Evidence map›Paper›PMID 40804659›Full record

ArticleBMC gastroenterology2025

Evaluation of PINK1 protein expression as a predictive marker for the efficacy of adjuvant chemotherapy in colorectal cancer: a retrospective study.

Takatsugu Fujii, Masataka Hirasaki, Yasuo Kamakura, Tomonori Kawasaki, Satoshi Yamasaki, Yasuhiro Ishiyama, Chikashi Hiranuma, Tetsuya Hamaguchi, Yasumitsu Hirano, Shinichi Sakuramoto

Erratum issuedAbstract read
In one paragraph

Article in BMC gastroenterology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

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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

1 citing paper in PubMed.

  1. Effects of copper overload on mitochondrial parameters in GBM-1, U-87 MG, and C6 glioma cell lines.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors.

Takatsugu FujiiDepartment of Gastroenterological Surgery, Saitama Medical University International Medical Center, Saitama, Japan.
Masataka HirasakiDepartment of Clinical Cancer Genomics, Saitama Medical University International Medical Center, 1397-1 Yamane, Hidaka, 350-1298, Saitama, Japan. hirasaki@saitama-med.ac.jp.
Yasuo KamakuraDepartment of Clinical Cancer Genomics, Saitama Medical University International Medical Center, 1397-1 Yamane, Hidaka, 350-1298, Saitama, Japan.
Tomonori KawasakiDepartment of Pathology, Saitama Medical University International Medical Center, 1397-1 Yamane, Hidaka, 350-1298, Saitama, Japan.
Satoshi YamasakiDepartment of Clinical Cancer Genomics, Saitama Medical University International Medical Center, 1397-1 Yamane, Hidaka, 350-1298, Saitama, Japan.
Yasuhiro IshiyamaDepartment of Gastroenterological Surgery, Saitama Medical University International Medical Center, Saitama, Japan.
Chikashi HiranumaDepartment of Gastroenterological Surgery, Saitama Medical University International Medical Center, Saitama, Japan.
Tetsuya HamaguchiDepartment of Clinical Cancer Genomics, Saitama Medical University International Medical Center, 1397-1 Yamane, Hidaka, 350-1298, Saitama, Japan.
Yasumitsu HiranoDepartment of Gastroenterological Surgery, Saitama Medical University International Medical Center, Saitama, Japan.
Shinichi SakuramotoDepartment of Gastroenterological Surgery, Saitama Medical University International Medical Center, Saitama, Japan.

Funding

Hidaka Research Project 4-D-1-13
6 · The paper itself

Abstract

backgroundPTEN-induced kinase 1 (PINK1) is involved in mitochondrial quality control via mitophagy, and recent studies have reported that its overexpression is associated with chemoresistance and poor prognosis in multiple malignant tumors. However, the clinical significance of PINK1 expression in colorectal cancer remains unclear. In this study, we investigated the association among PINK1 protein expression, clinicopathological factors, and prognosis in patients with colorectal cancer who underwent adjuvant chemotherapy after curative surgery.

methodsWe retrospectively analyzed 83 patients with colorectal cancer who underwent curative surgery and fluoropyrimidine-based adjuvant chemotherapy in 2016. Expression of PINK1 and autophagy-related protein LC3 was evaluated by immunohistochemical staining, and the percentage of positive cells and staining intensity were scored. The association between PINK1 expression and the prognosis of 25 patients with confirmed recurrence was analyzed in detail. Survival analysis was performed using the Kaplan-Meier method and Cox proportional hazards models. Furthermore, in 11 cases with RNA sequencing analysis available among the recurrent cases, gene expression profiles were compared based on PINK1 expression levels, and biological characteristics were evaluated.

resultsPINK1 high expression was observed in 42.2% of the cases. No significant association was found between PINK1 and LC3 expression and overall survival (OS) or recurrence-free survival (RFS). However, in the recurrence group (n = 25), PINK1 high expression was significantly associated with a shorter OS (p = 0.024). In multivariate analysis, histological differentiation grade and high PINK1 expression were identified as independent prognostic factors (PINK1: hazard ratio 5.345, 95% confidence interval, 1.343-21.276; p = 0.017). RNA sequencing revealed increased expression of genes associated with autophagy and amino acid transport in the high PINK1 expression group.

conclusionsHigh PINK1 expression is associated with poor prognosis in colorectal cancer recurrence and may be involved in the promotion of chemotherapy resistance and cellular stress tolerance. PINK1 is a promising biomarker as a prognostic predictor and a new therapeutic target for adjuvant chemotherapy after surgery.

Indexed as

Biomarkers, TumorColorectal NeoplasmsProtein KinasesAdultAgedChemotherapy, AdjuvantFemaleHumansMaleMicrotubule-Associated ProteinsMiddle AgedNeoplasm Recurrence, LocalPrognosisPTEN-Induced Putative KinaseRetrospective StudiesBiomarkers, TumorMAP1LC3A protein, humanMicrotubule-Associated ProteinsProtein KinasesPTEN-Induced Putative KinaseAdjuvant chemotherapyAutophagyChemoresistanceColorectal cancerLC3PINK1Single nucleotide polymorphism

Identifiers

PMID40804659
PMCPMC12351948

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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.