Evidence map›Paper›PMID 25128497›Full record

ArticleGenes & development2014

CDK9-mediated transcription elongation is required for MYC addiction in hepatocellular carcinoma.

Chun-Hao Huang, Amaia Lujambio, Johannes Zuber, Darjus F Tschaharganeh, Michael G Doran, Michael J Evans, Thomas Kitzing, Nan Zhu, Elisa de Stanchina, Charles L Sawyers and 4 more

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 134 papers.

0numbers the graph read from it
0cells of the map it votes in
134citing papers in PubMed
–field-weighted citation impact
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

134 citing papers in PubMed, 200 citations in OpenAlex.

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  9. KRAS Withdrawal in Cholangiocarcinoma Leads to Immune Infiltration and Tumor Regression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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74 more citing papers are in PubMed but not listed here.

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

14 authors at 5 institutions in 2 countries.

Chun-Hao HuangMemorial Sloan-Kettering Cancer Center, New York, New York 10065, USA; Cell and Developmental Biology Program, Weill Graduate School of Medical Sciences, Cornell University, New York, New York 10065, USA; Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA;
Amaia LujambioMemorial Sloan-Kettering Cancer Center, New York, New York 10065, USA; Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA;
Johannes ZuberCold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA; Research Institute of Molecular Pathology, Vienna, 1030, Austria;
Darjus F TschaharganehMemorial Sloan-Kettering Cancer Center, New York, New York 10065, USA;
Michael G DoranMemorial Sloan-Kettering Cancer Center, New York, New York 10065, USA;
Michael J EvansMemorial Sloan-Kettering Cancer Center, New York, New York 10065, USA;
Thomas KitzingMemorial Sloan-Kettering Cancer Center, New York, New York 10065, USA; Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA;
Nan ZhuMemorial Sloan-Kettering Cancer Center, New York, New York 10065, USA;
Elisa de StanchinaMemorial Sloan-Kettering Cancer Center, New York, New York 10065, USA;
Charles L SawyersMemorial Sloan-Kettering Cancer Center, New York, New York 10065, USA; Howard Hughes Medical Institute, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA;
Scott A ArmstrongMemorial Sloan-Kettering Cancer Center, New York, New York 10065, USA;
Jason S LewisMemorial Sloan-Kettering Cancer Center, New York, New York 10065, USA;
Charles J SherrHoward Hughes Medical Institute, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA;
Scott W LoweMemorial Sloan-Kettering Cancer Center, New York, New York 10065, USA; Cell and Developmental Biology Program, Weill Graduate School of Medical Sciences, Cornell University, New York, New York 10065, USA; Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA; Howard Hughes Medical Institute, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA; lowes@mskcc.org.
Kettering University · USMemorial Sloan Kettering Cancer Center · USCold Spring Harbor Laboratory · USHoward Hughes Medical Institute · USResearch Institute of Molecular Pathology · AT

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Nicholas D Socci · 1985 to 2026
$347.4M
VIRAL TRANSACTIVATIONP01CA013106 · NCI · COLD SPRING HARBOR LABORATORY · PI William Richard McCombie · 1985 to 2026
$116.8M
COMPUTATIONAL AND FUNCTIONAL APPROACHES TO VALIDATING CANCER GENOME TARGETSU01CA168409 · NCI · COLD SPRING HARBOR LABORATORY · PI POWERS, SCOTT · 2012 to 2016
$7.3M
Annotating Oncogene Status in Prostate Cancer with Zr-89-transferrin PETR01CA176671 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI EVANS, MICHAEL JOHN, LEWIS, JASON S. · 2013 to 2017
$3.1M
Noninvasive measurement of oncogenic signaling pathways with 89Zr-transferrinR00CA172695 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI EVANS, MICHAEL JOHN · 2014 to 2016
$728k
Howard Hughes Medical InstituteNCI NIH HHS 5U01 CA168409-02NCI NIH HHS CA008748NCI NIH HHS CA013106NCI NIH HHS CA176671NCI NIH HHS P01 CA013106NCI NIH HHS P30 CA008748NCI NIH HHS R00 CA172695NCI NIH HHS R01 CA176671NCI NIH HHS U01 CA168409
6 · The paper itself

Abstract

One-year survival rates for newly diagnosed hepatocellular carcinoma (HCC) are <50%, and unresectable HCC carries a dismal prognosis owing to its aggressiveness and the undruggable nature of its main genetic drivers. By screening a custom library of shRNAs directed toward known drug targets in a genetically defined Myc-driven HCC model, we identified cyclin-dependent kinase 9 (Cdk9) as required for disease maintenance. Pharmacological or shRNA-mediated CDK9 inhibition led to robust anti-tumor effects that correlated with MYC expression levels and depended on the role that both CDK9 and MYC exert in transcription elongation. Our results establish CDK9 inhibition as a therapeutic strategy for MYC-overexpressing liver tumors and highlight the relevance of transcription elongation in the addiction of cancer cells to MYC.

Indexed as

AnimalsCarcinoma, HepatocellularCell Line, TumorCell ProliferationCyclin-Dependent Kinase 9FemaleGene ExpressionGene LibraryHep G2 CellsHumansLiver NeoplasmsMicePositive Transcriptional Elongation Factor BProto-Oncogene Proteins c-mycRNA InterferenceRNA, Small InterferingCyclin-Dependent Kinase 9Myc protein, mousePositive Transcriptional Elongation Factor BProto-Oncogene Proteins c-mycRNA, Small InterferingCDK9MYConcogene addictionRNAi screentranscription elongation

Identifiers

PMID25128497
PMCPMC4197965
OpenAlexW2052279652

What OpenQuestion holds

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LicenceCC BY-NC
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.