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Precision Oncology

Precision Oncology is an international, peer-reviewed, open access journal in the field of precision oncology, published quarterly online by MDPI.
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  • Rapid Publication: first decisions in 18 days; acceptance to publication in 7 days (median values for MDPI journals in the first half of 2026).
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All Articles (13)

  • Review
  • Open Access

Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal solid malignancies, characterised by rising incidence, poor long-term survival, and profound resistance to systemic therapy. Its poor prognosis reflects late diagnosis, early metastatic spread, and a uniquely desmoplastic, immunosuppressive tumour microenvironment that limits both drug delivery and effective antitumour immunity. Although cytotoxic chemotherapy remains the therapeutic backbone, its clinical benefit is modest. In parallel, molecular profiling has revealed a limited but expanding set of actionable vulnerabilities; however, immuno-oncology has not yet replicated in PDAC the transformative impact observed in other tumour types. This review examines the evolving immuno-oncology landscape in PDAC, focusing on four principal domains: immune checkpoint blockade in MSI-H/dMMR disease, tumour microenvironment-directed therapies, adoptive cellular therapies, and therapeutic cancer vaccines. Taken together, available evidence suggests that progress in PDAC immuno-oncology will depend on biomarker-guided patient selection, earlier disease settings, minimal residual disease-directed approaches, and rational combinations that address immune exclusion, stromal and myeloid barriers, impaired T-cell priming, and adaptive resistance. While durable clinical benefit remains limited and most strategies remain in early-phase evaluation, emerging data from molecularly selected cohorts, adoptive cellular therapies, and personalised or shared-antigen vaccines provide a compelling rationale for continued refinement of immune-based approaches in PDAC.

Precis. Oncol.

28 September 2026

Immuno-oncology targets within the PDAC tumour microenvironment. Schematic overview of key cellular and molecular interactions contributing to immune exclusion and immune suppression in PDAC, including tolerogenic dendritic cells, regulatory T cells, suppressive myeloid populations, tumour-associated macrophages, cancer-associated fibroblasts, endothelial cells, NK cells and CD8+ T cells. Annotated therapeutic strategies correspond to approaches discussed in this review. Therapeutic vaccines aim to enhance antigen presentation and T-cell priming; CD40, STING and TLR agonists target antigen-presenting cells and innate immune activation; immune checkpoint inhibitors target inhibitory PD-1/PD-L1 and CTLA-4 signalling; TIL/TCR-T-cell therapies and CAR-T/CAR-NK therapies supply or redirect tumour-reactive effector cells; PEGPH20 and certepetide/CEND-1 target stromal barriers and tumour penetration; CCR2, CCR2/CCR5 and CXCR4 blockade target suppressive myeloid recruitment and chemokine-mediated immune exclusion; and FAK and TGF-β pathway inhibition aim to remodel stromal and immune-suppressive signalling. Abbreviations: Arg-1: arginase-1; CAF: cancer-associated fibroblast; CAR: chimeric antigen receptor; CEA: carcinoembryonic antigen; CSF2: colony-stimulating factor 2; CSF3: colony-stimulating factor 3; CTLA-4: cytotoxic T lymphocyte-associated protein-4; CXCL12: C-X-C motif chemokine 12; DC: dendritic cell; FAK: focal adhesion kinase; FGF2: fibroblast growth factor; IL-1β: interleukin-1β; IL-4: interleukin-4; IL-6: interleukin-6; IL-8: interleukin-8; IL-10: interleukin-10; IL-27: interleukin-27; IL-35: interleukin-35; IDO: indoleamine 2,3-dioxygenase; iNOS: inducible nitric oxide synthase; LAG-3: lymphocyte-activation gene 3; MDSC: myeloid-derived suppressor cell; MMP: matrix metalloprotease; NK: natural killer; NO: nitric oxide; PD-1: programmed cell death protein-1; ROS: reactive oxygen species; TAA: tumour-associated antigen; TAM: tumour-associated macrophage; TCR-T: T-cell receptor-engineered T cell; TIL: tumour-infiltrating lymphocyte; TGFβ: transforming growth factor-β; TLR: Toll-like receptor; TNFα: tumour necrosis factor-α; TRAIL: TNF-related apoptosis-inducing ligand; Treg: regulatory T cell; VEGF: vascular endothelial growth factor. The graphic was created with BioRender.com.
  • Case Report
  • Open Access

Background/Objectives: Gestational choriocarcinoma is an uncommon neoplasia related to pregnancy. Signs and symptoms remain unspecific, while abnormal uterine bleeding is the main symptom. Methods: We report a case of a 40-year-old woman with gestational choriocarcinoma presenting as cervical ectopic pregnancy and a review of the literature. Results: After emergency evaluation, acute blood loss was controlled surgically. Diagnosis was set by histological examination of the uterus. Histological confirmation typically is difficult, due to high vascularization of the lesions. Conclusions: Diagnosis requires a high level of clinical suspicion, correlation with laboratory findings and specialized histopathological confirmation in cases which biopsy is offered. Treatment with chemotherapy is the main way of management, achieving treatment and fertility preservation. Surgical intervention is required for cases complicated by hemorrhage leading to hemodynamic instability.

Precis. Oncol.

17 September 2026

Transvaginal ultrasound of cervical lesion.
  • Review
  • Open Access

Immune checkpoint inhibitors (ICIs) have translated the scope of cancer therapy, but their immune-restorative mechanism can lead to immune-related adverse events (irAEs), which can affect several organs with varying severity. Early identification of patients at risk of irAEs is prudent to inform clinical decisions in precision oncology and remains a challenge as current clinical and biomarker methods still lack predictive accuracy. Artificial Intelligence (AI) presents a promising strategy for improving early detection, risk stratification as well as monitoring of irAEs. This narrative review summarizes the current AI modalities for detecting and predicting irAEs risk occurring with ICI therapy, including clinical Machine Learning models, radiomics-based approaches, natural language processing (NLP) systems and the integration of modalities with multimodal AI frameworks. Clinical Machine Learning models demonstrate moderate predictive performance whereas radiomics-derived modeling appears promising for pneumonitis. NLP and language models have achieved higher accuracy for retrospective irAEs detection. Multimodal AI applications offer theoretical potential through diverse data integration that captures the complex biology of irAEs; however, current evidence is limited. All these modalities face limitations of inadequate sample sizes, retrospective design, heterogeneous outcome definitions, class imbalance, and insufficient external validation. AI-based models have significant potential for personalized immunotherapy monitoring but require prospective multicenter validation, standardized datasets and clinically interpretable frameworks prior to implementation. Future advances in multimodal modeling can also enable precise prediction and early detection of irAEs, ultimately improving the safety and effectiveness of cancer immunotherapy.

Precis. Oncol.

27 July 2026

Overview of proposed multimodal AI predictive pipeline. The framework integrates diverse heterogenous data modalities ranging from structured to unstructured data, radiomics and biomarkers. The data streams are processed through modality-specific encoders and unified using feature-fusion network to generate clinically predictive outputs. Key elements required to enrich model learning as well as validation have been described. Despite significant potential for enhanced clinical decision support, current limitations, albeit resolvable, hinder applicability.
  • Review
  • Open Access

Modulating the Actin Cytoskeleton to Regulate Autophagy and Overcome Chemotherapy Resistance in Tumours

  • María Ruso-López,
  • Armando Jesús Pérez-Díaz and
  • Francisco Prieto-Ruiz

Macroautophagy is a key adaptive process that enables tumour cells to withstand the cytotoxic stress induced by standard antitumour treatments, thereby contributing to therapeutic resistance. In this context, identifying regulators capable of modulating autophagy is crucial for restoring sensitivity to these treatments. The actin cytoskeleton has emerged as a regulatory axis of autophagy, governing both its dynamics and its functional control. Drugs that target actin, and in particular actin-binding proteins (ABPs), can modulate the autophagy triggered by antitumour treatments and thereby sensitise cancer cells. This review summarises recent advances in ABP-targeted strategies for modulating autophagy across different tumour contexts and examines their potential in combination therapies.

Precis. Oncol.

26 June 2026

Overview of the autophagy process and points of regulation by the actin cytoskeleton. Autophagy is initiated by stress signals such as nutrient deprivation, hypoxia, reactive oxygen species (ROS) or chemotherapy, which inhibit mTORC1 and promote ULK1 activation. This leads to the recruitment of the PI3KC3-C1 complex to endoplasmic reticulum-associated omegasomes, triggering phagophore nucleation. Subsequent membrane expansion is driven by two ubiquitin-like conjugation systems (ATG12–ATG5–ATG16L1 and ATG8/LC3), resulting in autophagosome formation. The mature autophagosome then undergoes transport and fusion with lysosomes to form the autolysosome, where cargo degradation and recycling occur. The actin cytoskeleton and its associated actin-binding proteins (ABPs) regulate multiple stages of this process, including phagophore nucleation, membrane remodelling, vesicular trafficking and autophagosome–lysosome fusion.

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Precis. Oncol. - ISSN 3042-7614