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PubMed2026

Technical note: reconstructing dose distributions from manually planned electron boosts in breast radiotherapy.

PURPOSE: In breast radiotherapy, delivery of manually-calculated electron boosts limits retrospective dose-response analyses as dose distribution is unavailable. This work evaluates the feasibility of reconstructing dose distributions from manually planned electron boosts in breast-conserving radiotherapy. METHODS: Only 72 out of 198 breast cancer patients had complete stored dose distributions from sequential electron boosts in the REQUITE study. Arbitrary data from 70/72 patients were used to develop and validate dose reconstruction method. Twenty patients were used to determine optimal parameters for Monte-Carlo-based (MC) electron dose reconstruction on RayStation (v.11B-R), considering CT-calibration curve, MC-history number, andcalculation grid resolution. Remaining 50 patients were used to quantify dose reconstruction accuracy. The similarity between reconstructed and stored dose was evaluated using 3D-gamma index and dosimetric parameters extracted from breast and tumour bed contours. Dose difference location was evaluated using dose-location histogram. RESULTS: Calculation grid resolution significantly impacted electron dose distribution (p < 0.01), where the finest grid (0.15 cm) showed highest similarity to stored doses. CT-calibration curve and MC-history number had a negligible influence on dose reconstruction. Dosimetric difference between reconstructed and stored doses was < 1 Gy for breast and tumour bed. Reconstructed dose was achieved > 90% gamma passing rate in the validation set. However, around 2.5 Gy dose differences were observed at the skin and tissue interface regions. CONCLUSIONS: Retrospective electron boost dose reconstruction is feasible with acceptable accuracy, and could increase data completeness in large cohort studies. Caution is advised when assessing dose near tissue interface and further validation is needed outside the REQUITE dataset.

Electrons↗

PubMed2026

Association of Therapeutic Mammoplasty and Radiotherapy Side-effects.

INTRODUCTION: Patients with larger breast size and volume are at increased risk of side-effects (toxicity) from radiotherapy. Therapeutic mammoplasty (TM) extends breast-conserving surgery by combining wide local excision of the cancer with breast reduction and mastopexy techniques. The aim of this study was to determine the effect of TM using level 2 oncoplastic techniques on the incidence of early and long-term radiotherapy side-effects. PATIENTS AND METHODS: Breast cancer patients recruited prospectively into the multicenter REQUITE cohort study (www.requite.eu) at a single institution (n = 346) were included. Radiotherapy side-effects (CTCAE v4.0) were scored at baseline, following radiotherapy, and at 2-year follow-up. The association of TM and specimen resection weight were investigated in multivariable regression models. RESULTS: At 2 years, 20.1 % of patients had grade ≥ 2 atrophy, 23.2% grade ≥ 1 tumor bed induration (fibrosis), 12.6% grade ≥ 1 breast induration, and 12.1% grade ≥ 1 telangiectasia. 22.5 % of patients (n = 78) underwent TM. TM patients had larger tumors (P = .006) and specimen resection weights (P < .001). TM but not specimen resection weight was associated with reduced tumor bed induration (Odds ratio = 0.12, 95% confidence interval [CI] 0.035-0.395, P = .001), breast induration (OR 0.19, CI 0.043-0.852, P = .03) and telangiectasia (OR 0.12, CI 0.020-0.736, P = .02). Neither TM nor specimen weight had any effect on atrophy or early radiotherapy side-effects. CONCLUSION: TM but not resected specimen weight was associated with fewer long-term radiotherapy side-effects. This implies that the incidence of side-effects is affected not by reducing the overall radiotherapy target volume but by re-shaping the breast, which is likely to reduce dose inhomogeneity.

Humans↗

PubMed2026

Oncotype DX: Clinical Utility, Evidence, and Future Trends in Personalized Breast Cancer Management.

The Oncotype DX assay has revolutionized the management of early-stage, hormone receptor-positive, HER2-negative breast cancer. Developed in 2004, it quantifies 21 genes to generate a recurrence score that predicts distant recurrence risk and guides adjuvant chemotherapy. Multiple studies have validated its reliability and clinical utility in enabling more precise risk stratification and individualized treatment planning, thereby minimizing unnecessary chemotherapy exposure and improving patient outcomes. Leading oncology organizations such as the American Society of Clinical Oncology and National Comprehensive Cancer Network have incorporated it into their clinical guidelines. Beyond its well-established role in adjuvant chemotherapy decision-making, Oncotype DX is increasingly being investigated in broader clinical contexts, including lymph node-positive breast cancer, neoadjuvant therapy, radiotherapy, and ductal carcinoma in situ. Ongoing research and technological advancements, such as artificial intelligence-based predictive models and novel biomarker identification, hold significant promise for further enhancing its predictive accuracy and expanding its applications. This review synthesizes current evidence supporting the clinical utility of Oncotype DX, discusses evolving applications, and highlights future directions for integrating this genomic tool into precision oncology practice.

Humans↗

PubMed2026

Robust optimisation for photon radiotherapy: A scoping review of models, paradigms, and reporting.

BACKGROUND AND PURPOSE: Robust optimisation offers an alternative to conventional margin-based photon radiotherapy planning by explicitly modelling uncertainty, but practice is variable and not standardised. MATERIALS AND METHODS: A scoping review was conducted to map robust optimisation for photon external beam radiotherapy. Electronic searches of Scopus, PubMed and Google Scholar (2000-2025, English language) identified planning studies that incorporated modelled uncertainties into the optimisation process and reported at least one robustness-related outcome. Data were charted on clinical context, uncertainty models, optimisation paradigms, robustness metrics and evidence for clinical implementation. RESULTS: Seventy-one studies were included. Most investigated prostate, breast or lung cancer and used intensity-modulated radiotherapy or volumetric-modulated arc therapy in commercial or research treatment planning systems. Scenario-based worst-case (minimax) optimisation was the dominant paradigm in clinically oriented work, while chance-constrained, conditional value at-risk, distributionally robust and adaptive formulations were confined to small methodological series. Uncertainty modelling focused mainly on rigid set-up error; fewer studies incorporated respiratory motion, inter-fraction anatomical change, dose-calculation uncertainty or biological variation. Robustness was evaluated with diverse scenario-based dose-volume metrics, probabilistic coverage measures, composite robustness indices and, less often, biological endpoints. Direct clinical implementation reports were scarce. CONCLUSION: Robust photon planning is technically feasible and generally maintains or improves target coverage and organ sparing compared with margin-based planning. However, heterogeneity in uncertainty models, optimisation configuration and robustness reporting limits comparison and synthesis. Pragmatic minimum standards are proposed to support future consensus and wider clinical adoption.

Humans↗

PubMed2026

Availability and public reimbursement of early breast cancer care across European expert centres: a PORTRAIT from an EUSOMA initiative.

BACKGROUND: Cross-country disparities in access to guideline-recommended early breast cancer care persist across Europe. PORTRAIT is a clinician-reported, cross-sectional access study mapping availability and state reimbursement of key services across the early breast cancer pathway. METHODS: A 49-item survey covering diagnostics, pathology and genomics, systemic therapy, surgery, radiotherapy, and supportive care was emailed from June to September 2024 to multidisciplinary teams at one expert breast centre in 42 European countries. Respondents provided a consensus perspective on service availability and reimbursement. Descriptive proportions with full, partial, or no access were calculated. RESULTS: Thirty-nine countries responded (93%). Core diagnostics were widely available, but gaps persisted: MRI-guided biopsy was absent in 29% of countries and vacuum-assisted biopsy was fully reimbursed in 66%. Genomic assays were unavailable in 14% and not fully reimbursed in 35%. Public funding gaps were reported for PARP inhibitors (33%) and CDK4/6 inhibitors (26%). Immediate implant-based reconstruction and biological meshes lacked reimbursement in 21% and 33%, respectively. Despite broad availability of hypofractionated radiotherapy, 38% of countries still used per-fraction reimbursement. Psycho-oncology was limited in 35%, fertility preservation in 46%, and patient-reported outcome measures absent in 43%. CONCLUSION: Basic services are nearly universal, but gaps persist in advanced imaging, molecular testing, targeted therapies, radiotherapy reimbursement, reconstructive/oncoplastic surgery, and survivorship care. PORTRAIT identifies practical targets for policy audit, reimbursement alignment, and resource stewardship. Findings reflect clinician perspectives from expert centres, potentially representing best specialist care rather than average national care, and are not population-representative estimates or direct measures of patient outcomes.

Humans↗

PubMed2025

Genome-wide DNA methylation regulation analysis provides novel insights on post-radiation breast cancer.

Breast cancer (BC) is the most common malignancy with a poor prognosis. Radiotherapy is one of the leading traditional treatments for BC. However, radiotherapy-associated secondary diseases are severe issues for the treatment of BC. The present study integrated multi-omics data to investigate the molecular and epigenetic mechanisms involved in post-radiation BC. The differences in the expression of radiation-associated genes between post-radiation and pre-radiation BC samples were determined. Enrichment analysis revealed that these radiation-associated genes involved diverse biological functions and pathways in BC. Combining epigenetic data, we identified radiation-associated genes whose transcriptional changes might be associated with aberrant methylation. Then, we identified potential therapeutic targets and chemical drugs for post-radiation BC patient treatment by constructing a drug-target association network. Specifically, four radiation-associated genes (CD248, CCDC80, GADD45B, and MMP2) whose increased expression might be regulated by hypomethylation of the corresponding enhancer region were found to have excellent diagnostic effects and clinical prognostic value. Finally, we further used independent samples to verify CD248 expression and established a simple epigenetic regulatory model. In summary, this study provides novel insights for understanding the regulation of target genes mediated by DNA methylation and developing potential biomarkers for radiation-associated secondary diseases in BC.

Humans↗

PubMed2026

Selective Omission of Oncotype Dx Genomic Testing in Ultra-Low-Risk Luminal A Breast Cancer.

INTRODUCTION: Older women with early-stage luminal A breast cancer have an excellent prognosis with a 5-year relative survival >99%. Research on curtailing overtreatment has challenged historical standards of care by reducing radiotherapy dose and volume, and selectively omitting sentinel lymph node biopsy. This study assessed the utility of Oncotype Dx genomic testing in ultra-low-risk luminal A breast cancer. PATIENTS AND METHODS: A community hospital cancer registry was queried to identify consecutive breast cancer patients from 2014 to 2022. An ultra-low-risk population was defined as age ≥60 years, hormone-receptor positive, HER2-negative, pathologic stage T1b-T2N0 without lymphovascular invasion, and Ki-67 ≤13.25%. Analyses examined the distribution of Oncotype Dx scores categorized as low risk (0-18), intermediate risk (19-25), or high risk (26-100), as well as recurrence and overall survival. RESULTS: Of 1711 patients, 91 met ultra-low-risk eligibility criteria with available Oncotype Dx results. The median age was 70 years with a median follow-up of 5.1 years, and no patients received chemotherapy. Only 1 patient (1.1%) had a high-risk Oncotype Dx score of ≥26, while 12 (13.2%) had intermediate scores and 78 (85.7%) were low risk. Five-year local control and overall survival were 100% and 93%, respectively. Ten non-breast cancer deaths occurred, and no patients developed distant metastases. CONCLUSION: We describe a pragmatic method using common clinical and pathological features to define an ultra-low-risk cohort. Older luminal A patients with favorable pathology have a very low probability of receiving a high-risk Oncotype Dx score and demonstrate an excellent prognosis with standard adjuvant therapy.

Chemotherapy↗

PubMed2026

The landscape of clonal hematopoiesis of indeterminate potential in long-term breast cancer survivors.

BACKGROUND: Clonal hematopoiesis of indeterminate potential (CHIP) can confound blood-based genomics and may be shaped by cytotoxic therapy; clarifying its persistence after breast-cancer chemotherapy is relevant for long-term survivorship follow-up. PATIENTS AND METHODS: Buffy-coat whole-exome sequencing was performed in 189 stage I-III breast-cancer survivors with blood collected a median 136.5 months after diagnosis. CHIP was assessed using a prespecified 100-gene hematopoietic-driver compendium and exome-wide interrogation. Clinical associations were assessed with univariable tests and multivariable logistic regression including chemotherapy, radiotherapy, age, smoking and obesity. RESULTS: Within the 100-gene compendium, 54/189 (28.6%) patients harbored ≥1 variant, predominantly missense, with DNMT3A and TET2 predominating and multi-hit cases rare. In multivariable models, chemotherapy was not associated with panel-defined CHIP (OR 0.77; 95% CI 0.40-1.48; p = 0.432). Similarly, age, adjuvant radiotherapy, obesity and smoking status were not significantly associated with panel-defined CHIP. Gene-level comparisons showed no differences by chemotherapy exposure. Exome-wide, 67/189 (35.4%) patients carried ≥1 variant; chemotherapy was not associated with exome-wide variant positivity (OR 0.89; 95% CI 0.48-1.67; p = 0.721), and no locus differed between chemotherapy-exposed and never-exposed women. CONCLUSION: Buffy-coat WES performed in long-term breast cancer survivors shows no cohort-level association between prior chemotherapy and increased CHIP.

Humans↗

PubMed2026

Re-evaluating the α/β ratio in 2026: A systematic review and quantitative reappraisal in the era of molecular radiobiology.

The linear-quadratic (LQ) model and its derived ratio, α/β, have served as the cornerstone of radiotherapy dose-fractionation decisions. The period from 2015 to 2026 has witnessed a substantial re-evaluation of this paradigm, driven by the clinical success of hypofractionation in prostate and breast cancer, stereotactic body radiation therapy (SBRT), and radiogenomics. A systematic review with narrative synthesis was conducted to evaluate quantitative estimates of α/β derived from clinical and preclinical studies over the last decade, updating classical assumptions using modern trial data. Extensive Phase III data in prostate cancer consistently define an α/β of 1.2 to 2.0 Gy. Microscopic models in breast cancer align with an α/β of ∼2.7 Gy. Conversely, lung SBRT data present a high modeled α/β driven by hypoxia artifacts. Genomic integration via the Genomic Adjusted Radiation Dose (GARD) reveals that α/β operates as a dynamic, patient-specific phenotype. In the molecular era, static α/β assumptions must be integrated with disease-specific kinetics, microenvironmental data, and genomic intrinsic radiosensitivity.

Hypofractionation↗

PubMed2025

Partial Breast Irradiation for High Molecular Risk Early-Stage Breast Cancer.

PURPOSE: Partial breast irradiation (PBI) is a suitable and well-tolerated alternative to whole breast irradiation (WBI) following lumpectomy for many forms of low-risk, early-stage breast cancer. Molecular risk scores, such as the Oncotype DX recurrence score (ODX RS), are increasingly guiding systemic treatment decisions. However, molecular/genomic profiling for radiation therapy (RT) decision-making remains investigational, and it is unclear whether a high ODX RS should preclude the use of PBI. We compared oncologic outcomes among patients with high ODX RS (>25) treated with PBI versus WBI. METHODS AND MATERIALS: Patients who underwent breast conservation followed by PBI or WBI with ODX RS > 25 were ascertained from a prospectively maintained institutional database. Comparable PBI and WBI cohorts were generated in 1:5 fashion using propensity score matching based on salient clinicopathologic features. We evaluated the incidence of local recurrence (LR) as a function of RT approach. RESULTS: We identified 968 patients with an ODX RS > 25 who were treated with adjuvant RT, with a median age of 59 years (range, 25-86) and a median 5.3 years of follow-up. In a propensity matched cohort analysis that included 28 patients who received PBI matched to 140 who received WBI, we observed 3 LR events among those receiving PBI (2 of which were in different quadrants from the primary lesion) and 5 events among those receiving WBI. Among this cohort with ODX RS > 25, the 72-month cumulative incidence of LR following PBI was 7.9% (95% CI, 1.3%-23%) compared to 4.8% (95% CI, 1.6%-11%) following WBI (P = .6). CONCLUSIONS: In this cohort of patients with high ODX RS, few LRs were observed, and no statistically significant difference in LR was identified between PBI and WBI. Although these findings suggest that PBI may be considered in carefully-selected high-genomic-risk patients, larger studies with longer follow-up are needed to definitively establish the safety of this approach.

Humans↗

PubMed2026

Unveiling novel transcriptomic prognostic biomarkers for specific breast cancer subtypes and treatment regimens.

BACKGROUND: Breast cancer (BRCA) is the most common cancer in women worldwide, yet current gene expression panels offer limited insight into treatment responses across different subtypes and therapies. This study aimed to identify reliable biomarkers for predicting treatment outcomes in specific BRCA subtypes and treatment regimens. METHODS: This study analyzed transcriptomic data from The Cancer Genome Atlas to identify differentially expressed genes (DEGs) in patient groups treated with different combinations of hormone therapy (H), chemotherapy (C), radiotherapy (R), and targeted therapy (T). Non-negative matrix factorization clustering was performed to stratify patients into clusters representing different BRCA subtypes. Functional enrichment analysis was performed, and survival assessments were conducted using the METABRIC dataset. RESULTS: A total of 1,148 DEGs were identified across treatment regimens, with 75 common DEGs shared across multiple regimens. Among these, 12 candidate biomarkers were associated with luminal subtypes treated with H, including LRP1B, of which high expression predicted cancer recurrence. In triple-negative breast cancer (TNBC) treated with C, 76 candidate biomarkers were identified, including TTYH1 for recurrence and ANXA8L1 and MPZ for non-recurrence. Functional analyses identified intermediate filament organization and keratinization as pathways associated with specific candidate biomarkers of TNBC following C. Survival analysis using METABRIC strengthened the prognostic ability of LRP1B and TTYH1 to predict worse survival and ANXA8L1 and MPZ to predict prolonged survival, with four additional prognostic biomarkers. CONCLUSION: This study identified gene expression prognostic biomarkers for luminal and TNBC subtypes, thereby supporting personalized therapies. Further experimental validation is required to confirm these findings for clinical application. CLINICAL TRIAL REGISTRY: No.

Breast cancer↗

PubMed2017

MicroRNA‑27a promotes tumorigenesis via targeting AKT in triple negative breast cancer.

Altered microRNA (miRNA/miR) expression regulates tumor development and progression in triple‑negative breast cancer (TNBC). The present study examined the effect of miR‑27a on proliferation, migration and invasion of TNBC cells in vitro and in vivo. An MTT assay was performed to examine the proliferation of MDA‑MB‑231 and MDA‑MB‑468 breast cancer cells with either overexpression of miR‑27a or downregulation of miR‑27a, in the presence or absence of radiation. The migratory and invasive abilities of MDA‑MB‑231 and MDA‑MB‑468 breast cancer cells were assessed by Transwell migration and Matrigel invasion assays. The protein expression levels were examined by western blotting. The caspase‑Glo3/7 assay was performed to examine the effect of miR‑27a on radiation‑induced apoptosis in MDA‑MB‑231 and MDA‑MB‑468 breast cancer cells. A luciferase assay was performed to evaluate the effect of miR‑27a on phosphatase and tensin homolog (PTEN) and B cell lymphoma (Bcl)‑2 associated X, apoptosis regulator (BAX) expression. Immunodeficient nude mice were used to examine tumor growth following injection of MDA‑MB‑231 breast cancer cells. miR‑27a promoted proliferation in vitro and in vivo, and enhanced migration and invasion in TNBC cells. miR‑27a improved the survival of TNBC cells following irradiation. miR‑27a inhibited radiation‑induced apoptosis in TNBC cells by regulation of caspase 3/7 and Bcl‑2 expression. Furthermore, the expression levels of PTEN and phosphorylated protein kinase B in MDA‑MB‑231 and MDA‑MB‑468 cells was altered following overexpression of miR‑27a. The luciferase assay demonstrated that miR‑27a regulated PTEN and BAX expression by binding to 3'‑untranslated regions. Overall, miR‑27a exhibits an essential role in tumor development and progression in TNBC and may be used as a potential biomarker to predict radiotherapy response and prognosis for the disease.

3' Untranslated Regions↗

PubMed2026

Recent advances in immunotherapy for breast cancer: An updated review.

Immunotherapy has revolutionized the treatment landscape of breast cancer, particularly for triple-negative breast cancer (TNBC), yet primary and acquired resistance remain formidable obstacles limiting durable clinical benefit. This review provides a comprehensive update on recent advances in breast cancer immunotherapy, with a focused emphasis on the molecular and cellular mechanisms driving treatment resistance and emerging strategies to overcome them. We dissect tumor-intrinsic resistance pathways, including loss of tumor antigens, defects in antigen processing and presentation machinery, insensitivity to interferon-γ signaling, metabolic reprogramming, and epigenetic dysregulation. Tumor-extrinsic mechanisms, such as infiltration of immunosuppressive cells, abnormal angiogenesis, extracellular matrix remodeling, and FGF/FGFR genomic amplification, are highlighted as key barriers to effective immune checkpoint blockade. Emerging evidence implicates novel resistance mediators, including the DUSP22-LGALS1 axis, THSD4-driven T cell exclusion, and the MTDH-SND1 complex impairing antigen presentation, etc. We critically evaluate current strategies to surmount resistance, encompassing combination regimens with chemotherapy, targeted therapies, radiotherapy, and novel immunomodulators. The review also addresses challenges in managing immune-related adverse events, controversies surrounding patient selection biomarkers, and the urgent need for optimized efficacy evaluation systems beyond RECIST criteria. Finally, we discuss future directions, including novel immune checkpoints, microbiome modulation, artificial intelligence-assisted decision-making, and innovative trial designs. By integrating mechanistic insights with clinical evidence, this review provides a framework for understanding and overcoming immunotherapy resistance, advancing the paradigm from "effective" to "precise" immuno-oncology in breast cancer.

Humans↗

PubMed2026

The emerging landscape of polymerase θ in tumor pathogenesis and precision treatment.

DNA polymerase θ (Polθ) has emerged as a central yet paradoxical regulator of genome stability and tumor progression. Unlike conventional DNA repair factors, Polθ governs an error-prone double-strand break repair pathway-termed theta-mediated end joining (TMEJ)-which becomes essential for survival in homologous recombination (HR)-deficient cancers while simultaneously fueling genomic instability. This review presents a comprehensive and updated synthesis of Polθ's structural architecture, regulatory networks, and context-dependent functions across major malignancies, including ovarian, breast, lung, and colorectal cancers. We highlight recently uncovered mechanisms, such as the iron-FTH1/FTL-POLQ-RAD51 axis in platinum-resistant ovarian cancer, the differential POLQ regulation under methionine restriction in BRCA1-mutant breast cancer, and the identification of germline POLQ mutations defining a novel hereditary colorectal cancer subtype. Beyond DNA repair, we integrate emerging evidence linking Polθ to replication stress tolerance, base excision repair, and immune modulation via type I interferon activation and macrophage polarization. The review also provides a critical evaluation of current Polθ inhibitors-including ART558, RP-6685, novobiocin, and AB25583-focusing on their mechanisms, synthetic lethality profiles, and ability to overcome PARP inhibitor resistance. By bridging molecular mechanisms with tumor biology and therapeutic translation, this review offers a unique framework for understanding Polθ as both a prognostic biomarker and a precision oncology target, with implications for combination therapies involving radiotherapy, immunotherapy, and chemotherapy.

Cancer therapy↗