Molecular mechanisms of fenofibrate-induced metabolic catastrophe and glioblastoma cell death.
Topics: Adenosine Triphosphate; Animals; Antineoplastic Agents; Astrocytes; Brain Neoplasms; Cell Death; Cel | 2015 |
Fenofibrate subcellular distribution as a rationale for the intracranial delivery through biodegradable carrier.
Topics: Animals; Biodegradable Plastics; Brain; Brain Neoplasms; Cell Line, Tumor; Drug Carriers; Female; Fe | 2015 |
ROS accumulation and IGF-IR inhibition contribute to fenofibrate/PPARalpha -mediated inhibition of glioma cell motility in vitro.
Topics: Adenosine Triphosphate; Base Sequence; Brain Neoplasms; Cell Line, Tumor; Cell Movement; Fenofibrate | 2010 |
Molecular pathways: radiation-induced cognitive impairment.
Topics: Animals; Brain; Brain Neoplasms; Cognition Disorders; Fenofibrate; Humans; Neurogenesis; Peroxisome | 2013 |