ReviewMedical oncology (Northwood, London, England)2025
Regulatory roles of MKP7/DUSP16 in cancer.
Review in Medical oncology (Northwood, London, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Article
- DUSP family phosphatases in cell signaling, inflammation, and chronic diseases.Journal of biomedical science · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Mitogen-activated protein kinase phosphatases (MKPs), also known as dual-specificity phosphatases (DUSPs), are key regulatory factors within the mitogen-activated protein kinase (MAPK) pathway. MKP7/DUSP16, a member of the MKP family, has been identified in vitro as a phosphatase with specificity for p38 mitogen-activated protein kinase (p38) and c-jun amino-terminal kinase (JNK), with a stronger inhibitory effect on JNK compared to other MAPKs. In recent years, MKP7/DUSP16 has recently attracted increasing interest, with accumulating evidence suggesting its dysfunction is correlated with the progression and drug resistance of various cancers, making it a potential prognostic biomarker. However, research into the specific mechanisms by which MKP7/DUSP16 regulates cancer cells remains limited. Current studies suggest that MKP7/DUSP16 may promote cancer progression through the regulation of the MAPK pathway, mitochondrial apoptosis pathways, and the induction of cancer cell proliferation by immune cells. This review summarizes the mechanisms by which MKP7/DUSP16 may promote tumor proliferation. Further studies are needed to clarify its specific regulatory roles in cancer.
Indexed as
Identifiers
41320681What OpenQuestion holds
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.