Evidence map›Paper›PMID 29432497›Full record

ArticlePloS one2018

Autologous T cells expressing the oncogenic transcription factor KLF6-SV1 prevent apoptosis of chronic lymphocytic leukemia cells.

Parviz Kokhaei, Mohammad Hojjat-Farsangi, Fariba Mozaffari, Ali Moshfegh, Fatemeh Pak, Ali Rashidy-Pour, Marzia Palma, Lotta Hansson, Anders Österborg, Håkan Mellstedt

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.2field-weighted citation impact, top 48% 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

5 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
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  4. Review
  5. 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

10 authors at 3 institutions in 2 countries.

Parviz KokhaeiImmune and Gene Therapy Laboratory, Cancer Centre Karolinska, Department of Oncology and Pathology, Karolinska Institute, Stockholm, Sweden.
Mohammad Hojjat-FarsangiImmune and Gene Therapy Laboratory, Cancer Centre Karolinska, Department of Oncology and Pathology, Karolinska Institute, Stockholm, Sweden.
Fariba MozaffariImmune and Gene Therapy Laboratory, Cancer Centre Karolinska, Department of Oncology and Pathology, Karolinska Institute, Stockholm, Sweden.
Ali MoshfeghImmune and Gene Therapy Laboratory, Cancer Centre Karolinska, Department of Oncology and Pathology, Karolinska Institute, Stockholm, Sweden.
Fatemeh PakCancer Research Center and Department of Immunology, Semnan University of Medical Sciences, Semnan, Iran.
Ali Rashidy-PourPhysiology Research Center and Department of Physiology, Semnan University of Medical Sciences, Semnan, Iran.
Marzia PalmaImmune and Gene Therapy Laboratory, Cancer Centre Karolinska, Department of Oncology and Pathology, Karolinska Institute, Stockholm, Sweden.
Lotta HanssonImmune and Gene Therapy Laboratory, Cancer Centre Karolinska, Department of Oncology and Pathology, Karolinska Institute, Stockholm, Sweden.
Anders ÖsterborgImmune and Gene Therapy Laboratory, Cancer Centre Karolinska, Department of Oncology and Pathology, Karolinska Institute, Stockholm, Sweden.
Håkan MellstedtImmune and Gene Therapy Laboratory, Cancer Centre Karolinska, Department of Oncology and Pathology, Karolinska Institute, Stockholm, Sweden.ORCID 0000-0001-6756-0609
Karolinska Institutet · SEKarolinska University Hospital · SESemnan University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Crosstalk between leukemic cells and the tumor microenvironment is of importance in chronic lymphocytic leukemia (CLL). T cells seem to sustain the survival of CLL cells by various mechanisms. The Krüppel-like family of transcription factors (KLFs) are identified as regulators of proliferation and cell death. In the present study, we analyzed the expression of the wild type (WT) gene KLF6 and the oncogenic splice variant 1 (KLF6-SV1) at the mRNA level in subsets of T cells from CLL patients (n = 29), multiple myeloma patients (n = 6) and normal donors (n = 10). RNA Silencing was used for wtKLF6 and KLF6-SV1. Tumor cell apoptosis was measured. A significant overexpression of wtKLF6 and KLF6-SV1 in T cells of CLL patients compared to normal donors and myeloma patients was noted (p<0.002). Western blot showed that both wtKLF6 and KLF6-SV1 were expressed in purified T cells from CLL patients. KLF6-SV1 siRNA transfection induced a significant down-regulation of KLF6-SV1 in CLL T cells, which lost the capability to sustain the growth of leukemic cells. However, no such a significant effect was seen after wtKLF6 transfection of the autologous T cells. The results suggest that KLF6-SV1 may play a role in the regulation of survival CLL cells.

Indexed as

AgedAged, 80 and overApoptosisFemaleGene ExpressionHumansKruppel-Like Factor 6Leukemia, Lymphocytic, Chronic, B-CellMaleMiddle AgedMultiple MyelomaOncogenesProtein IsoformsRNA InterferenceRNA, MessengerRNA, NeoplasmKLF6 protein, humanKruppel-Like Factor 6Protein IsoformsRNA, MessengerRNA, NeoplasmRNA, Small Interfering

Identifiers

PMID29432497
PMCPMC5809069
OpenAlexW2790054050

What OpenQuestion holds

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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.