Evidence map›Paper›PMID 39950924›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025

LINC01235 Promotes Clonal Evolution through DNA Replication Licensing-Induced Chromosomal Instability in Breast Cancer.

Qi Zhang, Xuliren Wang, Zhibo Shao, Yi Zhang, Liyi Zhang, Ming Chen, Xujie Zhou, Han Zhu, Yue Zhou, Xinya Lu and 9 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Article
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  4. Review
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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

19 authors.

Qi ZhangDepartment of Breast Surgery, Key Laboratory of Breast Cancer in Shanghai, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Xuliren WangDepartment of Breast Surgery, Key Laboratory of Breast Cancer in Shanghai, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Zhibo ShaoDepartment of Breast Surgery, Key Laboratory of Breast Cancer in Shanghai, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Yi ZhangDepartment of Breast Surgery, Key Laboratory of Breast Cancer in Shanghai, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Liyi ZhangDepartment of Breast Surgery, Key Laboratory of Breast Cancer in Shanghai, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Ming ChenDepartment of Breast Surgery, Key Laboratory of Breast Cancer in Shanghai, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Xujie ZhouDepartment of Breast Surgery, Key Laboratory of Breast Cancer in Shanghai, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Han ZhuDepartment of Breast Surgery, Key Laboratory of Breast Cancer in Shanghai, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Yue ZhouDepartment of Breast Surgery, Key Laboratory of Breast Cancer in Shanghai, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Xinya LuDepartment of Breast Surgery, Key Laboratory of Breast Cancer in Shanghai, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Pei LiDepartment of Breast Surgery, Key Laboratory of Breast Cancer in Shanghai, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Weiru ChiDepartment of Breast Surgery, Key Laboratory of Breast Cancer in Shanghai, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Lun LiDepartment of Breast Surgery, Key Laboratory of Breast Cancer in Shanghai, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Zhi-Ming ShaoDepartment of Breast Surgery, Key Laboratory of Breast Cancer in Shanghai, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Shenglin HuangFudan University Shanghai Cancer Center, Key Laboratory of Medical Epigenetics and Metabolism, Institutes of Biomedical Sciences, Fudan University, Shanghai, 200032, China.
Jingyan XueDepartment of Breast Surgery, Key Laboratory of Breast Cancer in Shanghai, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Yayun ChiDepartment of Breast Surgery, Key Laboratory of Breast Cancer in Shanghai, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Jiong WuDepartment of Breast Surgery, Key Laboratory of Breast Cancer in Shanghai, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Bingqiu XiuDepartment of Breast Surgery, Key Laboratory of Breast Cancer in Shanghai, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.ORCID https://orcid.org/0000-0002-0771-591X

Funding

National Natural Science Foundation of China 82002795National Natural Science Foundation of China 82072919National Natural Science Foundation of China 82173274National Natural Science Foundation of China 82373357
6 · The paper itself

Abstract

Despite the development of HER2-targeting drugs such as trastuzumab and T-DXd, treatment resistance is a substantial challenge, often leading to relapse and distant metastasis. Tumor heterogeneity in HER2-positive breast cancer drives the evolution of resistant clones following therapeutic stress. However, the targetable drivers of anti-HER2 treatment resistance are not thoroughly identified. This study aims to use neoadjuvant-targeted therapy cohorts and a patient-derived organoid in vitro treatment model to uncover the potential targetable drivers of anti-HER2 treatment resistance. it is found that LINC01235 significantly enhances DNA replication licensing and chromosomal instability, fostering clonal expansion and evolution, and ultimately increasing resistance to therapeutic interventions. LINC01235 regulates global H3K27ac, H3K9ac, and H3K36me3 modifications, promotes H2A.Z expression in regulatory regions, and increases the accessibility of DNA licensing factors to their promoter regions. XRCC5 is identified as a key component for maintaining genomic stability, crucial for LINC01235's role in replication licensing. Furthermore, therapeutic strategies targeting LINC01235, including the use of antisense oligonucleotides or ATR inhibitors, which showed promise in overcoming treatment resistance are explored. These findings underscore the pivotal role of LINC01235 in driving resistance mechanisms and highlight novel avenues for targeted therapies to improve the outcomes of patients with HER2-positive breast cancer.

Indexed as

Breast NeoplasmsChromosomal InstabilityClonal EvolutionDNA ReplicationRNA, Long NoncodingCell Line, TumorDrug Resistance, NeoplasmFemaleHumansRNA, Long NoncodingATR inhibitorschromosomal instabilitiesDNA replication licensingHER2‐positive breast cancersLINC01235

Identifiers

PMID39950924
PMCPMC11984920

What Socratic holds

Textmetadata
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.