Evidence map›Paper›PMID 31468695›Full record

ArticleEMBO reports2019

CDK12 drives breast tumor initiation and trastuzumab resistance via WNT and IRS1-ErbB-PI3K signaling.

Hee-Joo Choi, Sora Jin, Hani Cho, Hee-Young Won, Hee Woon An, Ga-Young Jeong, Young-Un Park, Hyung-Yong Kim, Mi Kyung Park, Taekwon Son and 5 more

Open access · greenAbstract read
In one paragraph

Article in EMBO reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
4.9field-weighted citation impact, top 4% 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, 117 citations in OpenAlex.

  1. Trial
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  5. Response to Lehrer.Journal of the National Cancer Institute · 2026
    Article
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  7. CDK12 and CDK13 in oncology: from RNA regulation to therapeutic targeting.Cellular oncology (Dordrecht, Netherlands) · 2026
    Review
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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

15 authors at 3 institutions in 1 country.

Hee-Joo ChoiInstitute for Bioengineering and Biopharmaceutical Research (IBBR), Hanyang University, Seoul, Korea.
Sora JinDepartment of Pathology, College of Medicine, Hanyang University, Seoul, Korea.
Hani ChoDepartment of Pathology, College of Medicine, Hanyang University, Seoul, Korea.
Hee-Young WonDepartment of Pathology, College of Medicine, Hanyang University, Seoul, Korea.
Hee Woon AnDepartment of Pathology, College of Medicine, Hanyang University, Seoul, Korea.
Ga-Young JeongDepartment of Pathology, College of Medicine, Hanyang University, Seoul, Korea.
Young-Un ParkDepartment of Pathology, College of Medicine, Hanyang University, Seoul, Korea.
Hyung-Yong KimDepartment of Pathology, College of Medicine, Hanyang University, Seoul, Korea.
Mi Kyung ParkNational Cancer Center, Goyang, Korea.
Taekwon SonCollege of Pharmacy, Seoul National University, Seoul, Korea.
Kyueng-Whan MinDepartment of Pathology, College of Medicine, Hanyang University, Seoul, Korea.ORCID 0000-0002-4757-9211
Ki-Seok JangDepartment of Pathology, College of Medicine, Hanyang University, Seoul, Korea.
Young-Ha OhDepartment of Pathology, College of Medicine, Hanyang University, Seoul, Korea.
Jeong-Yeon LeeDepartment of Medicine, College of Medicine, Hanyang University, Seoul, Korea.ORCID 0000-0003-1298-7466
Gu KongInstitute for Bioengineering and Biopharmaceutical Research (IBBR), Hanyang University, Seoul, Korea.ORCID 0000-0001-9206-8210
Hanyang University · KRNational Cancer Center · KRSeoul National University · KR

Funding

National Research Foundation of Korea (NRF) 2019R1A2C3006305
6 · The paper itself

Abstract

Cyclin-dependent kinase 12 (CDK12) has emerged as an effective therapeutic target due to its ability to regulate DNA damage repair in human cancers, but little is known about the role of CDK12 in driving tumorigenesis. Here, we demonstrate that CDK12 promotes tumor initiation as a novel regulator of cancer stem cells (CSCs) and induces anti-HER2 therapy resistance in human breast cancer. High CDK12 expression caused by concurrent amplification of CDK12 and HER2 in breast cancer patients is associated with disease recurrence and poor survival. CDK12 induces self-renewal of breast CSCs and in vivo tumor-initiating ability, and also reduces susceptibility to trastuzumab. Furthermore, CDK12 kinase activity inhibition facilitates anticancer efficacy of trastuzumab in HER2

Indexed as

Drug Resistance, NeoplasmSignal TransductionAnimalsBreast NeoplasmsCarcinogenesisCell Line, TumorCell ProliferationChromosomes, Human, Pair 17Cyclin-Dependent KinasesFemaleGene Expression Regulation, NeoplasticHumansInsulin Receptor Substrate ProteinsMiceNeoplastic Stem CellsPhosphatidylinositol 3-KinasesCDK12 protein, humanCyclin-Dependent KinasesInsulin Receptor Substrate ProteinsIRS1 protein, humanPhosphatidylinositol 3-KinasesProtein Kinase InhibitorsReceptor, ErbB-3Trastuzumabbreast cancercancer stem cellsCDK12HER2trastuzumab

Identifiers

PMID31468695
PMCPMC6776914
OpenAlexW2971050114

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.