Evidence map›Paper›PMID 37800872›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2023

Targeting sphingosine kinase 1 in p53KO thymic lymphoma.

Fabiola N Velazquez, Jeffrey L Stith, Leiqing Zhang, Amira M Allam, John Haley, Lina M Obeid, Ashley J Snider, Yusuf A Hannun

Open access · bronzeAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.3field-weighted citation impact, top 36% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  1. Article
  2. Review
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

8 authors at 3 institutions in 1 country.

Fabiola N VelazquezDepartment of Medicine, Stony Brook University, Stony Brook, New York, USA.ORCID 0000-0001-5692-848X
Jeffrey L StithDepartment of Medicine, Stony Brook University, Stony Brook, New York, USA.
Leiqing ZhangDepartment of Medicine, Stony Brook University, Stony Brook, New York, USA.
Amira M AllamDepartment of Medicine, Stony Brook University, Stony Brook, New York, USA.
John HaleyBiological Mass Spectrometry Center, Stony Brook Medicine, Stony Brook University, Stony Brook, New York, USA.ORCID 0000-0002-0283-6413
Lina M ObeidDepartment of Medicine, Stony Brook University, Stony Brook, New York, USA.
Ashley J SniderDepartment of Medicine, Stony Brook University, Stony Brook, New York, USA.ORCID 0000-0002-1515-4171
Yusuf A HannunDepartment of Medicine, Stony Brook University, Stony Brook, New York, USA.ORCID 0000-0003-3349-3369
Stony Brook University · USStony Brook Medicine · USUniversity of Arizona · US

Funding

Sphingolipids in Cancer Therapy and AngiogenesisP01CA097132 · NCI · STATE UNIVERSITY NEW YORK STONY BROOK · PI Daniel Canals · 2003 to 2026
$30.8M
NCI NIH HHS P01 CA097132
6 · The paper itself

Abstract

Sphingosine kinase 1 (SK1) is a key sphingolipid enzyme that is upregulated in several types of cancer, including lymphoma which is a heterogenous group of malignancies. Treatment for lymphoma has improved significantly by the introduction of new therapies; however, subtypes with tumor protein P53 (p53) mutations or deletion have poor prognosis, making it critical to explore new therapeutic strategies in this context. SK1 has been proposed as a therapeutic target in different types of cancer; however, the effect of targeting SK1 in cancers with p53 deletion has not been evaluated yet. Previous work from our group suggests that loss of SK1 is a key event in mediating the tumor suppressive effect of p53. Employing both genetic and pharmacological approaches to inhibit SK1 function in Trp53KO mice, we show that targeting SK1 decreases tumor growth of established p53KO thymic lymphoma. Inducible deletion of Sphk1 or its pharmacological inhibition drive increased cell death in tumors which is accompanied by selective accumulation of sphingosine levels. These results demonstrate the relevance of SK1 in the growth and maintenance of lymphoma in the absence of p53 function, positioning this enzyme as a potential therapeutic target for the treatment of tumors that lack functional p53.

Indexed as

NeoplasmsTumor Suppressor Protein p53AnimalsMicePhosphotransferases (Alcohol Group Acceptor)SphingosineSphingosine KinasePhosphotransferases (Alcohol Group Acceptor)SphingosineSphingosine KinaseTumor Suppressor Protein p53apoptosislymphomamicep53sphingosinesphingosine kinase 1

Identifiers

PMID37800872
PMCPMC11740227
OpenAlexW4387393393

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.