Evidence map›Paper›PMID 27074052›Full record

ArticleLeukemia & lymphoma2016

Modulation of p73 isoforms expression induces anti-proliferative and pro-apoptotic activity in mantle cell lymphoma independent of p53 status.

Hesham M Hassan, Michelle L Varney, Nagendra K Chaturvedi, Shantaram S Joshi, Dennis D Weisenburger, Rakesh K Singh, Bhavana J Dave

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Leukemia & lymphoma, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.2field-weighted citation impact, top 40% 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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Article
  3. 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

7 authors at 3 institutions in 1 country.

Hesham M Hassana Department of Pathology and Microbiology , University of Nebraska Medical Center , Omaha , NE , USA.
Michelle L Varneya Department of Pathology and Microbiology , University of Nebraska Medical Center , Omaha , NE , USA.
Nagendra K Chaturvedib Department of Genetics, Cell Biology and Anatomy , University of Nebraska Medical Center , Omaha , NE , USA.
Shantaram S Joshib Department of Genetics, Cell Biology and Anatomy , University of Nebraska Medical Center , Omaha , NE , USA.
Dennis D Weisenburgerc Department of Pathology , City of Hope Medical Center , Duarte , CA , USA.
Rakesh K Singha Department of Pathology and Microbiology , University of Nebraska Medical Center , Omaha , NE , USA.
Bhavana J Davea Department of Pathology and Microbiology , University of Nebraska Medical Center , Omaha , NE , USA.
University of Nebraska Medical Center · USCity Of Hope National Medical Center · USNebraska Medical Center · US

Funding

Research Pilot Project ProgramP30GM106397 · NIGMS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI JOHNSON, KEITH R · 2013 to 2017
$4.9M
Molecular Regulation of Human Melanoma MetastasisR01CA072781 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI SINGH, RAKESH K · 2005 to 2007
$580k
NCI NIH HHS R01 CA072781NIGMS NIH HHS P30 GM106397
6 · The paper itself

Abstract

Mantle cell lymphoma (MCL) is characterized by a clinically aggressive course with frequent relapse and poor survival. The p53 pathway is frequently dysregulated and p53 status predicts clinical outcome. In this report, we investigated whether modulation of p73 isoforms by diclofenac inhibits cell growth, induces apoptosis and/or cell cycle arrest in MCL relative to p53 status. Wild-type p53 [Granta-519 and JVM-2], mutant p53 [Jeko-1 and Mino-1] expressing cells, therapy resistant cell lines, and primary human cells isolated from MCL patients were used. Overexpression of pro-apoptotic TAp73 enhanced MCL cell apoptosis. Diclofenac induced a concentration- and duration-dependent increase in TAp73, cell cycle arrest, cell death, and inhibited MCL cell growth independent of p53 status. Diclofenac treatment was associated with increased activity of caspases 3, 7, and 8 and induction of p53 transcriptional target genes. These studies demonstrate the potential for diclofenac as novel therapeutic agent in MCL independent of p53 status.

Indexed as

Gene Expression Regulation, NeoplasticApoptosisCaspasesCell CycleCell Cycle CheckpointsCell Line, TumorCell ProliferationDiclofenacHumansLymphoma, Mantle-CellProtein IsoformsTumor Protein p73Tumor Suppressor Protein p53CaspasesDiclofenacProtein IsoformsTumor Protein p73Tumor Suppressor Protein p53Apoptosiscell cyclediclofenacmantle cell lymphomap73 isoforms

Identifiers

PMID27074052
PMCPMC5967247
OpenAlexW2338898247

What OpenQuestion holds

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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.