ReviewClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2026
Genotoxicity of cancer therapies and the risk of secondary malignancies: toward personalized prevention.
Review in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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.
Who cites it
1 citing paper in PubMed.
- PEGylated PLGA Nanoformulations For Effective Immunomodulatory Actors In Non-Small Cell Lung Cancer.International journal of nanomedicine · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The evolution of cancer therapies has dramatically improved patient survival but has also revealed a critical challenge: the long-term genotoxic effects that can lead to secondary primary malignancies (SPMs). This review synthesizes current knowledge on how diverse treatment modalities, including chemotherapy, radiotherapy, targeted agents, and immunotherapies, induce DNA damage in normal tissues. It details the distinct mechanisms of genotoxicity, from the direct DNA lesions caused by cytotoxic drugs and ionizing radiation to the indirect damage mediated by oxidative stress and inflammation from newer therapies. The article identifies a range of multifactorial risk factors for SPMs, encompassing patient-specific variables such as age, genetic predisposition, and lifestyle, as well as therapy-related factors such as dose, duration, and combination regimens. It then evaluates the progression of monitoring methods, from traditional cytogenetic assays to advanced molecular and multi-omics biomarkers, highlighting their potential to predict individual susceptibility and inform risk stratification. By exploring pharmacogenomics and its role in genotype-guided dosing, the review proposes a framework for personalized prevention strategies. These strategies include risk-adapted regimens, prophylactic interventions, and the use of AI-driven predictive models. Ultimately, this comprehensive analysis underscores the urgent need to advance personalized prevention in oncology to balance therapeutic efficacy with long-term genomic safety for cancer survivors.
Indexed as
Identifiers
41637000What OpenQuestion holds
Registered trials
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.