Evidence map›Paper›PMID 32977496›Full record

ReviewBiomolecules2020

Sphingolipid Metabolism in Glioblastoma and Metastatic Brain Tumors: A Review of Sphingomyelinases and Sphingosine-1-Phosphate.

Cyntanna C Hawkins, Tomader Ali, Sasanka Ramanadham, Anita B Hjelmeland

Open access · goldAbstract readReview
In one paragraph

Review in Biomolecules, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.4field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

39 citing papers in PubMed, 55 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 2 countries.

Cyntanna C HawkinsDepartment of Cell, Developmental, and Integrative Biology, University of Birmingham at Alabama, Birmingham, AL 35233, USA.ORCID 0000-0001-6488-0244
Tomader AliResearch Department, Imperial College London Diabetes Centre, Abu Dhabi P.O. Box 48338, UAE.ORCID 0000-0002-9327-2675
Sasanka RamanadhamDepartment of Cell, Developmental, and Integrative Biology, University of Birmingham at Alabama, Birmingham, AL 35233, USA.
Anita B HjelmelandDepartment of Cell, Developmental, and Integrative Biology, University of Birmingham at Alabama, Birmingham, AL 35233, USA.
University of Alabama at Birmingham · USImperial College London Diabetes Centre · AE

Funding

iPLA2beta-mediated alternative splicing and -cell death in type 1 diabetesR01DK126444 · NIDDK · UNIVERSITY OF VIRGINIA · PI CHALFANT, CHARLES E., EIZIRIK, DECIO LAKS · 2021 to 2024
$2.0M
Biosynthetic Metabolic Pathway Regulation of Glioma GrowthR01NS104339 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI HJELMELAND, ANITA BORTON · 2018 to 2022
$1.9M
Contribution of β-Cell- & Immune Cell-Derived Lipids to β-Cell Death and DiabetesR01DK110292 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI RAMANADHAM, SASANKA · 2016 to 2019
$1.7M
Importance of immune-cell lipid signaling in events leading to type 1 diabetesR21AI146743 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI RAMANADHAM, SASANKA · 2019 to 2020
$408k
NIAID NIH HHS R21 AI146743NIDDK NIH HHS R01 DK110292NIDDK NIH HHS R01 DK126444NINDS NIH HHS R01 NS104339
6 · The paper itself

Abstract

Glioblastoma (GBM) is a primary malignant brain tumor with a dismal prognosis, partially due to our inability to completely remove and kill all GBM cells. Rapid tumor recurrence contributes to a median survival of only 15 months with the current standard of care which includes maximal surgical resection, radiation, and temozolomide (TMZ), a blood-brain barrier (BBB) penetrant chemotherapy. Radiation and TMZ cause sphingomyelinases (SMase) to hydrolyze sphingomyelins to generate ceramides, which induce apoptosis. However, cells can evade apoptosis by converting ceramides to sphingosine-1-phosphate (S1P). S1P has been implicated in a wide range of cancers including GBM. Upregulation of S1P has been linked to the proliferation and invasion of GBM and other cancers that display a propensity for brain metastasis. To mediate their biological effects, SMases and S1P modulate signaling via phospholipase C (PLC) and phospholipase D (PLD). In addition, both SMase and S1P may alter the integrity of the BBB leading to infiltration of tumor-promoting immune populations. SMase activity has been associated with tumor evasion of the immune system, while S1P creates a gradient for trafficking of innate and adaptive immune cells. This review will explore the role of sphingolipid metabolism and pharmacological interventions in GBM and metastatic brain tumors with a focus on SMase and S1P.

Indexed as

Brain NeoplasmsCell ProliferationGlioblastomaHumansLysophospholipidsNeoplasm MetastasisPhospholipase DSphingolipidsSphingomyelin PhosphodiesteraseSphingosineType C PhospholipasesLysophospholipidsPhospholipase DSphingolipidsSphingomyelin PhosphodiesteraseSphingosinesphingosine 1-phosphateType C Phospholipasesglioblastomametastasissphingolipidsphingomyelinsphingomyelinasesphingosine-1-phosphate

Identifiers

PMID32977496
PMCPMC7598277
OpenAlexW3088637885

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.