Evidence map›Paper›PMID 39080255›Full record

ArticleCell death discovery2024

Myeloid PTEN loss affects the therapeutic response by promoting stress granule assembly and impairing phagocytosis by macrophages in breast cancer.

Yan Li, Chao Xu, Xiaojun Qian, Gang Wang, Chaoqiang Han, Hui Hua, Menghao Dong, Jian Chen, Haiyang Yu, Rutong Zhang and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Phase separation and the tumor microenvironment.Cell communication and signaling : CCS · 2026
    Review
  2. Review
  3. Article
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.

Yan Li *Department of Clinical Oncology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, 230001, China.
Chao Xu *Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, 230001, China.
Xiaojun QianDepartment of Clinical Oncology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, 230001, China.
Gang WangDivision of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, 230001, China.
Chaoqiang HanDivision of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, 230001, China.
Hui HuaDivision of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, 230001, China.
Menghao DongDivision of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, 230001, China.
Jian ChenDepartment of Clinical Oncology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, 230001, China.
Haiyang YuDivision of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, 230001, China.
Rutong ZhangDivision of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, 230001, China.ORCID http://orcid.org/0009-0003-2694-6654
Xiaoxi FengDivision of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, 230001, China.
Zhenye YangDivision of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, 230001, China. zhenye@ustc.edu.cn.ORCID http://orcid.org/0000-0001-7797-5891
Yueyin PanDepartment of Clinical Oncology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui, 230001, China. panyueyin@ustc.edu.cn.ORCID http://orcid.org/0000-0003-0532-5368

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82102905National Natural Science Foundation of China (National Science Foundation of China) 82172775
6 · The paper itself

Abstract

Breast cancer (BRCA) has become the most common type of cancer in women. Improving the therapeutic response remains a challenge. Phosphatase and tensin homologue deleted on chromosome 10 (PTEN) is a classic tumour suppressor with emerging new functions discovered in recent years, and myeloid PTEN loss has been reported to impair antitumour immunity. In this study, we revealed a novel mechanism by which myeloid PTEN potentially affects antitumour immunity in BRCA. We detected accelerated stress granule (SG) assembly under oxidative stress in PTEN-deficient bone marrow-derived macrophages (BMDMs) through the EGR1-promoted upregulation of TIAL1 transcription. PI3K/AKT/mTOR (PAM) pathway activation also promoted SG formation. ATP consumption during SG assembly in BMDMs impaired the phagocytic ability of 4T1 cells, potentially contributing to the disruption of antitumour immunity. In a BRCA neoadjuvant cohort, we observed a poorer response in myeloid PTEN

Identifiers

PMID39080255
PMCPMC11289284

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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.