Evidence map›Paper›PMID 40095310›Full record

ArticleAnnals of surgical oncology2025

DNA Polymerase Delta 2 Activates Cell Cycle in Lung Adenocarcinoma, Leading to High Malignancy and Poor Prognosis.

Asato Hashinokuchi, Fumihiko Kinoshita, Makoto Iimori, Keisuke Kosai, Yuya Ono, Takumi Tomonaga, Bassi Giacomo, Kyoto Matsudo, Taichi Nagano, Takaki Akamine and 4 more

Abstract read
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Article in Annals of surgical oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Comprehensive analysis ofJournal of thoracic disease · 2026
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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

14 authors.

Asato HashinokuchiDepartment of Surgery and Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Fumihiko KinoshitaDepartment of Surgery and Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Makoto IimoriOral Medicine Research Center, Fukuoka Dental College, Fukuoka, Japan.
Keisuke KosaiDepartment of Thoracic Oncology, National Hospital Organization Kyushu Cancer Center, Fukuoka, Japan.
Yuya OnoDepartment of Surgery, Kyushu University Beppu Hospital, Beppu, Oita, Japan.
Takumi TomonagaDepartment of Anatomic Pathology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Bassi GiacomoDepartment of Surgery and Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Kyoto MatsudoDepartment of Surgery and Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Taichi NaganoDepartment of Surgery and Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Takaki AkamineDepartment of Surgery and Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Mikihiro KohnoDepartment of Surgery and Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Tomoyoshi TakenakaDepartment of Surgery and Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. takenaka.tomoyoshi.473@m.kyushu-u.ac.jp.
Yoshinao OdaDepartment of Anatomic Pathology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Tomoharu YoshizumiDepartment of Surgery and Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDNA polymerase delta 2 (POLD2) plays a crucial role in DNA repair and replication. POLD2 is upregulated and related to poor prognosis in several types of cancer. However, the biological and clinical importance of POLD2 in lung adenocarcinoma remains unclear. PATIENTS AND

methodsWe investigated the relationship between POLD2 expression and tumor malignancy in lung adenocarcinoma cell lines. Immunohistochemistry (IHC) was performed on 373 patients with completely resected lung adenocarcinoma, and the association between POLD2 expression, clinicopathological features, and prognosis was examined.

resultsPOLD2 knockdown decreases cell proliferation and migration, resulting in apoptosis and G1 arrest in the cell cycle in lung adenocarcinoma cells. Additionally, POLD2 knockdown attenuates MYC expression, which may decrease the expression of cyclin-dependent kinases 4 and 6, pRb, Rb, and E2F1. Furthermore, among 373 patients with completely resected lung adenocarcinoma, smoking history, advanced pathological stage, and vascular invasion were significantly more prevalent in patients with high POLD2 expression (n = 146, 39.3%) than in those with low POLD2 expression (n = 227, 60.7%). Patients with high POLD2 expression also had a significantly worse recurrence-free survival (RFS) and overall survival. In the multivariable analysis, high POLD2 expression was an independent poor prognostic factor of RFS.

conclusionsWe provide the possibility of POLD2 as a potential new therapeutic target because high POLD2 expression is associated with high malignancy and poor prognosis in specimens from patients with lung adenocarcinoma and POLD2 depletion triggers the suppression of cell migration, cell cycle progression, and cell proliferation.

Indexed as

AdenocarcinomaBiomarkers, TumorCell CycleDNA Polymerase IIILung NeoplasmsAdenocarcinoma of LungAgedApoptosisCell MovementCell ProliferationFemaleFollow-Up StudiesHumansMaleMiddle AgedPrognosisBiomarkers, TumorDNA Polymerase IIIApoptosisCell cycleDNA polymerase delta 2 (POLD2)Lung adenocarcinomaMYC

Identifiers

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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 Socratic graph.