Evidence map›Paper›PMID 38993645›Full record

ReviewFrontiers in oncology2024

Our current understanding of the biological impact of endometrial cancer mtDNA genome mutations and their potential use as a biomarker.

Pabitra Khadka, Carolyn K J Young, Ravi Sachidanandam, Laurent Brard, Matthew J Young

Abstract readReview
In one paragraph

Review in Frontiers in oncology, 2024. 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. Review
  2. Review
  3. Review
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

5 authors.

Pabitra Khadka *Department of Biomedical Sciences, Division of Biochemistry & Molecular Biology, Southern Illinois University School of Medicine, Carbondale, IL, United States.
Carolyn K J YoungDepartment of Biomedical Sciences, Division of Biochemistry & Molecular Biology, Southern Illinois University School of Medicine, Carbondale, IL, United States.
Ravi SachidanandamGirihlet Inc, Oakland, CA, United States.
Laurent BrardObstetrics & Gynecology, Southern Illinois University School of Medicine, Springfield, IL, United States.
Matthew J Young *Department of Biomedical Sciences, Division of Biochemistry & Molecular Biology, Southern Illinois University School of Medicine, Carbondale, IL, United States.

Funding

Defining the cellular and molecular mechanisms of how toxicants disrupt mitochondrial DNA homeostasisR15ES033394 · NIEHS · SOUTHERN ILLINOIS UNIVERSITY CARBONDALE · PI YOUNG, MATTHEW J · 2021 to 2021
$463k
NIEHS NIH HHS R15 ES033394
6 · The paper itself

Abstract

Endometrial cancer (EC) is a devastating and common disease affecting women's health. The NCI Surveillance, Epidemiology, and End Results Program predicted that there would be >66,000 new cases in the United States and >13,000 deaths from EC in 2023, and EC is the sixth most common cancer among women worldwide. Regulation of mitochondrial metabolism plays a role in tumorigenesis. In proliferating cancer cells, mitochondria provide the necessary building blocks for biosynthesis of amino acids, lipids, nucleotides, and glucose. One mechanism causing altered mitochondrial activity is mitochondrial DNA (mtDNA) mutation. The polyploid human mtDNA genome is a circular double-stranded molecule essential to vertebrate life that harbors genes critical for oxidative phosphorylation plus mitochondrial-derived peptide genes. Cancer cells display aerobic glycolysis, known as the Warburg effect, which arises from the needs of fast-dividing cells and is characterized by increased glucose uptake and conversion of glucose to lactate. Solid tumors often contain at least one mtDNA substitution. Furthermore, it is common for cancer cells to harbor mixtures of wild-type and mutant mtDNA genotypes, known as heteroplasmy. Considering the increase in cancer cell energy demand, the presence of functionally relevant carcinogenesis-inducing or environment-adapting mtDNA mutations in cancer seems plausible. We review 279 EC tumor-specific mtDNA single nucleotide variants from 111 individuals from different studies. Many transition mutations indicative of error-prone DNA polymerase γ replication and C to U deamination events were present. We examine the spectrum of mutations and their heteroplasmy and discuss the potential biological impact of recurrent, non-synonymous, insertion, and deletion mutations. Lastly, we explore current EC treatments, exploiting cancer cell mitochondria for therapy and the prospect of using mtDNA variants as an EC biomarker.

Indexed as

cancer biomarkerDNA polymerase gammaendometrial cancer (EC)endometrial cancer treatmentheteroplasmyhomoplasmymetabolismmitochondrial DNA (mtDNA)

Identifiers

PMID38993645
PMCPMC11236604

What Socratic holds

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LicenceCC BY
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 Socratic graph.