Evidence map›Paper›PMID 30104286›Full record

ReviewJournal of clinical pathology2018

CDK12: an emerging therapeutic target for cancer.

Goldie Y L Lui, Carla Grandori, Christopher J Kemp

Open access · greenAbstract readReview
In one paragraph

Review in Journal of clinical pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 5% 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

70 citing papers in PubMed, 1 synthesis or guideline pooled it, 133 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. CDK12 and CDK13 in oncology: from RNA regulation to therapeutic targeting.Cellular oncology (Dordrecht, Netherlands) · 2026
    Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. Article

10 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

3 authors at 2 institutions in 1 country.

Goldie Y L LuiFred Hutchinson Cancer Research Center, Human Biology Division, Seattle, Washington, USA glui@fredhutch.org.
Carla GrandoriSEngine Precision Medicine, Seattle, Washington, USA.
Christopher J KempFred Hutchinson Cancer Research Center, Human Biology Division, Seattle, Washington, USA.
Fred Hutch Cancer Center · USPrecision for Medicine (United States) · US

Funding

Research Education About Cancer and Health (REACH) CoreU54CA132381 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI KAREN R PETERSON · 2007 to 2026
$25.3M
Undergraduate Student Training in Cancer ResearchU54CA132383 · NCI · NEW MEXICO STATE UNIVERSITY LAS CRUCES · PI MICHELE Irene SHUSTER · 2007 to 2026
$21.4M
Personalized cancer models to discover and develop new therapeutic targets.U01CA217883 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI KEMP, CHRISTOPHER J · 2017 to 2021
$4.3M
An integrated computational and functional genomics discovery engine for precliniU01CA176303 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI KEMP, CHRISTOPHER J · 2013 to 2016
$4.1M
An Academic-Industry Partnership to Advance Functional Genomics for Personalized Oncology.R01CA214428 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI KEMP, CHRISTOPHER J · 2018 to 2022
$3.0M
NCI NIH HHS R01 CA214428NCI NIH HHS U01 CA176303NCI NIH HHS U01 CA217883NCI NIH HHS U54 CA132381NCI NIH HHS U54 CA132383
6 · The paper itself

Abstract

Cyclin-dependent kinase 12 (CDK12) belongs to the cyclin-dependent kinase (CDK) family of serine/threonine protein kinases that regulate transcriptional and post-transcriptional processes, thereby modulating multiple cellular functions. Early studies characterised CDK12 as a transcriptional CDK that complexes with cyclin K to mediate gene transcription by phosphorylating RNA polymerase II. CDK12 has been demonstrated to specifically upregulate the expression of genes involved in response to DNA damage, stress and heat shock. More recent studies have implicated CDK12 in regulating mRNA splicing, 3' end processing, pre-replication complex assembly and genomic stability during embryonic development. Genomic alterations in CDK12 have been detected in oesophageal, stomach, breast, endometrial, uterine, ovarian, bladder, colorectal and pancreatic cancers, ranging from 5% to 15% of sequenced cases. An increasing number of studies point to CDK12 inhibition as an effective strategy to inhibit tumour growth, and synthetic lethal interactions have been described with MYC, EWS/FLI and PARP/CHK1 inhibition. Herein, we discuss the present literature on CDK12 in cell function and human cancer, highlighting important roles for CDK12 as a clinical biomarker for treatment response and potential as an effective therapeutic target.

Indexed as

AnimalsAntineoplastic AgentsBiomarkers, TumorCyclin-Dependent KinasesGene Expression Regulation, EnzymologicGene Expression Regulation, NeoplasticHumansMolecular Targeted TherapyMutationNeoplasmsProtein Kinase InhibitorsSignal TransductionAntineoplastic AgentsBiomarkers, TumorCDK12 protein, humanCyclin-Dependent KinasesProtein Kinase Inhibitorsbreast cancercancer geneticscell biologyC-MYC oncogeneovarian cancer

Identifiers

PMID30104286
PMCPMC6242340
OpenAlexW2887071858

What OpenQuestion holds

Textmetadata
LicenceTDM
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.