Evidence map›Paper›PMID 20919655›Full record

ReviewAdvances in experimental medicine and biology2010

Cancer treatment strategies targeting sphingolipid metabolism.

Babak Oskouian, Julie D Saba

Abstract readReview
In one paragraph

Review in Advances in experimental medicine and biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed, 1 pooled it
21.2field-weighted citation impact, top 1% 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

79 citing papers in PubMed, 1 synthesis or guideline pooled it, 140 citations in OpenAlex.

  1. Pooled it
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  10. Sphingolipid metabolism and regulated cell death in malignant melanoma.Apoptosis : an international journal on programmed cell death · 2024
    Review
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19 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Babak OskouianChildren's Hospital Oakland Research Institute, 5700 Martin Luther King Jr. Way, Oakland, California, 94609-1673, USA.
Julie D Saba
Martin Luther King, Jr. Multi-Service Ambulatory Care Center · US

Funding

S1P Lyase in colon cancerR01CA129438 · NCI · CHILDREN'S HOSPITAL & RES CTR AT OAKLAND · PI SABA, JULIE D · 2007 to 2017
$3.2M
SPHINGOSINE--REGULATION AND POTENTIAL ROLE IN CANCERR01CA077528 · NCI · CHILDREN'S HOSPITAL &RES CTR AT OAKLAND · PI SABA, JULIE D · 1998 to 2009
$2.8M
NCI NIH HHS CA129438NCI NIH HHS CA77528NCI NIH HHS R01 CA077528NCI NIH HHS R01 CA129438
6 · The paper itself

Abstract

Ceramide and sphingosine-1-phosphate are related sphingolipid metabolites that can be generated through a de novo biosynthetic route or derived from the recycling of membrane sphingomyelin. Both these lipids regulate cellular responses to stress, with generally opposing effects. Sphingosine-1-phosphate functions as a growth and survival factor, acting as a ligand for a family of G protein-coupled receptors, whereas ceramide activates intrinsic and extrinsic apoptotic pathways through receptor-independent mechanisms. A growing body of evidence has implicated ceramide, sphingosine-1-phosphate and the genes involved in their synthesis, catabolism and signaling in various aspects of oncogenesis, cancer progression and drug- and radiation resistance. This may be explained in part by the finding that both lipids impinge upon the PI3K/ AKT pathway, which represses apoptosis and autophagy. In addition, sphingolipids influence cell cycle progression, telomerase function, cell migration and stem cell biology. Considering the central role of ceramide in mediating physiological as well as pharmacologically stimulated apoptosis, ceramide can be considered a tumor-suppressor lipid. In contrast, sphingosine-1-phosphate can be considered a tumor-promoting lipid, and the enzyme responsible for its synthesis functions as an oncogene. Not surprisingly, genetic mutations that result in reduced ceramide generation, increased sphingosine-1-phosphate synthesis or which reduce steady state ceramide levels and increase sphingosine-1-phosphate levels have been identified as mechanisms of tumor progression and drug resistance in cancer cells. Pharmacological tools for modulating sphingolipid pathways are being developed and represent novel therapeutic strategies for the treatment of cancer.

Indexed as

AnimalsAntineoplastic AgentsApoptosisAutophagyCell CycleCeramidesHumansLysophospholipidsModels, BiologicalNeoplasmsSignal TransductionSphingolipidsSphingosineAntineoplastic AgentsCeramidesLysophospholipidsSphingolipidsSphingosinesphingosine 1-phosphate

Identifiers

PMID20919655
PMCPMC3076281
OpenAlexW1830948261

What OpenQuestion holds

Textmetadata
LicenceTDM
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.