Evidence map›Paper›PMID 42339120›Full record

ReviewFrontiers in oncology2026

Radiogenomics and the DNA damage response: opportunities for biomarker-guided radiosensitization in pancreatic cancer.

Marie Nour Karam, Joseph Hajj, Christopher H Crane, Paul Ramia, Fady Geara, Nadim Hamadeh, Jacob G Scott, Stephen Grobmyer, Rachael Almond, Eileen M O'Reilly and 1 more

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

11 authors.

Marie Nour KaramDepartment of Medicine, Indiana University School of Medicine, Indianapolis, IN, United States.
Joseph HajjHeart, Vascular, and Thoracic Institute, Cleveland Clinic Foundation, Cleveland, OH, United States.
Christopher H CraneDepartment of Radiation Oncology, Memorial Sloan Kettering Cancer Center, New York, NY, United States.
Paul RamiaDepartment of Radiation Oncology, Cleveland Clinic, Abu Dhabi, United Arab Emirates.
Fady GearaDepartment of Radiation Oncology, Cleveland Clinic, Abu Dhabi, United Arab Emirates.
Nadim HamadehFaculty of Medicine, American University of Beirut, Beirut, Lebanon.
Jacob G ScottDepartment of Radiation Oncology, Cleveland Clinic Foundation, Cleveland, OH, United States.
Stephen GrobmyerDepartment of Radiation Oncology, Cleveland Clinic, Abu Dhabi, United Arab Emirates.
Rachael AlmondM42, Abu Dhabi, United Arab Emirates.
Eileen M O'ReillyDepartment of Medical Oncology, Memorial Sloan Kettering Cancer Center, New York, NY, United States.
Carla HajjDepartment of Radiation Oncology, Cleveland Clinic, Abu Dhabi, United Arab Emirates.

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI SELWYN M VICKERS · 1985 to 2026
$347.4M
NCI NIH HHS P30 CA008748
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is associated with poor prognosis, despite significant research efforts. The use of radiotherapy (RT) in PDAC treatment is constrained by intrinsic PDAC radioresistance and concern for normal tissue toxicity. Radiogenomics, the study of how genetic variants may influence RT response, could be incorporated into PDAC treatment. This approach offers a framework for personalized RT dosing guided by individual genomic data. Additionally, DNA damage response (DDR) inhibitors may sensitize PDAC to ionizing radiation to increase the targeted effectiveness of RT. This review examines the history and progress of radiogenomics, spanning from genome-wide approaches to more recent algorithm-based indices such as the radiosensitivity index (RSI) and the genomic-adjusted radiation dose (GARD). These approaches are promising but require additional validation in PDAC due to inconsistent findings across studies and inadequate PDAC-specific data. We also evaluate clinical advances in the development of inhibitors targeting key DDR elements such as ATR, ATM, CHK1/2, WEE1, DNA-PKcs, and PARP. Finally, we highlight emerging strategies for targeting KRAS G12D in PDAC. Collectively, these approaches offer an avenue for reducing radioresistance in PDAC while improving treatment response and minimizing normal tissue toxicity. Future research directions should include the incorporation of multi-omics data into predictive models for appropriate treatment selection, additional large-scale, biomarker-driven clinical trials, and continued integration of biomarker-targeting drug therapy, radiotherapy, and immunotherapy into treatment regimens.

Indexed as

DNA damage responsegenomic-adjusted radiation dose (GARD)KRAS G12Dpancreatic ductal adenocarcinomaPARP inhibitorsradiogenomicsradiosensitization

Identifiers

PMID42339120
PMCPMC13283891

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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.