Evidence map›Paper›PMID 30733502›Full record

ArticleScientific reports2019

Evaluation of cationic channel TRPV2 as a novel biomarker and therapeutic target in Leukemia-Implications concerning the resolution of pulmonary inflammation.

Kodappully S Siveen, Kirti S Prabhu, Aeijaz S Parray, Maysaloun Merhi, Abdelilah Arredouani, Mohamed Chikri, Shahab Uddin, Said Dermime, Ramzi M Mohammad, Martin Steinhoff and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.1field-weighted citation impact, top 16% 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

13 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. The TRPV2 cation channels: from urothelial cancer invasiveness to glioblastoma multiforme interactome signature.Laboratory investigation; a journal of technical methods and pathology · 2020
    Review
  12. Review
  13. Article
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

12 authors at 4 institutions in 2 countries.

Kodappully S SiveenTranslational Research Institute, Academic Health System, Hamad Medical Corporation, Doha, Qatar.
Kirti S PrabhuTranslational Research Institute, Academic Health System, Hamad Medical Corporation, Doha, Qatar.
Aeijaz S ParrayTranslational Research Institute, Academic Health System, Hamad Medical Corporation, Doha, Qatar.
Maysaloun MerhiNational Center for Cancer Care and Research-Hamad Medical Corporation, Doha, Qatar.
Abdelilah ArredouaniQatar Biomedical Research Institute, Qatar Foundation, Doha, Qatar.
Mohamed ChikriQatar Biomedical Research Institute, Qatar Foundation, Doha, Qatar.
Shahab UddinTranslational Research Institute, Academic Health System, Hamad Medical Corporation, Doha, Qatar.ORCID 0000-0003-1886-6710
Said DermimeNational Center for Cancer Care and Research-Hamad Medical Corporation, Doha, Qatar.ORCID 0000-0002-5526-7496
Ramzi M MohammadDepartment of Oncology, Karmanos Cancer Institute, Wayne State University, Detroit, Michigan, USA.
Martin SteinhoffTranslational Research Institute, Academic Health System, Hamad Medical Corporation, Doha, Qatar.
Ibrahim A JanahiDivision of Pediatric Pulmonology Sidra Medicine, Doha, Qatar.
Fouad AziziTranslational Research Institute, Academic Health System, Hamad Medical Corporation, Doha, Qatar. fazizi@hamad.qa.
Hamad Medical Corporation · QANational Center for Cancer Care and Research · QAQatar Foundation · QAWayne State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Patients treated during leukemia face the risk of complications including pulmonary dysfunction that may result from infiltration of leukemic blast cells (LBCs) into lung parenchyma and interstitium. In LBCs, we demonstrated that transient receptor potential vanilloid type 2 channel (TRPV2), reputed for its role in inflammatory processes, exhibited oncogenic activity associated with alteration of its molecular expression profile. TRPV2 was overexpressed in LBCs compared to normal human peripheral blood mononuclear cells (PBMCs). Additionally, functional full length isoform and nonfunctional short form pore-less variant of TRPV2 protein were up-regulated and down-regulated respectively in LBCs. However, the opposite was found in PBMCs. TRPV2 silencing or pharmacological targeting by Tranilast (TL) or SKF96365 (SKF) triggered caspace-mediated apoptosis and cell cycle arrest. TL and SKF inhibited chemotactic peptide fMLP-induced response linked to TRPV2 Ca

Indexed as

ADP-ribosyl Cyclase 1ApoptosisBiomarkersCalciumCell Cycle CheckpointsCell Line, TumorDown-RegulationHumansImidazolesLeukemiaLeukocytes, MononuclearMitogen-Activated Protein Kinasesortho-AminobenzoatesPneumoniaProtein IsoformsRNA Interference1-(2-(3-(4-methoxyphenyl)propoxy)-4-methoxyphenylethyl)-1H-imidazoleADP-ribosyl Cyclase 1BiomarkersCalciumImidazolesMitogen-Activated Protein Kinasesortho-AminobenzoatesProtein IsoformsRNA, Small InterferingtranilastTRPV2 protein, humanTRPV Cation Channels

Identifiers

PMID30733502
PMCPMC6367460
OpenAlexW2913311808

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.