Evidence map›Paper›PMID 39738117›Full record

ArticleScientific reports2024

D-loop mutations in mitochondrial DNA are a risk factor for chemotherapy resistance in esophageal cancer.

Takashi Harino, Koji Tanaka, Daisuke Motooka, Yasunori Masuike, Tsuyoshi Takahashi, Kotaro Yamashita, Takuro Saito, Kazuyoshi Yamamoto, Tomoki Makino, Yukinori Kurokawa and 3 more

Abstract read
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

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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

13 authors.

Takashi HarinoDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, 2-2-E2, Yamada-Oka, Suita, Osaka, 565-0871, Japan.
Koji TanakaDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, 2-2-E2, Yamada-Oka, Suita, Osaka, 565-0871, Japan. ktanaka@gesurg.med.osaka-u.ac.jp.
Daisuke MotookaGenome Information Research Center, Research Institute for Microbial Diseases, Osaka University, Suita, Japan.
Yasunori MasuikeDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, 2-2-E2, Yamada-Oka, Suita, Osaka, 565-0871, Japan.
Tsuyoshi TakahashiDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, 2-2-E2, Yamada-Oka, Suita, Osaka, 565-0871, Japan.
Kotaro YamashitaDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, 2-2-E2, Yamada-Oka, Suita, Osaka, 565-0871, Japan.
Takuro SaitoDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, 2-2-E2, Yamada-Oka, Suita, Osaka, 565-0871, Japan.
Kazuyoshi YamamotoDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, 2-2-E2, Yamada-Oka, Suita, Osaka, 565-0871, Japan.
Tomoki MakinoDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, 2-2-E2, Yamada-Oka, Suita, Osaka, 565-0871, Japan.
Yukinori KurokawaDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, 2-2-E2, Yamada-Oka, Suita, Osaka, 565-0871, Japan.
Kiyokazu NakajimaDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, 2-2-E2, Yamada-Oka, Suita, Osaka, 565-0871, Japan.
Hidetoshi EguchiDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, 2-2-E2, Yamada-Oka, Suita, Osaka, 565-0871, Japan.
Yuichiro DokiDepartment of Gastroenterological Surgery, Graduate School of Medicine, Osaka University, 2-2-E2, Yamada-Oka, Suita, Osaka, 565-0871, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Esophageal cancer is a highly aggressive disease, and acquired resistance to chemotherapy remains a significant hurdle in its treatment. mtDNA, crucial for cellular energy production, is prone to mutations at a higher rate than nuclear DNA. These mutations can accumulate and disrupt cellular function; however, mtDNA mutations induced by chemotherapy in esophageal cancer remain unexplored. We aimed to identify such mutations in esophageal cancer, pre- and post-chemotherapy, and explore the relationship between them and clinicopathological factors associated with chemotherapy resistance. We investigated mtDNA mutations in Human esophageal squamous cell carcinoma (ESCC) cancer cell lines (TE8 and TE11) and patient samples (27 pre- and post-chemotherapy, and 96 post-chemotherapy) using next-generation sequencing. Our analysis revealed a rise in mtDNA mutations following chemotherapy, particularly within the D-loop region. Moreover, mutations in a specific D-loop segment (hypervariable segment 1; HVS1) were associated with lower mtDNA copy number, poorer response to chemotherapy, and decreased five-year survival rates. These findings suggest that HVS1 mutations in mtDNA acquired after chemotherapy may contribute to treatment resistance and poorer clinical outcomes in patients with esophageal cancer. This study sheds light on the mechanisms of chemotherapy resistance and provides valuable insights for future research to overcome this challenge.

Indexed as

DNA, MitochondrialDrug Resistance, NeoplasmEsophageal NeoplasmsMutationAgedCell Line, TumorEsophageal Squamous Cell CarcinomaFemaleHumansMaleMiddle AgedRisk FactorsDNA, MitochondrialChemotherapyD-loopEsophageal cancerMitochondrial DNAMtDNA copy numberMutation

Identifiers

PMID39738117
PMCPMC11685473

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Registered trials

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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.