Evidence map›Paper›PMID 40564403›Full record

ArticleBioengineering (Basel, Switzerland)2025

Characterization of Parthanatos in Breast Cancer: Implications for Prognosis and PARP Inhibitor Resistance.

Junjie Tang, Qian Liu, Wei Du, Linxi Chen, Feiyang Qi, Ranxin Zhang, Bang H Hoang, David S Geller, Rui Yang, Jichuan Wang and 1 more

Abstract read
In one paragraph

Article in Bioengineering (Basel, Switzerland), 2025. 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. Review
  2. Article
  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

11 authors.

Junjie TangKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Familial & Hereditary Cancer Center, Peking University Cancer Hospital & Institute, Beijing 100142, China.ORCID 0009-0000-6103-6822
Qian LiuKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Familial & Hereditary Cancer Center, Peking University Cancer Hospital & Institute, Beijing 100142, China.
Wei DuBreast Center, Peking University People's Hospital, Beijing 100044, China.
Linxi ChenMusculoskleletal Tumor Center, Beijing Key Laboratory for Musculoskeletal Tumors, Peking University People's Hospital, Beijing 100041, China.
Feiyang QiMusculoskleletal Tumor Center, Beijing Key Laboratory for Musculoskeletal Tumors, Peking University People's Hospital, Beijing 100041, China.ORCID 0009-0001-7874-4312
Ranxin ZhangDepartment of Orthopedic Surgery, Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, NY 10467, USA.
Bang H HoangDepartment of Orthopedic Surgery, Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, NY 10467, USA.
David S GellerDepartment of Orthopedic Surgery, Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, NY 10467, USA.ORCID 0000-0002-4549-7124
Rui YangDepartment of Orthopedic Surgery, Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, NY 10467, USA.
Jichuan WangMusculoskleletal Tumor Center, Beijing Key Laboratory for Musculoskeletal Tumors, Peking University People's Hospital, Beijing 100041, China.ORCID 0009-0005-7194-0192
Li HuKey Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Familial & Hereditary Cancer Center, Peking University Cancer Hospital & Institute, Beijing 100142, China.

Funding

Leveraging Tumor Suppressor Inactivation for Osteosarcoma TherapyR01CA255643 · NCI · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI HOANG, BANG H · 2021 to 2024
$1.7M
Beijing Physician Scientist Training Project BJPSTP-2024-10Clinical Medicine Plus X - Young Scholars Project, Peking University, the Fundamental Research Funds for the Central Universities PKU2024LCXQ027National Natural Science Foundation of China 82303165, 82103223NCI NIH HHS R01 CA255643NIH HHS R01CA255643Peking University Clinical Scientist Training Program BMU2024PYJH026Peking University People's Hospital Scientific Research Development Funds RDX2022-01
6 · The paper itself

Abstract

Parthanatos, a novel form of programmed cell death mediated by PARP1 and driven by DNA damage, has not been comprehensively characterized in breast cancer (BC). Given the widespread clinical use of PARP1 inhibitors for treating BRCA-mutant breast cancers, understanding the role of parthanatos is crucial. In this study, we systematically analyzed the role and clinical significance of parthanatos in BC by integrating genomic, transcriptomic, and clinical data. Our analysis revealed significant differential expression of parthanatos-related genes between BC and normal breast tissues, with frequent copy number variations (CNVs) affecting gene expression. At the single-cell level, parthanatos-related genes were primarily expressed in breast cancer cells and macrophages, and genomic instability scores were positively correlated with parthanatos pathway scores. Unsupervised clustering identified two BC subtypes based on parthanatos-related gene expression: C1 (parthanatos-high) and C2 (parthanatos-low). C1 exhibited a poorer prognosis, reduced immune infiltration, and potential resistance to PARP inhibitors compared to C2. This study represents the first comprehensive investigation of parthanatos in BC, offering insights into its role in tumor progression and highlighting its potential link to PARP inhibitor resistance and poor clinical outcomes.

Indexed as

breast cancerparthanatossingle-cell sequencingsubtypestumor immune microenvironment

Identifiers

PMID40564403
PMCPMC12189614

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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.