Search Results (9,786)

Background: Immune checkpoint inhibitors (ICIs) have moved from the metastatic setting into neoadjuvant, adjuvant, and fully perioperative strategies across several solid tumors. This shift has created a new clinical interface between medical oncology, surgery, anesthesia, pathology and postoperative care because immune activation may improve pathological response and survival while also generating immune-related adverse events (irAEs) that mimic or aggravate perioperative complications. Methods: We conducted a scoping review according to PRISMA-ScR. PubMed/MEDLINE and Web of Science were searched for studies published between 2016 and 2026 that evaluated adult patients with solid tumors receiving ICIs in relation to surgery. Thirty-three studies were included and synthesized descriptively across surgical feasibility, perioperative safety, irAEs, anesthetic considerations, and oncological outcomes. Results: The strongest evidence was found in resectable non-small-cell lung cancer, where neoadjuvant or perioperative ICI-based regimens improved pathological response and, in several trials, event-free or overall survival. Evidence in triple-negative breast, bladder, gastric/gastroesophageal junction, and ovarian cancers supported broader applicability but remained heterogeneous, with variable efficacy across tumor types and treatment regimens. Surgery following ICI exposure was generally feasible, without a consistent increase in postoperative mortality. However, pneumonitis, myocarditis, endocrinopathies, hepatitis, colitis, and cytokine release syndrome may mimic conventional postoperative complications. Direct evidence comparing anesthetic or perioperative management strategies was scarce. Conclusions: Perioperative ICI-based therapy is no longer an experimental concept, but its safe implementation requires structured preoperative screening, individualized surgical timing, organ-specific toxicity surveillance, careful corticosteroid decision-making, and close multidisciplinary communication. Future prospective studies should integrate standardized perioperative endpoints, anesthesia-related variables, biomarker-driven risk stratification, and long-term oncological outcomes. Full article

Metastatic colorectal cancer remains associated with poor prognosis despite major therapeutic advances, highlighting the need for robust biomarkers to refine treatment selection and monitor disease dynamics. This review summarizes emerging predictive and prognostic biomarkers in metastatic colorectal cancer across molecular and cellular layers, encompassing both tissue and circulating biomarkers. At the tissue level, we discuss genomic alterations and mutational signatures, transcriptomic classification systems and immune-related gene expression tools, protein-level immune checkpoint markers, and cellular determinants including immune infiltrates, cancer-associated fibroblasts and microbiome features. At the circulating level, we review biomarkers derived from liquid biopsy and peripheral blood, including circulating tumor DNA kinetics, T-cell receptor repertoire diversity, soluble cytokines and proteins, immune cell phenotyping, and circulating tumor cells. We highlight major challenges limiting clinical translation, including tumor heterogeneity, methodological variability, and the absence of standardized analytical pipelines and thresholds. Finally, we discuss future perspectives, emphasizing the integration of multi-omics biomarkers and artificial intelligence-driven strategies to improve biomarker validation and enable more precise management of metastatic colorectal cancer, particularly for patients with microsatellite-stable tumors who derive limited benefit from immune checkpoint inhibition. Full article

Background: Emergency surgery for complicated colorectal cancer (CRC) presenting with obstruction, perforation, or uncontrolled bleeding has high postoperative mortality, especially in older patients. However, age-related risk and the roles of radical versus palliative treatment are not fully understood. This study aimed to measure 90-day and 36-month mortality after emergency CRC surgery and to analyze whether the relationship between age and mortality is nonlinear and influenced by operative intent. Methods: Retrospective cohort of consecutive adults undergoing emergency surgery for complicated CRC (2015–2024). The outcome was 90-day and 36-month all-cause mortality. Cox regression provided adjusted hazard ratios (HR) using two models: a primary whole-cohort model omitting pathological T/N stage, and a secondary resection-only model including pathological stage. Age was modeled with restricted cubic splines and predicted 90-day and 36-month mortality were plotted by operative intent. Results: In 496 patients, 90-day mortality was 19.7% (98/496), while 36-month mortality was 37.3% (185/496). In the primary whole-cohort Cox model, independent predictors of 36-month mortality included age ≥75 years (HR 2.09, 95% CI 1.48–2.95, p < 0.001), Charlson Comorbidity Index (HR 1.02, 95% CI 0.98–1.06, p = 0.31), obstruction (HR 1.69, 95% CI 1.18–2.42, p = 0.004), perforation (HR 2.05, 95% CI 1.24–3.39, p = 0.005), and metastatic disease (HR 2.30, 95% CI 1.62–3.27, p < 0.001); radical operative intent was independently associated with lower 36-month mortality (HR 0.461, 95% CI 0.30–0.71, p = 0.001). In a secondary resection-only model additionally adjusting for pathological T/N stage (n = 426 with available pathology), the association for radical intent was attenuated and no longer statistically significant (HR 0.67, 95% CI 0.43–1.03, p = 0.067). The 36-month mortality spline estimate indicated an increasing risk with advancing age; a likelihood-ratio test did not show that the spline model fit significantly better than a linear age term (χ² = 1.43, df = 1, p = 0.233), so this pattern is interpreted descriptively rather than as formal evidence of nonlinearity, and no formal interaction between age and operative intent was demonstrated. Conclusions: Ninety-day mortality after emergency colon cancer surgery remains significant. Age-related risk shows a predominantly monotonic, descriptive pattern and should not be assumed to vary by operative intent without formal interaction testing, emphasizing individualized risk assessment and shared decision-making. Full article

Ferulic acid, a natural phenolic phytotherapeutic, which is mainly found in plant cell walls, has attracted the attention of researchers for its multiple pharmacological properties, especially for its anti-tumor potential. As an efficient antioxidant, the compound counteracts oxidative stress and modulates key molecular pathways involved in carcinogenesis. Recent studies demonstrate that ferulic acid exerts antiproliferative, pro-apoptotic, and anti-metastatic effects in various tumor models, including colon, breast, liver, and lung cancers. Mechanistically, ferulic acid affects components of prosurvival-signaling pathways such as PI3K/Akt, MAPK, and NF-κB, and stimulates programmed cell death by diverse mechanisms, including apoptosis, autophagy and ferroptosis. Furthermore, its ability to sensitize cancer cells to chemotherapeutic drugs with low toxicity to normal cells underscores its therapeutic potential. Despite promising preclinical anti-tumor activity, low water solubility and bioavailability limit its clinical use. For this reason, several attempts, ranging from chemical derivatives to nanodevices, have been made to improve ferulicbioavailability and anti-tumor efficacy. This review highlights the most significant and recent strategies to ameliorate the anticancer ability of ferulic acid in the perspective of a clinical application. Full article

Background/Objectives: Stereotactic body radiation therapy (SBRT) is increasingly used for oligometastatic lung cancer. However, standard ablative SBRT (BED₁₀ of 100 Gy or higher) is not feasible when lesions abut critical organs or patients have poor performance status. This study aimed to evaluate the efficacy and safety of moderate-dose SBRT (BED₁₀ below 100 Gy but exceeding conventional palliative doses) in patients with oligometastatic lung cancer unfit for standard ablative SBRT. Methods: We retrospectively analyzed patients treated at a single institution between October 2019 and March 2025. Eligible patients had pathologically confirmed lung cancer with extracranial oligometastasis and received 25–40 Gy in 4–7 fractions. Patients with brain or bone metastases were excluded. The primary endpoint was local control. Secondary endpoints were event-free survival, disseminated disease-free survival, overall survival, and treatment-related toxicity. Results: Forty-three patients with 55 lesions were analyzed. The mean age was 66 years, and lymph node metastases were the most frequent site (69.1%). The most common regimen was 35 Gy in 5 fractions (63.6%). At a median follow-up of 14.7 months, objective response (complete or partial) was achieved in 54 of 55 lesions (98.2%). The 1-year and 2-year local recurrence-free survival rates were 89.7% and 86.9%, respectively, and the 1-year and 2-year overall survival rates were 83.2% and 56.1%, respectively. Local control differed by metastatic site, with 2-year rates of 95.5% for lymph node lesions and 56.2% for lesions of the lung and chest wall (p = 0.002), whereas smaller differences were observed by BED₁₀ and oligometastatic subtype. Treatment-related toxicities occurred in 8 of 43 patients (18.6%), all of grade 1–2, and radiation pneumonitis was the most common (9.3%). No grade 3 or higher events occurred. Conclusions: In this preliminary single-center experience, moderate-dose SBRT achieved favorable local control with acceptable toxicity in oligometastatic lung cancer patients unfit for standard ablative SBRT, supporting a risk-adapted approach. Full article

Feline mammary tumors are the third most common neoplasms in female cats and they are characterized by high aggressiveness and high metastatic rates. Given the pivotal role of iron in human breast cancer development, in this study, we preliminarily explore the immunohistochemical expression of proteins involved in iron uptake, storage and efflux [Transferrin Receptor 1 (TfR1), Transferrin Receptor 2 (TfR2), ferritin (FTH1), and ferroportin (SLC40A1)] in non-metastatic and metastatic feline mammary carcinomas and their tributary lymph node and the possible correlation with hypoxia-inducible factor-1 (HIF-1). Our results showed an increased expression of TfR1 and TfR2 in relation to tumor progression. FTH1 immunolabeling was mainly observed in cancer cells delimiting necrotic areas and in lymph node metastasis, indicating greater iron storage possibly associated with hypoxic environments, as suggested by increased expression of HIF-1α. Also, an increase in SLC40A1 labeling in tumoral cells suggested greater iron efflux. Although preliminary, our results underline interesting differences between feline normal and tumoral mammary tissues, which could pave the way to further in vitro studies to better understand the role of iron in the progression of feline mammary tumors. Full article

The kallikrein–kinin system (KKS) and the kallikrein-related peptidase (KLK) family are interconnected proteolytic networks that regulate inflammatory signaling, vascular permeability, extracellular matrix remodeling, and tissue barrier dynamics. Beyond their classical vasoactive and inflammatory functions, accumulating evidence indicates that kinin peptides, including bradykinin, Lys-bradykinin, and their des-Arg⁹ metabolites, together with selected KLKs, modulate cell–cell and cell–extracellular matrix adhesion. Through B1 and B2 kinin receptor activation, the KKS influences endothelial adhesion molecule expression, leukocyte integrin activation, neutrophil trafficking, focal adhesion kinase/Src signaling, cytoskeletal remodeling, and matrix metalloproteinase activity. In parallel, KLKs directly reshape the adhesive microenvironment by cleaving junctional proteins, including E-cadherin and desmosomal components, and extracellular matrix substrates such as fibronectin, laminin, vitronectin, fibrinogen, and collagens. These coordinated actions affect epithelial and endothelial barrier integrity, leukocyte transmigration, angiogenesis, fibrosis, epithelial–mesenchymal transition, tumor cell migration, invasion, and metastatic dissemination. This review critically summarizes current evidence linking KKS and KLK activity to adhesion-dependent processes in inflammation and cancer, emphasizing how proteolytic signaling may either preserve tissue homeostasis or promote pathological barrier disruption depending on cellular context, receptor expression, protease activity, and microenvironmental cues. Understanding these mechanisms may refine the identification of adhesion-related biomarkers and support the development of targeted therapeutic strategies for inflammatory disorders, fibrotic remodeling, and cancer progression. Full article

Lung cancer is characterized by profound molecular and clinical heterogeneity and remains the leading cause of cancer-related mortality worldwide. Its initiation and progression are shaped by complex genetic and epigenetic alterations that perturb key biological processes, including cell proliferation, apoptosis, metabolic reprogramming, invasion, metastasis, and immune evasion. Increasing evidence indicates that dysregulated alternative splicing (AS) represents a critical post-transcriptional regulatory mechanism involved in lung cancer pathogenesis. Although AS abnormalities are not the sole drivers of tumorigenesis, they contribute to malignant transformation, tumor progression, therapeutic resistance, and phenotypic plasticity, providing opportunities for biomarker development and therapeutic targeting. This review summarizes the multifaceted roles of AS in lung cancer biology, highlighting its contributions to tumor evolution, metastatic dissemination, and treatment resistance. Furthermore, subtype-specific AS landscapes between major lung cancer subtypes are discussed to elucidate their distinct molecular mechanisms and therapeutic implications. Representative AS-generated isoforms, including cluster of differentiation 44 variants (CD44v), are further discussed as examples of how aberrant splicing events regulate cancer stemness, tumor progression, and therapeutic responses. The regulatory mechanisms underlying CD44v generation, including upstream splicing factors and downstream signaling pathways, are also summarized. Collectively, this review highlights the emerging role of aberrant AS regulation in lung cancer and emphasizes its potential implications for biomarker discovery and precision therapeutic strategies targeting splicing dysregulation. Full article

Introduction: The “obesity paradox” describes the observed association between improved cancer-specific (CSS) and overall (OS) survival observed among obese (BMI ≥ 30 kg/m²) patients with RCC. Prior studies have reported lower stage/grade tumors among obese patients to explain this. This study aimed to evaluate subcutaneous (SFA) and visceral fat area (VFA) associations with CSS, OS, tumor stage and grade among patients with non-metastatic clear cell RCC. Methods: Following IRB approval, patients undergoing nephrectomy for clear cell RCC between 2000 and 2023 were screened for inclusion. Eligible patients were those with non-metastatic disease and available preoperative imaging within 90 days of surgery. SFA and VFA were determined using mid-L3 imaging and standardized Hounsfield Unit thresholds. Multivariable Cox models evaluated factors associated with 5-year CSS and OS, and multivariable logistic regression models evaluated associations with pathologic stage (pT) 3–4 and Fuhrman grade 3–4 disease. Results: 400 patients were included. Higher SFA quartiles were independently associated with improved CSS (Q3 HR 0.21, p = 0.029; Q4 HR 0.24, p = 0.042) and OS (Q2-Q4 HR range 0.35–0.52, all p < 0.05) compared to Q1. VFA was not independently associated with OS and showed only an isolated association with CSS in the third quartile (HR 2.95, p = 0.041). Neither SFA nor VFA were independently associated with RCC stage or grade. Conclusions: Greater subcutaneous adiposity was associated with improved 5-year CSS/OS, whereas visceral adiposity did not demonstrate consistent associations with survival outcomes. These findings refine the obesity paradox and reflect the importance of fat distribution as a more specific risk factor than weight-based measures such as BMI alone. Full article

Prostate cancer is formed of a heterogeneous population of cancer cells with different biological properties. They initially form a small part of the normal stromal microenvironment but are able, through cell-to-cell contact and via exosomes, small nanoparticles containing DNA, mRNA, microRNA, long non-coding RNA, enzymes, and chemokines and cytokines, to transform the normal stromal cells into tumour-associated cells to create an immunosuppressive environment as well as inhibit the antitumour immune response. Matrix metalloproteinases are able to degrade not only the basement membrane but also the extracellular matrix, allowing the exosomes to disseminate via the circulation. Exosomes are organotrophic, homing in to specific tissues such as bone. Here, they create the premetastatic niche devoid of cancer cells and cause an immunosuppressive environment, as well as induce changes in the host cells and produce myeloid-derived suppressor cells, of which some migrate to the primary tumour inhibiting the antitumour immune response further. Prostate cancer cells can disseminate even before the cancer is detected and thus escape curative therapy. If they survive the shear forces of the circulation and the antitumour immune response, they are able to implant in the premetastatic niche, transforming it into the metastatic niche. Here, they enter a latent state or dormancy period, which may last for months or years but later can “awake” to form metastasis. This review critically analyses the cellular and molecular mechanisms, which produce this process from cellular aspects to the signalling pathways responsible for this process. Multiple mechanisms are involved in a coordinated fashion to permit the survival of the cancer cells, from cellular changes in host cells and immunomodulation via chemokines and cytokines. It emphasizes the role of microRNAs and long non-coding RNAs in this process, and that patients with higher Gleason scores have a worse prognosis in terms of biochemical free survival at 10 years. Therefore, a precision medical approach may improve the biochemical free survival rate without affecting the role of the signalling pathways in normal cells. This includes the modulation of interleukin expression, elimination of exosomes, or the inhibition of important enzymes, such as MMP-2, thus mitigating the residual recurrence risk that persists with conventional therapy. Full article

Objective: To describe breast assessment before diagnosis among women with breast cancer (BC) and examine its association with stage at diagnosis. Methods: This single-center cross-sectional study included 191 women with BC attending a medical oncology clinic. Participants completed a face-to-face questionnaire on breast self-examination (BSE), clinical breast examination (CBE), mammography, and patient characteristics. The stage was obtained from medical records. Mammography history was self-reported, and screening mammography could not be distinguished from diagnostic imaging. Exploratory logistic regression compared stage IV with stages I–III. Results: At diagnosis, 41 women (21.5%) had stage IV disease. Regular monthly BSE, regular CBE, and biennial mammography were reported by 8.4%, 3.7%, and 21.4%, respectively. Metastatic disease was present in 7.3% of women who reported biennial mammography and in 25.3% of other women (p = 0.013). In the exploratory multivariable model, biennial mammography was associated with lower odds of metastatic disease (adjusted OR 0.242, 95% CI 0.067–0.869), whereas later menarche was associated with higher odds (adjusted OR 1.273, 95% CI 1.017–1.592). Smoking and hormonal medication use also showed inverse associations, but these findings may reflect confounding or selection and should not be viewed as protective. Conclusions: Self-reported biennial mammography was associated with earlier stage and lower odds of metastatic disease at diagnosis. This cross-sectional study of women with BC cannot establish causality or screening-program effectiveness. Full article

Objectives: This study evaluated the association between maintenance therapy and survival outcomes following first-line bevacizumab-based combination chemotherapy in metastatic colorectal cancer (mCRC) using real-world data. Methods: This retrospective study included 94 mCRC patients achieving disease control, defined as complete response (CR), partial response (PR), or stable disease (SD), after first-line bevacizumab-based chemotherapy (2015–2025). Patients were divided into maintenance (fluoropyrimidine ± bevacizumab, n = 44) and active surveillance (n = 50) groups. Progression-free survival (PFS) and overall survival (OS) were analyzed using a landmark approach, Kaplan–Meier methods, and Cox regression models. Results: The overall patient cohort (n = 94) had a median age of 62 years and a male predominance of 61.7%. Median OS was significantly longer with maintenance therapy than surveillance (24.8 vs. 18.0 months; p = 0.045); PFS differences were not statistically significant (11.3 vs. 6.7 months; p = 0.077). In multivariable analysis, maintenance was not independently associated with OS or PFS. Male sex, comorbidities, multiple metastases, and non-resected primary tumors independently predicted worse OS. No statistically significant treatment-by-subgroup interactions were identified in the exploratory analyses. Conclusions: These real-world data suggest a potential survival advantage associated with maintenance therapy following first-line bevacizumab-based combination chemotherapy in patients with mCRC who achieve disease control. However, this association was not maintained after multivariable adjustment, suggesting that baseline differences may have contributed to the observed findings. Trial Registration: This retrospective observational study was not prospectively registered. Full article

Background: In advanced cancer care, routine clinical assessment often focuses on symptoms, treatment tolerance, and disease status, while spiritual well-being remains insufficiently explored despite its relevance to quality of life (QoL). Standardized patient-reported tools may help identify spiritual and existential vulnerability in patients receiving palliative treatment. This study evaluated the EORTC QLQ-SWB32 as a structured spiritual well-being assessment tool in advanced cancer care through its cultural adaptation and clinical validation among Romanian patients. Furthermore, it evaluated the tool’s feasibility and explored the association between spiritual well-being and QoL in individuals receiving palliative systemic therapy. Methods: Following EORTC Quality of Life Group guidelines, the QLQ-SWB32 was translated and pilot-tested with ten cancer patients. A prospective, cross-sectional observational study was then conducted at the Regional Institute of Oncology in Iași, Romania. Over six months, 42 adult patients with metastatic or locally advanced inoperable malignancies undergoing palliative systemic therapy were enrolled. Participants completed the EORTC QLQ-SWB32 and EORTC QLQ-C15-PAL questionnaires, while sociodemographic and clinical variables were collected using structured case report forms. Results: The translated instrument showed good linguistic clarity and clinical acceptability during pilot testing. The study cohort was predominantly aged 40–64 years (52.38%) and was socio-culturally homogeneous, with all patients identifying as Romanian and most as Eastern Orthodox (92.85%). The Relationship with God/the Divine (RSG) domain showed a stronger association with QoL in male patients than in female patients, particularly in subsequent treatment lines. In the subsequent-line subgroup, residential environment reached statistical significance (p = 0.021), with a stronger RSG–QoL correlation among rural residents. Age-related inversion patterns in the RSG–QoL association were also observed across treatment lines. Conclusions: Spiritual well-being assessment may provide clinically relevant patient-reported information in advanced cancer care. The Romanian EORTC QLQ-SWB32 demonstrated feasibility, linguistic clarity, and clinical validity as a structured assessment tool. The association between the Relationship with God/the Divine domain and QoL varied according to sex, age, residential environment, and treatment trajectory, supporting the integration of standardized spiritual assessment into individualized palliative oncology care. Full article

Objectives: Eligibility for Lutetium-177 labeled prostate-specific membrane antigen ([¹⁷⁷Lu]Lu-PSMA) radioligand therapy depends on PSMA PET/CT interpretation and may vary across observers and centres. We aimed to identify imaging and clinical correlates of VISION-like PSMA PET-defined eligibility and to compare exploratory clinical, PET-based, and combined models. Materials and Methods: Seventy-six consecutive patients with de novo metastatic prostate cancer undergoing PSMA PET/CT were retrospectively assessed for [¹⁷⁷Lu]Lu-PSMA eligibility. Candidacy was determined by consensus of two nuclear medicine physicians using VISION-like criteria. Three stepwise logistic regression models used clinical variables, PSMA PET/CT variables, or both, and were internally validated with bootstrap out-of-bag predictions. Results: Forty-three patients (56.6%) met VISION-like criteria for RLT. Internally validated area under the curve (AUC) values were 0.731, 0.817, and 0.829 for the clinical, PSMA PET/CT, and combined models. PET-defined candidacy was associated with higher PSMA-positive lesion count, greater PET-derived tumour burden, and higher mean standardised uptake value (SUVmean). Clinically, CHAARTED low-volume disease and prior docetaxel exposure were linked to lower probability, whereas disease state at imaging was not significant. In the combined multivariable model, SUVmean was independently associated with higher candidacy (odds ratio [OR]: 1.22, 95% confidence interval [CI]: 1.04–1.42; p = 0.015), whereas prior docetaxel showed the opposite association (OR: 0.10, 95% CI: 0.0129–0.776; p = 0.028). Conclusions: PSMA-positive lesion count and SUVmean were the most reproducible determinants of VISION-like eligibility. Prior docetaxel exposure was associated with lower candidacy in the combined model, although the exposed subgroup was small and the confidence interval wide. Whether systemic therapy modifies PSMA expression, and with it access to subsequent PSMA-targeted lines, requires paired imaging before and after treatment in the same patients. Full article

Background/Objectives: This study engineered and evaluated a targeted, folate-functionalized chitosan nanoparticle (CS-FA NP) delivery system to enhance the therapeutic efficacy of standard quercetin and Coriandrum sativum seed extract against breast cancer. Methods: Phytochemical profiling confirmed a 14% crude yield for the methanolic extract, with gas chromatography–mass spectrometry (GC-MS) and high-performance liquid chromatography (HPLC) identifying quercetin as the principal bioactive agent. The synthesized CS-FA NPs exhibited a core size of 7–20 nm, an average hydrodynamic diameter of 150–160 nm, a stable zeta potential of −55 mV, and high encapsulation efficiencies (87.2% for quercetin and 80.5% for coriander). Kinetic assessments confirmed a biphasic, diffusion-controlled release matching Higuchi matrix kinetics. Anticancer activity was evaluated in vitro using MTT cytotoxicity, Annexin V-FITC/PI apoptosis analysis, RT-qPCR, and ex vivo rat aortic ring assays, followed by validation in a syngeneic 4T1 mammary tumor mouse model. Results: In vitro, folate-receptor-targeted quercetin nanoparticles (T4) demonstrated superior, selective cytotoxicity, particularly against triple-negative MDA-MB-231 cells, while sparing normal fibroblasts. Annexin V-FITC/PI apoptosis profiling and ex vivo aortic ring assays revealed profound, cell-line-dependent programmed cell death and up to 90% inhibition of microvessel sprout outgrowth. Mechanistically, RT-qPCR verified that nano-formulations induced complete transcriptional silencing of NANOG, MMP-1, VEGFA, TSPAN8, TWIST, EMMPRIN, and CDK1, alongside marked upregulation of P27^KIP1 and P21^CIP1. In vivo, these nano-formulations successfully improved tumor-associated pathological features, reduced aggressive tumor spindle-cell proliferation, and suppressed elevated serum CA15-3 and arginase biomarkers. Conclusions: Folate-functionalized chitosan nano-formulations significantly enhanced the anticancer efficacy of quercetin and Coriandrum sativum seed extract through improved targeted delivery, potent antiproliferative, anti-angiogenic, and pro-apoptotic activities, together with favorable modulation of multiple molecular pathways associated with breast cancer progression. These findings support their potential as promising targeted nanotherapeutic strategies for breast cancer treatment. Full article