Evidence map›Paper›PMID 31506496›Full record

ArticleScientific reports2019

Aberrant Regulation of RAD51 Promotes Resistance of Neoadjuvant Endocrine Therapy in ER-positive Breast Cancer.

Yan Jia, Yueshuai Song, Guolei Dong, Chunfang Hao, Weipeng Zhao, Shufen Li, Zhongsheng Tong

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.5field-weighted citation impact, top 17% of its field
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

12 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. International journal of oncology · 2025
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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

7 authors at 2 institutions in 1 country.

Yan JiaDepartment of Breast Oncology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, and Key Laboratory of Cancer Prevention and Therapy, Huanhuxi Road, Tianjin, 300060, China. jiayantiantian@163.com.
Yueshuai SongDepartment of Otolaryngology Head-Neck Surgery, Beijing Friendship Hospital, Capital Medical University, Yong'an Road, Beijing, 100032, China.
Guolei DongDepartment of Breast Oncology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, and Key Laboratory of Cancer Prevention and Therapy, Huanhuxi Road, Tianjin, 300060, China.
Chunfang HaoDepartment of Breast Oncology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, and Key Laboratory of Cancer Prevention and Therapy, Huanhuxi Road, Tianjin, 300060, China.
Weipeng ZhaoDepartment of Breast Oncology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, and Key Laboratory of Cancer Prevention and Therapy, Huanhuxi Road, Tianjin, 300060, China.
Shufen LiDepartment of Breast Oncology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, and Key Laboratory of Cancer Prevention and Therapy, Huanhuxi Road, Tianjin, 300060, China.
Zhongsheng TongDepartment of Breast Oncology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, and Key Laboratory of Cancer Prevention and Therapy, Huanhuxi Road, Tianjin, 300060, China. tongzhongsheng@tjmuch.com.
Tianjin Medical University Cancer Institute and Hospital · CNCapital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Breast cancer is one of the most common malignant cancers affecting females. Estrogen receptor (ER)-positive breast cancer is responsive to endocrine therapy. Although current therapies offer favorable prospects for improving survival, the development of resistance remains a severe problem. In this study, we explored the resistance mechanisms of ER-positive breast cancer to neoadjuvant endocrine therapy. Microarray data of GSE87411 contained 109 pairs of samples from Z1031 trial, including untreated samples and post-treated samples with neoadjuvant aromatase inhibitor (AI) therapy. The differentially expressed genes (DEGs) were obtained from two different comparisons: untreated samples versus post-treated samples with AIs, and post-treated samples sensitive versus resistant to AIs. Multiple bioinformatic methods were applied to evaluate biological function, protein-protein network and potential binding between target protein and aromatase inhibitor. Then, regulation of gene expression, DNA methylation and clinicopathological factors of breast cancer were further analyzed with TCGA data. From GSE87411 dataset, 30 overlapped DEGs were identified. Cell division was found to be the main function of overlapped DEGs by functional enrichment and gene ontology (GO) analysis. RAD51 recombinase (RAD51), a key protein of homologous recombination, was detected to interact with BReast CAncer genes 2 (BRCA2). Moreover, according to the docking simulation, RAD51 might potentially bind to AIs. Overexpressed RAD51 was associated with hypermethylation of BRCA2, resistance to AIs and poor overall survival of patients with ER-positive breast cancer. Furthermore, RAD51 was found to be a better indicator than MKI67 for predicting resistance in neoadjuvant setting. The results indicated that methylation of BRCA2 led to incomplete suppression on RAD51, which caused an increased expression of RAD51, subsequently AI-resistance and poor prognosis in ER-positive breast cancer. RAD51 could be a new candidate used as a predicative marker and therapeutic target in neoadjuvant endocrine treatment.

Indexed as

Gene Expression Regulation, NeoplasticAntineoplastic Agents, HormonalAromatase InhibitorsBiomarkers, TumorBreast NeoplasmsDrug Resistance, NeoplasmFemaleGene Expression ProfilingHumansRad51 RecombinaseReceptors, EstrogenAntineoplastic Agents, HormonalAromatase InhibitorsBiomarkers, TumorRAD51 protein, humanRad51 RecombinaseReceptors, Estrogen

Identifiers

PMID31506496
PMCPMC6736845
OpenAlexW2972318155

What OpenQuestion 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 OpenQuestion graph.