Evidence map›Paper›PMID 30260324›Full record

ArticleThe Journal of clinical investigation2018

PLK1 stabilizes a MYC-dependent kinase network in aggressive B cell lymphomas.

Yuan Ren, Chengfeng Bi, Xiaohong Zhao, Tint Lwin, Cheng Wang, Ji Yuan, Ariosto S Silva, Bijal D Shah, Bin Fang, Tao Li and 15 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
8.3field-weighted citation impact, top 2% 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

59 citing papers in PubMed, 91 citations in OpenAlex.

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  15. Targeting ST8SIA6-AS1 counteracts KRASExperimental hematology & oncology · 2023
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

25 authors at 4 institutions in 2 countries.

Yuan RenDepartment of Laboratory Medicine and Hematopathology, Moffitt Cancer Center & Research Institute, Tampa, Florida, USA.
Chengfeng BiDepartment of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, Nebraska, USA.
Xiaohong ZhaoDepartment of Laboratory Medicine and Hematopathology, Moffitt Cancer Center & Research Institute, Tampa, Florida, USA.
Tint LwinDepartment of Laboratory Medicine and Hematopathology, Moffitt Cancer Center & Research Institute, Tampa, Florida, USA.
Cheng WangDepartment of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, Nebraska, USA.
Ji YuanDepartment of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, Nebraska, USA.
Ariosto S SilvaDepartment of Cancer Imaging and Metabolism.
Bijal D ShahDepartment of Malignant Hematology, and.
Bin FangProteomics Core Facility, Moffitt Cancer Center & Research Institute, Tampa, Florida, USA.
Tao LiDepartment of Laboratory Medicine and Hematopathology, Moffitt Cancer Center & Research Institute, Tampa, Florida, USA.
John M KoomenProteomics Core Facility, Moffitt Cancer Center & Research Institute, Tampa, Florida, USA.
Huijuan JiangDepartment of Laboratory Medicine and Hematopathology, Moffitt Cancer Center & Research Institute, Tampa, Florida, USA.
Julio C ChavezDepartment of Malignant Hematology, and.
Lan V PhamDepartment of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Praneeth R SudalaguntaDepartment of Cancer Imaging and Metabolism.
Lixin WanDepartment of Molecular Oncology and.
Xuefeng WangDepartment of Biostatics and Bioinformatics, Moffitt Cancer Center & Research Institute, Tampa, Florida, USA.
William S DaltonDepartment of Malignant Hematology, and.
Lynn C MoscinskiDepartment of Laboratory Medicine and Hematopathology, Moffitt Cancer Center & Research Institute, Tampa, Florida, USA.
Kenneth H ShainDepartment of Malignant Hematology, and.
Julie VoseDepartment of Internal Medicine, University of Nebraska Medical Center, Omaha, Nebraska, USA.
John L ClevelandDepartment of Tumor Biology, Moffitt Cancer Center & Research Institute, Tampa, Florida, USA.
Eduardo M SotomayorDepartment of Hematology & Oncology, George Washington University, Washington, DC, USA.
Kai FuDepartment of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, Nebraska, USA.
Jianguo TaoDepartment of Laboratory Medicine and Hematopathology, Moffitt Cancer Center & Research Institute, Tampa, Florida, USA.
Moffitt Cancer Center · USUniversity of Nebraska Medical Center · USGeorge Washington University · USThe University of Texas MD Anderson Cancer Center · US

Funding

TRANSLATIONAL RESEARCHP30CA076292 · NCI · UNIVERSITY OF SOUTH FLORIDA · PI KENNETH Lynn WRIGHT · 1998 to 2026
$93.5M
UNMC/EPPLEY CANCER CENTER SUPPORT GRANTP30CA036727 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI Apar Kishor Ganti · 1985 to 2026
$55.0M
"Research Supplement to Promote Diversity in Health-Related Research", as part of Moffitt PS-OC, "Cancer as a Complex adaptive System"U54CA193489 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI ANDERSON, ALEXANDER ROBERTSON ALLAN, GATENBY, ROBERT A · 2015 to 2020
$12.5M
Targeting Negative Regulatory Pathways for Immunotherapy of B-Cell LymphomasR01CA134807 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI TAO, JIANGUO · 2010 to 2014
$2.3M
Role of Specific Histone Deacetylases in Lymphoma Immunobiology and TherapyR01CA179062 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI SOTOMAYOR, EDUARDO M., TAO, JIANGUO · 2015 to 2019
$1.8M
Tageting BAFF and BAFF-Induced Non-Canonical NF-kB Pathways for Enhancing Mantle R01CA137123 · NCI · H. LEE MOFFITT CANCER CTR & RES INST · PI TAO, JIANGUO · 2009 to 2013
$1.3M
NCI NIH HHS P30 CA036727NCI NIH HHS P30 CA076292NCI NIH HHS R01 CA134807NCI NIH HHS R01 CA137123NCI NIH HHS R01 CA179062NCI NIH HHS U54 CA193489
6 · The paper itself

Abstract

Concordant activation of MYC and BCL-2 oncoproteins in double-hit lymphoma (DHL) results in aggressive disease that is refractory to treatment. By integrating activity-based proteomic profiling and drug screens, polo-like kinase-1 (PLK1) was identified as an essential regulator of the MYC-dependent kinome in DHL. Notably, PLK1 was expressed at high levels in DHL, correlated with MYC expression, and connoted poor outcome. Further, PLK1 signaling augmented MYC protein stability, and in turn, MYC directly induced PLK1 transcription, establishing a feed-forward MYC-PLK1 circuit in DHL. Finally, inhibition of PLK1 triggered degradation of MYC and of the antiapoptotic protein MCL-1, and PLK1 inhibitors showed synergy with BCL-2 antagonists in blocking DHL cell growth, survival, and tumorigenicity, supporting clinical targeting of PLK1 in DHL.

Indexed as

ProteolysisSignal TransductionAnimalsCell Cycle ProteinsCell Line, TumorFemaleHumansLymphoma, Large B-Cell, DiffuseMaleMiceMice, Inbred NODMice, SCIDMyeloid Cell Leukemia Sequence 1 ProteinPolo-Like Kinase 1Protein Serine-Threonine KinasesProtein StabilityCell Cycle ProteinsMCL1 protein, humanMYC protein, humanMyeloid Cell Leukemia Sequence 1 ProteinPolo-Like Kinase 1Protein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-mycCancerHematologyLymphomasMolecular biologyOncology

Identifiers

PMID30260324
PMCPMC6264635
OpenAlexW2894397394

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.