ReviewMedical oncology (Northwood, London, England)2023
The evolving landscape of involvement of DTYMK enzymes in cancer.
Review in Medical oncology (Northwood, London, England), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
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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.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Unraveling lung cancer dynamics: a new metabolic signature improving the prediction of recurrence in resected lung adenocarcinoma.Journal of translational medicine · 2026Article
- Construction of a novel G2/M checkpoint-related gene signature for prognosis in hepatocellular carcinoma based on machine learning.Discover oncology · 2025Article
- Dualistic Role of MITF in Uveal Melanoma: Defining Two Distinct Cellular Subpopulations With Prognostic and Therapeutic Implications.Investigative ophthalmology & visual science · 2025Article
- The Effect of Circulating Proteins and Their Role in Mediating Adiposity's Effect on Endometrial Cancer Risk: Mendelian Randomization and Colocalization Analyses.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2025Article
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Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer cells require continuous synthesis of nucleotides for their uncontrolled proliferation. Deoxy thymidylate kinase (DTYMK) belongs to the thymidylate kinase family and is concerned with pyrimidine metabolism. DTYMK catalyzes the ATP-based conversion of deoxy-TMP to deoxy-TDP in both de novo and salvage pathways. Different studies demonstrated that DTYMK was increased in various types of cancers such as hepatocellular carcinoma, colon cancer, lung cancer, etc. Increased level of DTYMK was associated with poorer survival and prognosis, stage, grade and size of tumor, cell proliferation, colony formation, enhanced sensitivity to chemotherapy drugs, migration. Some studies were showed that knockdown of DTYMK reduced the signaling pathway of PI3K/AKT and downregulated expression of CART, MAPKAPK2, AKT1 and NRF1. Moreover, some microRNAs could suppress DTYMK expressions. On the other hand based on the TIMER database, the infiltration of macrophages, dendritic cells, neutrophils, B cells, CD4+ T cell and CD8+ T cell is affected by DTYMK. In the present review, we describe the genomic location, protein structure and isoforms of DTYMK and focus on its role in cancer development.
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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 Socratic graph.