Real-world oncology data are essential for clinical research and precision cancer care. However, genomic biomarkers are often embedded in scanned, unstructured clinical documents requiring manual abstraction before becoming available in cancer registries, delaying real-world evidence generation. This study evaluated and compared three open-source optical character recognition (OCR) approaches, Tesseract, EasyOCR, and a hybrid implementation, to determine which best enables automated extraction of Oncotype DX recurrence scores and improves the timeliness and quality of real-world oncology data.

We evaluated the feasibility of automated genomic data extraction using 675 Oncotype DX reports from a Midwestern U.S. health system. EasyOCR, Tesseract, and a hybrid OCR approach were used to extract recurrence scores from scanned reports. OCR-derived values were compared with manually abstracted scores and local cancer registry data. Performance was assessed using agreement, precision, recall, F1 score, and processing time. Multivariable logistic regression was performed to identify factors associated with discordance between registry-reported and manually abstracted scores.

The hybrid OCR approach demonstrated the highest performance, achieving 97% agreement with manual abstraction, precision of 0.997, recall of 0.972, and an F1 score of 0.984. Registry abstraction demonstrated comparable performance but required greater manual effort. Automated extraction substantially reduced processing time while maintaining high accuracy. Logistic regression showed registry discordance was largely independent of patient and tumor characteristics, with unknown progesterone receptor (PR) status as the only significant predictor.

Automated extraction of genomic biomarkers represents a scalable approach to reducing delays in cancer data availability. Earlier capture of genomic information may support cancer registry modernization and improve real-world evidence generation in precision oncology.

Immunotherapy-targeted combination therapy has transformed hepatocellular carcinoma (HCC) treatment, yet longitudinal patient-reported outcome (PRO) trajectories remain poorly characterized. We prospectively examined decision regret, hope, fatigue and quality of life during first-line treatment.

This convergent mixed-methods study enrolled 33 patients initiating first-line immunotherapy-targeted therapy at a Taiwan medical center (December 2022-October 2023). PROs were assessed across six cycles using validated instruments, and all participants were interviewed. Strands were integrated through joint display analysis.

Twenty-one patients (63.6%) completed six cycles; 12 (36.4%) discontinued. Completers maintained stable PROs with low regret, whereas discontinuers declined faster in EQ-5D utility (interaction B =  - 0.169 per cycle, p = .007) and showed a larger, non-significant rise in regret (+ 9.58, p = .051, d = 0.50; between-group p = .042). Hope declined in both groups (- 1.48, p = .003), correlating negatively with regret (r =  - .383, p = .028). Interviews centered on treatment-related discomfort (24/33), sustained hope for disease control (31/33) and financial strain (25/33); where regret was voiced (3/33) it concerned earlier points in the illness course rather than the current treatment decision. Integration yielded four expanded meta-inferences and one discordance, between measured and voiced regret.

Treatment completers maintain stable PROs, but more than one-third discontinued and experienced worse fatigue and greater regret, supporting pre-treatment counselling that is honest and informative rather than reassuring. Discontinuation marks a psychologically vulnerable transition, while universal hope decline warrants psychosocial monitoring for all patients. Given the sample size, predictors of regret are hypothesis-generating.

Cancer therapy-related cardiovascular toxicity (CTR-CVT) is an umbrella term for myocardial, vascular, electrical, and inflammatory complications of cytotoxic, targeted, immune, and radiation-based therapies. Cancer therapy-related cardiac dysfunction (CTRCD) is used here more narrowly for treatment-related myocardial dysfunction, typically identified by changes in left ventricular ejection fraction, global longitudinal strain, and/or cardiac biomarkers. The pathophysiology of CTR-CVT is multifactorial, but the implicated pathways should not be interpreted as equally causal. The dominant initiating mechanism is therapy-specific - anthracycline injury is best supported by topoisomerase IIβ (TOP2B)-mediated DNA damage with secondary mitochondrial and redox injury; HER2-directed toxicity by disruption of NRG1-ERBB2/ERBB4 survival signalling; fluoropyrimidine toxicity by coronary vasomotor dysfunction; VEGF-pathway inhibition by endothelial dysfunction and hypertension; immune checkpoint inhibitor toxicity by loss of immune tolerance; and radiotherapy injury by endothelial and microvascular damage with progressive fibrosis. Mitochondrial dysfunction, oxidative stress, inflammation, calcium dysregulation, apoptosis, and ferroptosis frequently act as downstream or amplifying pathways, although the clinical relevance of several regulated cell-death mechanisms remains incompletely established. Genetic susceptibility may further modify risk, but the strength of evidence differs among reported loci. Replicated pharmacogenetic associations, rare variants in established cardiomyopathy genes, and preliminary candidate-gene findings should therefore be considered separately. Most available studies remain limited by small cohorts, heterogeneous phenotyping, ancestry imbalance, and incomplete external replication. This review critically evaluates the hierarchy and strength of mechanistic and genetic evidence and discusses the extent to which these findings can currently inform risk stratification, surveillance, prevention, and treatment in precision cardio-oncology.

Reliable biomarkers reflecting tumor biology and histopathological risk status in pheochromocytomas and paragangliomas (PPGL) remain limited. In this study, the expression of biomarkers associated with hypoxia, angiogenesis, and proliferation was evaluated, and their associations with histopathological differentiation in PPGL were investigated.

A total of 35 tumor foci from 31 patients with PPGL who were surgically treated were retrospectively examined. Expression levels of hypoxia-inducible factor-2 alpha (HIF-2α), vascular endothelial growth factor (VEGF), CD105 (endoglin), Ki-67, and succinate dehydrogenase subunit B (SDHB) were assessed using immunohistochemical methods. Associations between these markers and clinicopathological characteristics, Pheochromocytoma of the Adrenal Gland Scaled Score (PASS), and Grading System for Adrenal Pheochromocytoma and Paraganglioma (GAPP) scores were analyzed.

HIF-2α expression, CD105 microvessel density (MVD) score, and Ki-67 proliferation index were significantly higher in poorly differentiated tumors compared with moderately/well-differentiated tumors (p<0.05 for all). In contrast, VEGF expression did not differ significantly between the groups. The GAPP score showed positive correlations with HIF-2α (r=0.48; p<0.01), CD105 (r=0.54; p<0.001), and Ki-67 (r=0.77; p<0.001). In univariate analyses, bilateral disease, HIF-2α expression, CD105 MVD score, and loss of SDHB expression were associated with higher GAPP scores. However, in multivariable regression analysis, only CD105 was independently associated with the GAPP score (β=0.04; p=0.026).

Increased expression of CD105, HIF-2α, and Ki-67 was associated with poorer histopathological differentiation in PPGL. Among the biomarkers evaluated, only CD105 showed an independent association with the GAPP score, suggesting that tumor-associated neoangiogenesis may contribute to histopathological differentiation in PPGL. These findings support further investigation of CD105 as a potential biomarker for histopathological risk assessment. However, larger studies with long-term clinical outcome data are needed to establish its clinical prognostic value.

Cancer remains a major global health challenge, particularly as several tumors develop resistance to current therapies. Although doxorubicin is widely used to treat various cancers, its effectiveness is often limited by adverse effects, including cardiotoxicity and nephrotoxicity, which restrict its dosing. In search of safer and more effective options, a series of novel piperidine-embedded isoxazol-triazole conjugates (6a-6o) were designed, synthesized, and biologically evaluated against the MCF-7 cell line in this study. The synthesized compounds 6a-6o were characterized using FTIR, HRMS, and ¹H and ¹³C NMR spectroscopy analysis to confirm their structure and verify successful synthesis. The GI₅₀ (Growth Inhibition 50%) values of synthesized compounds 6a-6o were determined using the SRB assay. Among all synthesized compounds, 6m exhibited the most potent antiproliferative activity against MCF-7 cells, having GI50 <10 µg/mL (SI >5), comparable to adriamycin (doxorubicin, GI₅₀ <10 µg/mL). Overall, 6m is a novel anticancer agent with promising abilities against MCF-7 human breast cancer. The results support the compounds relevance as a biologically active agent with effective proliferation-suppressive properties.

Endometrial cancer (EC) is the most common gynecological malignancy in postmenopausal women. Patients with low estrogen receptor alpha (ERα) expression frequently develop aggressive pathological subtypes and have poor prognosis. The role of estradiol (E2) in ERα-low EC remains poorly understood. This study investigated the tumor-promoting effects of E2 using clinical data, in vitro functional assays, and a mouse xenograft model. We found that serum E2 levels were elevated in ERα-low patients, of whom 67.7% showed high tumor expression of G protein-coupled estrogen receptor (GPER). High GPER expression correlated with increased E2 levels, enhanced sphingosine kinase 1 (SphK1) activity, and higher Ki67 proliferation index. In vitro, E2 promoted proliferation, migration, and invasion of HEC-1A cells (low ERα, high GPER). These effects were suppressed by pharmacological inhibition or siRNA knockdown of GPER or SphK1. Mechanistically, E2 activated the ERK1/2 pathway via the GPER/SphK1 axis, leading to upregulation of Cyclin D1, Cyclin E1, and MMP-9. In vivo, E2 stimulated xenograft tumor growth, an effect mitigated by inhibitors of GPER, SphK1, and ERK. Our findings demonstrate that E2 drives progression of ERα-low endometrial cancer through the GPER/SphK1 signaling pathway, revealing potential therapeutic targets for this high-risk subgroup.

Ferroptosis, an iron-dependent form of regulated cell death, is frequently dysregulated in both tumor and immune cells, contributing to tumor progression and limiting the effectiveness of cancer immunotherapy. Defining the molecular mechanisms that govern ferroptosis and its effects within the tumor immune microenvironment is critical for understanding its dual role in cancer biology. While modulation of ferroptosis presents a promising therapeutic strategy, non-specific targeting may also impair normal tissues and tumor-infiltrating immune cells. In this context, nanoparticle-based delivery systems offer a potential approach to selectively regulate ferroptosis within tumors. Such strategies may enable precise remodeling of the tumor microenvironment and enhance antitumor immune responses, thereby improving immunotherapy outcomes. This review highlights the regulatory mechanisms linking ferroptosis and the tumor immune microenvironment, provides a critical discussion of recent developments in bionanomaterial-based therapeutic platforms, and outlines the challenges and prospects for clinical application of these platforms for immunotherapy.

Stroke is the second most common neurological complication in cancer patients after metastases. Cancer-associated coagulopathy (CAC) is an important mechanism of ischemic stroke in this population. We systematically reviewed the epidemiological, clinical, radiological, and pathophysiological features of CAC-related stroke, as well as associated biomarkers and treatment strategies.

A systematic search of PubMed/MEDLINE, Scopus, Cochrane Library, and Embase (2000-2025) was performed according to PRISMA 2020 guidelines. Search terms included "stroke", "cancer", "hypercoagulability", "coagulopathy", "disseminated intravascular coagulation", and "non-bacterial or marantic thrombotic endocarditis". Studies published in English or Spanish were included, whereas case reports and review articles were excluded. Data were synthesized qualitatively.

Eighty-two studies met inclusion criteria. CAC-related stroke occurs predominantly within six months of cancer diagnosis and is strongly associated with advanced or metastatic disease and a high risk of early recurrence. Adenocarcinoma, particularly lung and pancreatic cancer, is the most frequently associated histological subtype. Proposed mechanisms include mucin-mediated platelet aggregation, tissue factor-driven coagulation, extracellular vesicles, and neutrophil extracellular trap formation, leading to thromboinflammation and platelet-rich thrombi. D-dimer is the biomarker most consistently associated with recurrence and mortality, while C-reactive protein, fibrinogen, CA-125, and transcranial Doppler microembolic signals show limited specificity. Characteristic imaging findings include multiple infarcts involving more than two vascular territories, particularly the 'three territories sign'. Low-molecular-weight heparin and direct oral anticoagulants are the most commonly used secondary prevention strategies. Thirty-day mortality rates range from 25 to 50%.

CAC-related stroke is a distinct and underrecognized entity characterized by specific biological and radiological features and poor outcomes. Earlier recognition and optimized antithrombotic strategies may improve prognosis.

IQGAP2 gene defects can lead to aberrant cell proliferation and are associated with multiple diseases. Previous studies suggest that IQGAP2 knockdown can activate AKT/mTORC1 and thereby promote aberrant cell proliferation. However, the upstream molecular regulatory mechanisms remain unclear. In our study, we found that IQGAP2 knockdown enhances PI3K activity, leading to accumulation of PI(3,4,5)P₃, thereby activating downstream AKT and mTORC1 activity. Integrative multi-omics and co-immunoprecipitation analyses revealed that IQGAP2 downregulation promotes PI3K activation within the IQGAP1 complex, while simultaneously activating the Wnt/β-catenin and AREG/EREG-EGFR signaling axes, thereby directly or indirectly enhancing PI3K activity. Furthermore, we found that the IQGAP1/IQGAP2 expression ratio is significantly elevated in tumor tissues and this ratio is associated with poor patient survival prognosis by TCGA pan-cancer analysis. This study provides insights into the signaling mechanisms associated with IQGAP2 downregulation, suggesting that the IQGAP1/IQGAP2 expression ratio may have clinical potential as a pan-cancer prognostic biomarker, and providing a basis for further investigation of targeted interventions for IQGAP2-related diseases.

Statins inhibit 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR) and reduce flux through the mevalonate pathway, which supplies both cholesterol and the non-sterol isoprenoids required for prenylation of small GTPases. Because this pathway is frequently activated in cancer, statins have become one of the most intensively studied candidates for oncological drug repurposing. Preclinical work indicates that statins can lower the threshold for apoptosis, modulate autophagy in either a pro-death or a cytoprotective direction, induce pyroptosis, and sensitize cells to ferroptosis, while also acting on CD8⁺ T cells, macrophages, dendritic cells, and cancer-associated fibroblasts within the tumor microenvironment. Clinical evidence, however, remains discordant with the strength of these mechanistic claims: favorable observational associations are susceptible to immortal-time bias, healthy-user bias, and confounding by indication, and randomized trials have been largely neutral for tumor-directed endpoints. This narrative review appraises the mechanistic, preclinical, and clinical literature using an explicit five-tier evidence hierarchy, and treats two constraints as analytical tools rather than closing caveats: the pharmacological heterogeneity of individual statins, and the one-to-two order-of-magnitude gap between concentrations used in cancer-cell experiments and free drug concentrations achievable in patients. We conclude that statins are biologically plausible but clinically unproven anticancer agents whose evaluation should proceed through biomarker-selected, pharmacodynamically validated combination trials rather than unselected add-on designs.