Evidence map›Paper›PMID 27466285›Full record

ArticleCancer research2016

Lack of p53 Augments Antitumor Functions in Cytolytic T Cells.

Anirban Banerjee, Krishnamurthy Thyagarajan, Shilpak Chatterjee, Paramita Chakraborty, Pravin Kesarwani, Myroslawa Soloshchenko, Mazen Al-Hommrani, Kristina Andrijauskaite, Kelly Moxley, Harinarayanan Janakiraman and 11 more

Open access · greenAbstract read
In one paragraph

Article in Cancer research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

27 citing papers in PubMed, 37 citations in OpenAlex.

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  10. The African-centric P47S Variant ofCancer research communications · 2023
    Article
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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

21 authors at 2 institutions in 1 country.

Anirban Banerjee *Department of Surgery, Medical University of South Carolina, Charleston, SC 29425.
Krishnamurthy Thyagarajan *Department of Surgery, Medical University of South Carolina, Charleston, SC 29425.
Shilpak Chatterjee *Department of Surgery, Medical University of South Carolina, Charleston, SC 29425.
Paramita ChakrabortyDepartment of Surgery, Medical University of South Carolina, Charleston, SC 29425.
Pravin KesarwaniDepartment of Surgery, Medical University of South Carolina, Charleston, SC 29425.
Myroslawa SoloshchenkoDepartment of Surgery, Medical University of South Carolina, Charleston, SC 29425.
Mazen Al-HommraniDepartment of Surgery, Medical University of South Carolina, Charleston, SC 29425.
Kristina AndrijauskaiteDepartment of Surgery, Medical University of South Carolina, Charleston, SC 29425.
Kelly MoxleyDepartment of Surgery, Oncology Institute, Loyola University, Maywood, IL 60153.
Harinarayanan JanakiramanDepartment of Oral Health Research, Medical University of South Carolina, Charleston, SC 29425.
Matthew J ScheffelDepartment of Microbiology & Immunology, Medical University of South Carolina, Charleston, SC 29425.
Kristi HelkeDepartment of Comparative Medicine, Medical University of South Carolina, Charleston, SC 29425.
Kent ArmensonDepartment of Public Health Sciences, Medical University of South Carolina, Charleston, SC 29425.
Viswanathan PalanisamyDepartment of Oral Health Research, Medical University of South Carolina, Charleston, SC 29425.
Mark P RubinsteinDepartment of Surgery, Medical University of South Carolina, Charleston, SC 29425.
Elizabeth-Garrett MayerDepartment of Public Health Sciences, Medical University of South Carolina, Charleston, SC 29425.
David J ColeDepartment of Surgery, Medical University of South Carolina, Charleston, SC 29425.
Chrystal M PaulosDepartment of Microbiology & Immunology, Medical University of South Carolina, Charleston, SC 29425.
Christina-Voelkel-JohnsonDepartment of Microbiology & Immunology, Medical University of South Carolina, Charleston, SC 29425.
Michael I NishimuraDepartment of Surgery, Oncology Institute, Loyola University, Maywood, IL 60153.
Shikhar MehrotraDepartment of Surgery, Medical University of South Carolina, Charleston, SC 29425.
Medical University of South Carolina · USLoyola University Medical Center · US

Funding

Translational Science Laboratory Shared ResourceP30CA138313 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI RAYMOND N. DUBOIS · 2009 to 2026
$42.7M
Institute for Integration of Medicine & Science: A Partnership to Improve HealthUL1TR001120 · NCATS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI CLARK, ROBERT A, HARGREAVES, KENNETH M · 2013 to 2017
$16.5M
TCR TRANSDUCED CDB T CELLS FOR ADOPTIVE IMMUNOTHERAPYP01CA154778 · NCI · LOYOLA UNIVERSITY CHICAGO · PI NISHIMURA, MICHAEL I. · 2011 to 2015
$15.4M
Mechanisms Of RNA-Binding Protein-Mediated Apoptosis In Oral MucositisR01DE022776 · NIDCR · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI PALANISAMY, VISWANATHAN · 2013 to 2017
$2.1M
Oxidative stress and AICD in memory T cell persistenceR01CA138930 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI MEHROTRA, SHIKHAR · 2010 to 2014
$1.5M
Isolation and Characterization of Prostrate Antigen Specific High Affinity TCRR21CA137725 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI MEHROTRA, SHIKHAR · 2009 to 2010
$357k
NCATS NIH HHS UL1 TR001120NCI NIH HHS P01 CA154778NCI NIH HHS P30 CA138313NCI NIH HHS R01 CA138930NCI NIH HHS R21 CA137725NIDCR NIH HHS R01 DE022776
6 · The paper itself

Abstract

Repetitive stimulation of T-cell receptor (TCR) with cognate antigen results in robust proliferation and expansion of the T cells, and also imprints them with replicative senescence signatures. Our previous studies have shown that life-span and antitumor function of T cells can be enhanced by inhibiting reactive oxygen species (ROS) or intervening with ROS-dependent JNK activation that leads to its activation-induced cell death. Because tumor suppressor protein p53 is also a redox active transcription factor that regulates cellular ROS generation that triggers downstream factor-mediating apoptosis, we determined if p53 levels could influence persistence and function of tumor-reactive T cells. Using h3T TCR transgenic mice, with human tyrosinase epitope-reactive T cells developed on p53 knockout (KO) background, we determined its role in regulating antitumor T-cell function. Our data show that as compared with h3T cells, h3T-p53 KO T cells exhibited enhanced glycolytic commitment that correlated with increased proliferation, IFNγ secretion, cytolytic capacity, expression of stemness gene signature, and decreased TGF-β signaling. This increased effector function correlated to the improved control of subcutaneously established murine melanoma after adoptive transfer of p53-KO T cells. Pharmacological inhibition of human TCR-transduced T cells using a combination of p53 inhibitors also potentiated the T-cell effector function and improved persistence. Thus, our data highlight the key role of p53 in regulating the tumor-reactive T-cell response and that targeting this pathway could have potential translational significance in adoptive T-cell therapy. Cancer Res; 76(18); 5229-40. ©2016 AACR.

Indexed as

Adoptive TransferAnimalsDisease Models, AnimalFlow CytometryHeterograftsHumansMelanomaMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicReal-Time Polymerase Chain ReactionReceptors, Antigen, T-CellT-Lymphocytes, CytotoxicTumor Suppressor Protein p53Receptors, Antigen, T-CellTumor Suppressor Protein p53

Identifiers

PMID27466285
PMCPMC5026612
OpenAlexW2486957823

What OpenQuestion holds

Textmetadata
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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.