Evidence map›Paper›PMID 26655503›Full record

ArticleOncotarget2016

Enhancement of anti-leukemia activity of NK cells in vitro and in vivo by inhibition of leukemia cell-induced NK cell damage.

Roberto Arriga, Sara Caratelli, Andrea Coppola, Giulio Cesare Spagnoli, Adriano Venditti, Sergio Amadori, Giulia Lanzilli, Davide Lauro, Patrizia Palomba, Tommaso Sconocchia and 6 more

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

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.7field-weighted citation impact, top 29% 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

8 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. TIMP-3 as a therapeutic target for cancer.Therapeutic advances in medical oncology · 2019
    Review
  5. Article
  6. Article
  7. Article
  8. 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

16 authors at 5 institutions in 3 countries.

Roberto ArrigaDepartment of Systems Medicine, University of Rome "Tor Vergata", Rome, Italy.
Sara CaratelliLaboratory of Tumor Immunology and Immunotherapy, Institute of Translational Pharmacology, Department of Biomedicine, National Research Council (CNR), Rome, Italy.
Andrea CoppolaDepartment of Systems Medicine, University of Rome "Tor Vergata", Rome, Italy.
Giulio Cesare SpagnoliInstitute for Surgical Research and Hospital Management, Department of Biomedicine, University of Basel, Basel, Switzerland.
Adriano VendittiHematology, Department of Biomedicine and Prevention, University of Rome "Tor Vergata", Rome, Italy.
Sergio AmadoriHematology, Department of Biomedicine and Prevention, University of Rome "Tor Vergata", Rome, Italy.
Giulia LanzilliLaboratory of Tumor Immunology and Immunotherapy, Institute of Translational Pharmacology, Department of Biomedicine, National Research Council (CNR), Rome, Italy.
Davide LauroDepartment of Systems Medicine, University of Rome "Tor Vergata", Rome, Italy.
Patrizia PalombaHematology, Department of Biomedicine and Prevention, University of Rome "Tor Vergata", Rome, Italy.
Tommaso SconocchiaLaboratory of Tumor Immunology and Immunotherapy, Institute of Translational Pharmacology, Department of Biomedicine, National Research Council (CNR), Rome, Italy.
Maria Ilaria Del PrincipeHematology, Department of Biomedicine and Prevention, University of Rome "Tor Vergata", Rome, Italy.
Luca MaurilloHematology, Department of Biomedicine and Prevention, University of Rome "Tor Vergata", Rome, Italy.
Francesco BuccisanoHematology, Department of Biomedicine and Prevention, University of Rome "Tor Vergata", Rome, Italy.
Barbara CapuaniDepartment of Systems Medicine, University of Rome "Tor Vergata", Rome, Italy.
Soldano FerroneDepartments of Surgery and Orthopedic Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Giuseppe SconocchiaLaboratory of Tumor Immunology and Immunotherapy, Institute of Translational Pharmacology, Department of Biomedicine, National Research Council (CNR), Rome, Italy.
University of Rome Tor Vergata · ITNational Research Council · ITHarvard University · USIstituto di Farmacologia Traslazionale · ITUniversity of Basel · CH

Funding

Therapuetic Immune Targeting of EphA2 Expressed by Melanoma & Its Tumor-AssociateP50CA121973 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BECICH, MICHAEL JOHN · 2008 to 2018
$22.9M
Combinatorial targeting of melanoma initiating cellsR01CA138188 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI FERRONE, SOLDANO · 2008 to 2012
$1.5M
NCI NIH HHS P50 CA121973NCI NIH HHS P50CA121973NCI NIH HHS R01 CA138188NCI NIH HHS R01CA138188
6 · The paper itself

Abstract

Acute myeloid leukemia (AML) cells induce, in vitro, NK cell abnormalities (NKCAs) including apoptosis and activating receptor down-regulation. The potential negative impact of AML cells on the therapeutic efficacy of NK cell-based strategies prompted us to analyze the mechanisms underlying NKCAs and to develop approaches to protect NK cells from NKCAs. NKCA induction by the AML leukemia cells target a subpopulation of peripheral blood NK cells and is interleukin-2 independent but is abrogated by a long-term culture of NK (LTNK) cells at 37°C. LTNK cells displayed a significantly enhanced ability to damage AML cells in vitro and inhibited the subcutaneous growth of ML-2 cells grafted into CB17 SCID mice. Actinomycin D restored the susceptibility of LTNK cells to NKCAs while TAPI-0, a functional analog of the tissue inhibitor of metalloproteinase (TIMP) 3, inhibits ML-2 cell-induced NKCAs suggesting that the generation of NK cell resistance to NKCAs involves RNA transcription and metalloproteinase (MPP) inactivation. This conclusion is supported by the reduced susceptibility to AML cell-induced NKCAs of LTNK cells in which TIMP3 gene and protein are over-expressed. This information may contribute to the rational design of targeted strategies to enhance the efficacy of NK cell-based-immunotherapy of AML with haploidentical NK cells.

Indexed as

AnimalsAntineoplastic AgentsApoptosisBiomarkers, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansIn Vitro TechniquesKiller Cells, NaturalLeukemia, Myeloid, AcuteLymphocytesMaleMiceMice, SCIDReal-Time Polymerase Chain ReactionReverse Transcriptase Polymerase Chain ReactionAntineoplastic AgentsBiomarkers, TumorRNA, Messengeracute myeloid leukemiaCD16NK cellNK cell abnormalitiesTIMP3

Identifiers

PMID26655503
PMCPMC4811516
OpenAlexW2232784070

What OpenQuestion holds

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LicenceCC BY
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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.