DNA damage response inhibitors in pancreatic cancer: progress and challenges.

Yeyao Wu, Wei Li, Mengyun Wu

Abstract readReview

In one paragraph

Review in Frontiers in oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it

0cells of the map it votes in

0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

3 authors.

Yeyao WuRadiology Laboratory, Department of Occupational Health and Radiological Health, Chongqing Center for Disease Control and Prevention, Chongqing, China.

Wei LiRadiology Laboratory, Department of Occupational Health and Radiological Health, Chongqing Center for Disease Control and Prevention, Chongqing, China.

Mengyun WuRadiology Laboratory, Department of Occupational Health and Radiological Health, Chongqing Center for Disease Control and Prevention, Chongqing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic cancer is one of the most lethal malignancies, with very limited treatment options beyond standard chemotherapy. The discovery of homologous recombination repair (HRR) deficiencies-such as BRCA1/2 and PALB2 mutations-has revealed a targetable vulnerability through the DNA damage response (DDR) pathway. This review systematically summarizes the application and current clinical landscape of DDR-targeted therapies in pancreatic cancer. We first discuss how DDR inhibitors have successfully translated from research into clinical practice as a targeted treatment option for pancreatic cancer patients. However, single-agent DDR inhibitors face major limitations, including a narrow beneficiary population, primary and acquired resistance, and dose-limiting toxicities. The central theme of this review is the paradigm shift from monotherapy to rational combination strategies. We therefore focus on emerging combination approaches, such as the PAD/PAD

Indexed as

ATR inhibitorscombination therapyDDR inhibitorsDNA damage response (DDR)homologous recombination deficiency (HRD)pancreatic cancerpancreatic ductal adenocarcinomaPARP inhibitors

Identifiers

PMID42376674

DOI10.3389/fonc.2026.1838580

PMCPMC13310779

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.