Evidence map›Paper›PMID 40569526›Full record

ArticleApoptosis : an international journal on programmed cell death2025

DNA damage repair inhibitors boost targeted radionuclide therapy and immunotherapy of prostate cancer.

Bin Xu, Lei Tao, Juan Sun, Jiangtao Yang, Fenghua Meng, Zhiyuan Zhong

Abstract read
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In one paragraph

Article in Apoptosis : an international journal on programmed cell death, 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. 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

6 authors.

Bin Xu *Biomedical Polymers Laboratory, College of Chemistry, Chemical Engineering and Materials Science, State Key Laboratory of Radiation Medicine and Protection, Soochow University, Suzhou, 215123, PR China.
Lei Tao *Biomedical Polymers Laboratory, College of Chemistry, Chemical Engineering and Materials Science, State Key Laboratory of Radiation Medicine and Protection, Soochow University, Suzhou, 215123, PR China.
Juan SunBiomedical Polymers Laboratory, College of Chemistry, Chemical Engineering and Materials Science, State Key Laboratory of Radiation Medicine and Protection, Soochow University, Suzhou, 215123, PR China.
Jiangtao YangBiomedical Polymers Laboratory, College of Chemistry, Chemical Engineering and Materials Science, State Key Laboratory of Radiation Medicine and Protection, Soochow University, Suzhou, 215123, PR China.
Fenghua MengBiomedical Polymers Laboratory, College of Chemistry, Chemical Engineering and Materials Science, State Key Laboratory of Radiation Medicine and Protection, Soochow University, Suzhou, 215123, PR China. fhmeng@suda.edu.cn.
Zhiyuan ZhongBiomedical Polymers Laboratory, College of Chemistry, Chemical Engineering and Materials Science, State Key Laboratory of Radiation Medicine and Protection, Soochow University, Suzhou, 215123, PR China. zyzhong@suda.edu.cn.

Funding

National Natural Science Foundation of China 52233007
6 · The paper itself

Abstract

Targeted radionuclide therapy (TRT) has emerged as a valuable treatment for metastatic castration-resistant prostate cancer (mCRPC) patients. The radioresistance coupled with heterogeneity and immunosuppressive tumor microenvironment of mCRPC, however, greatly restricts the clinical response and anticancer immunity. Here, we found that DNA damage repair inhibitors, in particular ATM inhibitor (ATMi), effectively boost TRT and immunotherapy of prostate cancer. ATMi significantly amplified TRT-induced DNA damage and immunogenic cell death in tumor cells, by impairing double-strand break repair and arresting cell cycle progression, which reshaped the tumor microenvironment and markedly improved tumor inhibition and survival rate in murine RM-1-hPSMA tumor model. Intriguingly, addition of αCTLA-4 antibody further resulted in 71% mice complete regression. TRT in combination with ATMi and αCTLA-4 appeared to boost adaptive and long-lasting anticancer immunity. Our results signify that ATM inhibitor not only sensitizes targeted radionuclide therapy but also effectively augments immune checkpoint inhibitor therapy.

Indexed as

DNA RepairImmunotherapyProstatic NeoplasmsProstatic Neoplasms, Castration-ResistantAnimalsAtaxia Telangiectasia Mutated ProteinsCell Line, TumorDNA DamageHumansImmune Checkpoint InhibitorsMaleMiceTumor MicroenvironmentAtaxia Telangiectasia Mutated ProteinsImmune Checkpoint InhibitorsDNA damage repair inhibitorsImmune checkpoint inhibitorsProstate cancerRadioresistanceTargeted radionuclide therapy

Identifiers

PMID40569526

What OpenQuestion holds

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Registered trials

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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.