Evidence map›Paper›PMID 28232743›Full record

ArticleLeukemia2017

Cobll1 is linked to drug resistance and blastic transformation in chronic myeloid leukemia.

S H Han, S-H Kim, H-J Kim, Y Lee, S-Y Choi, G Park, D-H Kim, A Lee, J Kim, J-M Choi and 4 more

Erratum issuedAbstract read
PubMed Publisher
In one paragraph

Article in Leukemia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

17 citing papers in PubMed, 26 citations in OpenAlex.

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  15. Expression ofHaematologica · 2018
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 6 institutions in 1 country.

S H Han *Department of Biological Sciences, Sungkyunkwan University, Suwon, Republic of Korea.
S-H Kim *Leukemia Research Institute, The Catholic University of Korea, Seoul, Republic of Korea.
H-J KimDepartment of Biological Sciences, Sungkyunkwan University, Suwon, Republic of Korea.
Y LeeCenter for Genomic Integrity Institute for Basic Science (IBS), Ulsan National Institute of Science and Technology, Ulsan, Republic of Korea.ORCID 0000-0001-7919-9048
S-Y ChoiLeukemia Research Institute, The Catholic University of Korea, Seoul, Republic of Korea.
G ParkDepartment of Pathology, Seoul St. Mary's Hospital, The Catholic University of Korea, Seoul, Republic of Korea.
D-H KimDepartment of Life Science, College of Natural Sciences, Hanyang University, Seoul, Republic of Korea.
A LeeDepartment of Life Systems, Sookmyung Women's University, Seoul, Republic of Korea.
J KimDepartment of Life Systems, Sookmyung Women's University, Seoul, Republic of Korea.
J-M ChoiDepartment of Life Science, College of Natural Sciences, Hanyang University, Seoul, Republic of Korea.
Y KimDepartment of Life Systems, Sookmyung Women's University, Seoul, Republic of Korea.ORCID 0000-0001-8574-4938
K MyungCenter for Genomic Integrity Institute for Basic Science (IBS), Ulsan National Institute of Science and Technology, Ulsan, Republic of Korea.
H KimDepartment of Biological Sciences, Sungkyunkwan University, Suwon, Republic of Korea.
D-W KimLeukemia Research Institute, The Catholic University of Korea, Seoul, Republic of Korea.
Institute for Basic Science · KRSookmyung Women's University · KRThe Catholic University of Korea Seoul St. Mary's Hospital · KRCatholic University of Korea · KRHanyang University · KRSungkyunkwan University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Drug resistance to BCR-ABL1 tyrosine kinase inhibitor (TKI) and disease progression to blast crisis (BC) are major clinical problems in chronic myeloid leukemia (CML); however, underlying mechanisms governing this process remain to be elucidated. Here, we report Cordon-bleu protein-like 1 (Cobll1) as a distinct molecular marker associated with drug resistance as well as progression to BC. In detail, Cobll1 increases IKKγ stability, leading to NF-κB activation and reduction of nilotinib-dependent apoptosis, suggesting Cobll1-mediated NF-κB could be involved in drug resistance. Recently, NF-κB signalling has been highlighted as a core mechanism for chronic phase (CP)-BC progression, stem cell survival and tyrosine kinase inhibitor resistance. We also demonstrated that high expression of Cobll1 confers drug resistance to tyrosine kinase inhibitors in CML cell line as well as patient samples. The analysis of large sets of primary CML samples (n=90) shows that Cobll1 expression is dramatically increased in BC but not in CP, which is correlated with a poor survival rate (P=0.002). Moreover, our studies show that Cobll1 is highly expressed in CD34

Indexed as

Blast CrisisCell Line, TumorDrug Resistance, NeoplasmFusion Proteins, bcr-ablHumansI-kappa B KinaseLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMicroRNAsNF-kappa BPyrimidinesTranscription FactorsBCR-ABL1 fusion protein, humanCOBLL1 protein, humanFusion Proteins, bcr-ablI-kappa B KinaseMicroRNAsMIRN424 microrna, humanMIRN503 microRNA, humanNF-kappa BnilotinibPyrimidinesTranscription Factors

Identifiers

PMID28232743
OpenAlexW2590257207

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.