Evidence map›Paper›PMID 23518499›Full record

ArticleCell cycle (Georgetown, Tex.)2013

CDK1 interacts with RARγ and plays an important role in treatment response of acute myeloid leukemia.

Andreas Hedblom, Kristian B Laursen, Regina Miftakhova, Martuza Sarwar, Lola Anagnostaki, Anders Bredberg, Nigel P Mongan, Lorraine J Gudas, Jenny L Persson

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

22 citing papers in PubMed, 38 citations in OpenAlex.

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  19. The expression of CDK1 is associated with proliferation and can be a prognostic factor in epithelial ovarian cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015
    Article
  20. Targeting cell cycle regulators in hematologic malignancies.Frontiers in cell and developmental biology · 2015
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 3 countries.

Andreas HedblomDepartment of Laboratory Medicine, Division of Experimental Cancer Research, Clinical Research Center, Lund University, Malmö, Sweden.
Kristian B Laursen
Regina Miftakhova
Martuza Sarwar
Lola Anagnostaki
Anders Bredberg
Nigel P Mongan
Lorraine J Gudas
Jenny L Persson
Lund University · SENew York Proton Center · USClinical Research Management · USUniversity of Nottingham · GB

Funding

Retinoic Acid Binding Proteins: Functional StudiesR01CA043796 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI GUDAS, LORRAINE J · 1987 to 2013
$5.0M
NCI NIH HHS R01 CA043796NCI NIH HHS R01CA043796
6 · The paper itself

Abstract

Alterations in cell cycle pathways and retinoic acid signaling are implicated in leukemogenesis. However, little is known about the roles of cyclin-dependent kinases (CDKs) in treatment response of leukemia. In this study, we observed that CDK1 expression was significantly higher in bone marrow from 42 patients with acute myeloid leukemia (AML) at recurrence than that at first diagnosis (p = 0.04). AML patients had higher level of nuclear CDK1 in their leukemic blasts tended to have poorer clinical outcome compared with those with lower levels. We showed that CDK1 function is required for all-trans retinoic acid (ATRA) to achieve the optimal effect in U-937 human leukemic cells. CDK1 modulates the levels of P27(kip) and AKT phosphorylation in response to ATRA treatment. Further, we show, for the first time, that RARγ in concert with ATRA regulates protein levels of CDK1 and its subcellular localization. The regulation of the subcellular content of CDK1 and RARγ by ATRA is an important process for achieving an effective response in treatment of leukemia. RARγ and CDK1 form a reciprocal regulatory circuit in the nucleus and influence the function and protein stability of each other and the level of P27(kip) protein. In addition, expression of wee1 kinase and Cdc25A/C phosphatases also coincide with CDK1 expression and its subcellular localization in response to ATRA treatment. Our study reveals a novel mechanism by which CDK1 and RARγ coordinate with ATRA to influence cell cycle progression and cellular differentiation.

Indexed as

AdultBone Marrow CellsCDC2 Protein KinaseCell CycleCell DifferentiationCell FractionationCyclin-Dependent Kinase Inhibitor p27DNA PrimersFlow CytometryHumansImmunohistochemistryKaplan-Meier EstimateLeukemia, Myeloid, AcuteNeoplasm Recurrence, LocalOncogene Protein v-aktPhosphorylationCDC2 Protein KinaseCDKN1B protein, humanCyclin-Dependent Kinase Inhibitor p27DNA PrimersOncogene Protein v-aktReceptors, Retinoic AcidRetinoic Acid Receptor gammaTretinoinAMLCDK1cell cycledifferentiationleukemiaretinoic acid receptortherapy

Identifiers

PMID23518499
PMCPMC3674090
OpenAlexW2071111320

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.