Evidence map›Paper›PMID 27461062›Full record

ReviewLeukemia2016

Therapeutic potential of targeting sphingosine kinases and sphingosine 1-phosphate in hematological malignancies.

C Evangelisti, C Evangelisti, F Buontempo, A Lonetti, E Orsini, F Chiarini, J T Barata, S Pyne, N J Pyne, A M Martelli

Open access · greenAbstract readReview
PubMed Publisher
In one paragraph

Review in Leukemia, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
2.6field-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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

  1. Pooled it
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  14. Nephrotoxicity in cancer treatment: An update.Advances in cancer research · 2022
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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

10 authors at 4 institutions in 3 countries.

C EvangelistiDepartment of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, Italy.
C EvangelistiInstitute of Molecular Genetics, National Research Council-Rizzoli Orthopedic Institute and Muscoloskeletal Cell Biology Laboratory, IOR, Bologna, Italy.
F BuontempoDepartment of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, Italy.
A LonettiDepartment of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, Italy.
E OrsiniDepartment of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, Italy.
F ChiariniInstitute of Molecular Genetics, National Research Council-Rizzoli Orthopedic Institute and Muscoloskeletal Cell Biology Laboratory, IOR, Bologna, Italy.
J T BarataInstituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa, Lisbon, Portugal.
S PyneStrathclyde Institute of Pharmacy and Biomedical Sciences, University of Strathclyde, Glasgow, Scotland, UK.
N J PyneStrathclyde Institute of Pharmacy and Biomedical Sciences, University of Strathclyde, Glasgow, Scotland, UK.
A M MartelliDepartment of Biomedical and Neuromotor Sciences, University of Bologna, Bologna, Italy.
University of Bologna · ITNational Research Council · ITUniversity of Strathclyde · GBUniversity of Lisbon · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sphingolipids, such as ceramide, sphingosine and sphingosine 1-phosphate (S1P) are bioactive molecules that have important functions in a variety of cellular processes, which include proliferation, survival, differentiation and cellular responses to stress. Sphingolipids have a major impact on the determination of cell fate by contributing to either cell survival or death. Although ceramide and sphingosine are usually considered to induce cell death, S1P promotes survival of cells. Sphingosine kinases (SPHKs) are the enzymes that catalyze the conversion of sphingosine to S1P. There are two isoforms, SPHK1 and SPHK2, which are encoded by different genes. SPHK1 has recently been implicated in contributing to cell transformation, tumor angiogenesis and metastatic spread, as well as cancer cell multidrug-resistance. More recent findings suggest that SPHK2 also has a role in cancer progression. This review is an overview of our understanding of the role of SPHKs and S1P in hematopoietic malignancies and provides information on the current status of SPHK inhibitors with respect to their therapeutic potential in the treatment of hematological cancers.

Indexed as

Disease ProgressionHematologic NeoplasmsHumansLysophospholipidsMolecular Targeted TherapyPhosphotransferases (Alcohol Group Acceptor)Protein Kinase InhibitorsSphingosineSphingosine KinaseLysophospholipidsPhosphotransferases (Alcohol Group Acceptor)Protein Kinase InhibitorsSphingosinesphingosine 1-phosphateSphingosine Kinasesphingosine kinase 2, human

Identifiers

PMID27461062
OpenAlexW2491756834

What OpenQuestion holds

Textmetadata
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.