Evidence map›Paper›PMID 40507948›Full record

ReviewInternational journal of molecular sciences2025

Clinical Significance of NUDT1 (MTH1) Across Cancer Types.

Radosław Misiak, Karol Białkowski, Ewelina Dondajewska

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
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

3 authors.

Radosław MisiakDepartment of Medical Biotechnology, Poznan University of Medical Sciences (PUMS), 61-701 Poznan, Poland.
Karol BiałkowskiDepartment of Clinical Biochemistry, Ludwik Rydygier Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University in Toruń, 87-100 Bydgoszcz, Poland.ORCID 0000-0002-3836-8076
Ewelina DondajewskaDepartment of Medical Biotechnology, Poznan University of Medical Sciences (PUMS), 61-701 Poznan, Poland.ORCID 0000-0001-9078-2015

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MTH1 (MutT Homolog 1) protein is one of the enzymes that protect cells from mutagenetic actions of reactive oxygen species. It sanitizes the pool of free nucleotides, making sure that oxidized dNTPs are not incorporated into the DNA. Any misfunction of it would lead to mutations. As such, it has attracted interest of cancer researchers, and multiple studies have been conducted over the years to determine its role in tumor cells. It has been found that MTH1 is not downregulated in most tumor tissues but, to the contrary, often overexpressed. This suggests that MTH1 is used by cancer as an adaptation to increased oxidative stress caused by metabolic reprogramming to support excessive proliferation. Based on this premise, many recent studies have evaluated MTH1 as either prognostic factor, general biomarker or therapeutic target in cancer. Here, we summarize all available research on MTH1 mRNA, protein and its enzymatic activity in clinical samples across various cancer types, identifying a subset of cancers where MTH1 plays an important role. This is particularly evident in cancers characterized by high metabolic activity and oxygen-rich environments, such as hepatocellular carcinoma, renal cell carcinoma, or non-small cell lung adenocarcinoma.

Indexed as

DNA Repair EnzymesNeoplasmsPhosphoric Monoester HydrolasesAnimalsBiomarkers, TumorClinical RelevanceGene Expression Regulation, NeoplasticHumansOxidative StressPrognosisReactive Oxygen Species8-oxodGTPaseBiomarkers, TumorDNA Repair EnzymesPhosphoric Monoester HydrolasesReactive Oxygen SpeciescancerMTH1NUDT1oxidative stressprognostic factorROS response

Identifiers

PMID40507948
PMCPMC12154510

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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.