ReviewOncology letters2022
The role of mediator subunit 12 in tumorigenesis and cancer therapeutics.
Review in Oncology letters, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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.
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.
Who cites it
13 citing papers in PubMed, 21 citations in OpenAlex.
- Molecular pathology of phyllodes tumours of the breast-much more than MED12.Histopathology · 2026Review
- X chromosome inactivation, X-linked disorders, and cancer.Frontiers in genetics · 2026Review
- Pancreatic cancer immunotherapy biomarkers: from traditional markers to multimodal integration and dynamic monitoring.Frontiers in immunology · 2026Review
- MED12 dysregulation: insights into cancer and therapeutic resistance.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- The MicroRNA miR-454 and the mediator complex component MED12 are regulators of the androgen receptor pathway in prostate cancer.Scientific reports · 2025Article
- The Cyclin-Dependent Kinase 8 Inhibitor E966-0530-45418 Attenuates Pulmonary FibrosisInternational journal of biological sciences · 2025Article
- A Pilot Study ofBalkan journal of medical genetics : BJMG · 2024Article
- Article
- Association of Fibroids, Endometriosis, and Gynecologic Surgeries with Breast Cancer Incidence and Hormone Receptor Subtypes.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2024Article
- Clinicopathological, immunohistochemical and molecular features of acinic cell carcinoma of the breast.Oncology letters · 2024Article
- PI3K/AKT/mTOR Dysregulation and Reprogramming Metabolic Pathways in Renal Cancer: Crosstalk with the VHL/HIF Axis.International journal of molecular sciences · 2023Review
- Emerging approaches to CDK inhibitor development, a structural perspective.RSC chemical biology · 2023Article
- High-accuracy prediction of colorectal cancer chemotherapy efficacy using machine learning applied to gene expression data.Frontiers in physiology · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mediator complex subunit 12 (MED12) is a subunit of Mediator, a large multi-subunit protein complex that acts an important regulator of transcription. Specifically, MED12 is an integral part of the kinase module of Mediator along with MED13, CyclinC (CycC) and CDK8. Structural studies have indicated that MED12 makes a direct connection to CycC through a specific interface and thereby functions to create a link between MED13 and CycC-CDK8. Disruption of the MED12-CycC interface often leads to dysregulated CDK8 kinase activity, which has important physiological implications. For example, a number of studies have indicated that mutations within MED12 can lead to the formation of benign or malignant tumors, either as a result of MED12-CycC disruption or through distinct independent mechanisms. Furthermore, recent studies have indicated that the N-terminal portion of MED12 forms a direct connection to CDK8. Mutations within MED12 do not appear to disrupt the physical connection to CDK8, but rather abrogate CDK8 kinase activity. Thus, mutations in MED12 can cause disruption of CDK8 kinase activity through two separate mechanisms. The aim of the present review article was to discuss the MED12 mutational landscape in a variety of benign and malignant tumors, as well as the mechanistic basis behind tumorigenesis. Furthermore, the link between MED12 and drug resistance has also been discussed, as well as potential cancer therapeutics related to MED12-altered tumors.
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Registered trials
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.