Evidence map›Paper›PMID 26242912›Full record

ArticleThe Journal of biological chemistry2015

Identification of a Dual Inhibitor of Janus Kinase 2 (JAK2) and p70 Ribosomal S6 Kinase1 (S6K1) Pathways.

Sanguine Byun, Semi Lim, Ji Young Mun, Ki Hyun Kim, Timothy R Ramadhar, Lee Farrand, Seung Ho Shin, N R Thimmegowda, Hyong Joo Lee, David A Frank and 3 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

11 citing papers in PubMed, 16 citations in OpenAlex.

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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

13 authors at 10 institutions in 2 countries.

Sanguine ByunFrom the Cutaneous Biology Research Center, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129, Advanced Institutes of Convergence Technology, Seoul National University, Suwon 443-270, Republic of Korea.
Semi LimWCU Biomodulation Major, Department of Agricultural Biotechnology, Seoul National University, Seoul 151-742, Republic of Korea.
Ji Young MunDepartment of Biomedical Laboratory Science, College of Health Sciences, Eulji University, Seongnam 461-463, Republic of Korea.
Ki Hyun KimDepartment of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, Massachusetts 02115, School of Pharmacy, Sungkyunkwan University, Suwon 440-746, Republic of Korea.
Timothy R RamadharDepartment of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, Massachusetts 02115.
Lee FarrandYuhan Research Institute, Yuhan Corp., Yongin 446-902, Republic of Korea.
Seung Ho ShinProgram in Biomedical Informatics and Computational Biology, University of Minnesota, Minneapolis, Minnesota 55455.
N R ThimmegowdaDepartment of Chemistry, Government Sri Krishnarajendra Silver Jubilee Technological Institute, Bangalore 560001, India, World Class Institute, Korea Research Institute of Bioscience and Biotechnology, Ochang 363-883, Korea.
Hyong Joo LeeWCU Biomodulation Major, Department of Agricultural Biotechnology, Seoul National University, Seoul 151-742, Republic of Korea.
David A FrankDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, and.
Jon ClardyDepartment of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, Massachusetts 02115, jon_clardy@hms.harvard.edu.
Sam W LeeFrom the Cutaneous Biology Research Center, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129, swlee@mgh.harvard.edu.
Ki Won LeeAdvanced Institutes of Convergence Technology, Seoul National University, Suwon 443-270, Republic of Korea, WCU Biomodulation Major, Department of Agricultural Biotechnology, Seoul National University, Seoul 151-742, Republic of Korea, kiwon@snu.ac.kr.
Harvard University · USSeoul National University · KRAdvanced Institute of Convergence Technology · KRDana-Farber Cancer Institute · USEulji University · KRKorea Research Institute of Bioscience and Biotechnology · KRMassachusetts General Hospital · USSungkyunkwan University · KRUniversity of Minnesota · USYuhan University · KR

Funding

Targeting ROS by a p53-activating agent for selective killing of cancer cellsR01CA142805 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI LEE, SAM W · 2010 to 2014
$1.7M
p53-GAMT pathway in cancer cell metabolism and DNA damage-induced carcinogenesisR01CA149477 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI LEE, SAM W · 2010 to 2014
$1.7M
Discovery of Potential Therapeutic Agents from Insect-Associated Symbiotic BacterF32GM108415 · NIGMS · HARVARD MEDICAL SCHOOL · PI RAMADHAR, TIMOTHY RAMESAR · 2014 to 2015
$106k
NCI NIH HHS 1R01CA142805NCI NIH HHS 1R01CA149477NCI NIH HHS R01 CA142805NCI NIH HHS R01 CA149477NIGMS NIH HHS F32 GM108415
6 · The paper itself

Abstract

Bioactive phytochemicals can suppress the growth of malignant cells, and investigation of the mechanisms responsible can assist in the identification of novel therapeutic strategies for cancer therapy. Ginger has been reported to exhibit potent anti-cancer effects, although previous reports have often focused on a narrow range of specific compounds. Through a direct comparison of various ginger compounds, we determined that gingerenone A selectively kills cancer cells while exhibiting minimal toxicity toward normal cells. Kinase array screening revealed JAK2 and S6K1 as the molecular targets primarily responsible for gingerenone A-induced cancer cell death. The effect of gingerenone A was strongly associated with relative phosphorylation levels of JAK2 and S6K1, and administration of gingerenone A significantly suppressed tumor growth in vivo. More importantly, the combined inhibition of JAK2 and S6K1 by commercial inhibitors selectively induced apoptosis in cancer cells, whereas treatment with either agent alone did not. These findings provide rationale for dual targeting of JAK2 and S6K1 in cancer for a combinatorial therapeutic approach.

Indexed as

ApoptosisCell Line, TumorDiarylheptanoidsEnzyme InhibitorsHumansJanus Kinase 2Ribosomal Protein S6 Kinases, 70-kDaDiarylheptanoidsEnzyme Inhibitorsgingerenone AJAK2 protein, humanJanus Kinase 2ribosomal protein S6 kinase, 70kD, polypeptide 1Ribosomal Protein S6 Kinases, 70-kDaanticancercancer biologycell deathcell signalingchemopreventiongingerenone AJAK2 signalingS6K1 signalingsmall molecule

Identifiers

PMID26242912
PMCPMC4583007
OpenAlexW1507948576

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.