Evidence map›Paper›PMID 27301701›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2016

Expression of CDK7, Cyclin H, and MAT1 Is Elevated in Breast Cancer and Is Prognostic in Estrogen Receptor-Positive Breast Cancer.

Hetal Patel, Rezvan Abduljabbar, Chun-Fui Lai, Manikandan Periyasamy, Alison Harrod, Carolina Gemma, Jennifer H Steel, Naina Patel, Claudia Busonero, Dena Jerjees and 13 more

Open access · bronzeAbstract read
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
3.8field-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

63 citing papers in PubMed, 99 citations in OpenAlex.

  1. Next-generation CDK inhibitors in HR+/HER2- breast cancer.The Journal of clinical investigation · 2026
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  17. Cimicifugin, a broad-spectrum inhibitor ofAntimicrobial agents and chemotherapy · 2024
    Article
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3 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

23 authors at 1 institution in 1 country.

Hetal PatelDepartment of Surgery and Cancer, Imperial College London, Hammersmith Hospital Campus, London, United Kingdom.
Rezvan AbduljabbarDepartment of Cancer and Stem Cells, School of Medicine, University of Nottingham, Nottingham, United Kingdom.
Chun-Fui LaiDepartment of Surgery and Cancer, Imperial College London, Hammersmith Hospital Campus, London, United Kingdom.
Manikandan PeriyasamyDepartment of Surgery and Cancer, Imperial College London, Hammersmith Hospital Campus, London, United Kingdom.
Alison HarrodDepartment of Surgery and Cancer, Imperial College London, Hammersmith Hospital Campus, London, United Kingdom.
Carolina GemmaDepartment of Surgery and Cancer, Imperial College London, Hammersmith Hospital Campus, London, United Kingdom.
Jennifer H SteelDepartment of Surgery and Cancer, Imperial College London, Hammersmith Hospital Campus, London, United Kingdom.
Naina PatelDepartment of Surgery and Cancer, Imperial College London, Hammersmith Hospital Campus, London, United Kingdom.
Claudia BusoneroDepartment of Surgery and Cancer, Imperial College London, Hammersmith Hospital Campus, London, United Kingdom.
Dena JerjeesDepartment of Cancer and Stem Cells, School of Medicine, University of Nottingham, Nottingham, United Kingdom.
Judit RemenyiDivision of Cancer Research, University of Dundee, Ninewells Hospital and Medical School, Dundee, United Kingdom.
Sally SmithCentre for Tumour Biology, Barts Cancer Institute, Queen Mary University of London, John Vane Science Centre, Charterhouse Square, London, United Kingdom.
Jennifer J GommCentre for Tumour Biology, Barts Cancer Institute, Queen Mary University of London, John Vane Science Centre, Charterhouse Square, London, United Kingdom.
Luca MagnaniDepartment of Surgery and Cancer, Imperial College London, Hammersmith Hospital Campus, London, United Kingdom.
Balázs GyőrffyMTA TTK Lendület Cancer Biomarker Research Group, Budapest, Hungary.
Louise J JonesCentre for Tumour Biology, Barts Cancer Institute, Queen Mary University of London, John Vane Science Centre, Charterhouse Square, London, United Kingdom.
Frances Fuller-PaceDivision of Cancer Research, University of Dundee, Ninewells Hospital and Medical School, Dundee, United Kingdom.
Sami ShoushaDepartment of Histopathology, Charing Cross Hospital, Imperial College London, United Kingdom.
Laki BuluwelaDepartment of Surgery and Cancer, Imperial College London, Hammersmith Hospital Campus, London, United Kingdom.
Emad A RakhaDepartment of Cancer and Stem Cells, School of Medicine, University of Nottingham, Nottingham, United Kingdom.
Ian O EllisDepartment of Cancer and Stem Cells, School of Medicine, University of Nottingham, Nottingham, United Kingdom.
R Charles CoombesDepartment of Surgery and Cancer, Imperial College London, Hammersmith Hospital Campus, London, United Kingdom.
Simak AliDepartment of Surgery and Cancer, Imperial College London, Hammersmith Hospital Campus, London, United Kingdom. simak.ali@imperial.ac.uk.
Semmelweis University · HU

Funding

Breast Cancer Now 2014MAYPR23Cancer Research UK 12011Cancer Research UK 18784Cancer Research UK A12011Cancer Research UK A12196Cancer Research UK A7283Cancer Research UK A9335
6 · The paper itself

Abstract

purposeCDK-activating kinase (CAK) is required for the regulation of the cell cycle and is a trimeric complex consisting of cyclin-dependent kinase 7 (CDK7), Cyclin H, and the accessory protein, MAT1. CDK7 also plays a critical role in regulating transcription, primarily by phosphorylating RNA polymerase II, as well as transcription factors such as estrogen receptor-α (ER). Deregulation of cell cycle and transcriptional control are general features of tumor cells, highlighting the potential for the use of CDK7 inhibitors as novel cancer therapeutics. EXPERIMENTAL

designmRNA and protein expression of CDK7 and its essential cofactors cyclin H and MAT1 were evaluated in breast cancer samples to determine if their levels are altered in cancer. Immunohistochemical staining of >900 breast cancers was used to determine the association with clinicopathologic features and patient outcome.

resultsWe show that expressions of CDK7, cyclin H, and MAT1 are all closely linked at the mRNA and protein level, and their expression is elevated in breast cancer compared with the normal breast tissue. Intriguingly, CDK7 expression was inversely proportional to tumor grade and size, and outcome analysis showed an association between CAK levels and better outcome. Moreover, CDK7 expression was positively associated with ER expression and in particular with phosphorylation of ER at serine 118, a site important for ER transcriptional activity.

conclusionsExpressions of components of the CAK complex, CDK7, MAT1, and Cyclin H are elevated in breast cancer and correlate with ER. Like ER, CDK7 expression is inversely proportional to poor prognostic factors and survival. Clin Cancer Res; 22(23); 5929-38. ©2016 AACR.

Indexed as

AdultBreast NeoplasmsCarrier ProteinsCell Cycle ProteinsCyclin-Dependent Kinase-Activating KinaseCyclin-Dependent KinasesCyclin HFemaleGene ExpressionHumansMiddle AgedPhosphorylationPrognosisReceptors, EstrogenSignal TransductionTranscription FactorsCarrier ProteinsCCNH protein, humanCDK7 protein, humanCell Cycle ProteinsCyclin-Dependent Kinase-Activating KinaseCyclin-Dependent KinasesCyclin HMNAT1 protein, humanReceptors, EstrogenTranscription Factors

Identifiers

PMID27301701
PMCPMC5293170
OpenAlexW2435390469

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.