Evidence map›Paper›PMID 29872115›Full record

ReviewCellular & molecular immunology2018

Biochemical mechanisms implemented by human acute myeloid leukemia cells to suppress host immune surveillance.

Inna M Yasinska, Isabel Gonçalves Silva, Svetlana Sakhnevych, Bernhard F Gibbs, Ulrike Raap, Elizaveta Fasler-Kan, Vadim V Sumbayev

Abstract readLetterReview
In one paragraph

Review in Cellular & molecular immunology, 2018. 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
–field-weighted citation impact
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.

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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

7 authors.

Inna M YasinskaMedway School of Pharmacy, Universities of Kent and Greenwich, Chatham Maritime, UK.
Isabel Gonçalves SilvaMedway School of Pharmacy, Universities of Kent and Greenwich, Chatham Maritime, UK.
Svetlana SakhnevychMedway School of Pharmacy, Universities of Kent and Greenwich, Chatham Maritime, UK.
Bernhard F GibbsDepartment of Dermatology and Allergy, University of Oldenburg, Oldenburg, Germany.
Ulrike RaapDepartment of Dermatology and Allergy, University of Oldenburg, Oldenburg, Germany.
Elizaveta Fasler-KanDepartment of Pediatric Surgery and Department of Biomedical Research, Children's Hospital, Inselspital, University of Bern, Bern, Switzerland.
Vadim V SumbayevMedway School of Pharmacy, Universities of Kent and Greenwich, Chatham Maritime, UK. V.Sumbayev@kent.ac.uk.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute myeloid leukaemia (AML) is a blood/bone marrow cancer originating from myeloid cell precusors capable of self-renewing. AML cells implement biochemical mechanisms which allow them not only to survive, but also to successfully escape immune surveillance. ln this work, we discuss crucial molecular mechanisms used by human AML cells in order to evade immune attack.

Indexed as

Leukemia, Myeloid, AcuteTumor EscapeHumansAcute myeloid leukaemiagalectin-9Immune surveillanceTim-3

Identifiers

PMID29872115
PMCPMC6207652

What OpenQuestion holds

Textmetadata
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.