Onco, Volume 5, Issue 3 (September 2025) – 7 articles

Prompt and accurate identification of liver metastases from neuroendocrine tumors, arising from the gastrointestinal system and from the pancreas, through the means of both anatomical and functional diagnostic imaging techniques is mandatory. A patient’s prognosis and treatment planning are dependent on these diagnostic procedures. The aim of this narrative review is to depict the common appearance of liver metastases, as well as to depict atypical imaging patterns. Moreover, this review will cover the differential diagnosis between liver metastases from neuroendocrine tumors and other primary and secondary malignant liver lesions, as well as benign liver lesions. Full article

Background: Many patients harbor minimal residual disease (MRD)—small clusters of residual tumor cells that survive therapy and evade conventional detection but drive recurrence. Although advances in molecular and computational methods have improved circulating tumor DNA (ctDNA)-based MRD detection, these approaches face challenges: ctDNA shedding fluctuates widely across tumor types, disease stages, and histological features. Additionally, low levels of driver mutations originating from healthy tissues can create background noise, complicating the accurate identification of bona fide tumor-specific signals. These limitations underscore the need for refined technologies to further enhance MRD detection beyond DNA sequences in solid malignancies. Methods: Profiling circulating cell-free mRNA (cfmRNA), which is hyperactive in tumor and non-tumor microenvironments, could address these limitations to inform postoperative surveillance and treatment strategies. This study reported the development of OncoMRD BREAST, a customized, gene signature-informed cfmRNA assay for residual disease monitoring in breast cancer. OncoMRD BREAST introduces several advanced technologies that distinguish it from the existing ctDNA-MRD tests. It builds on the patient-derived gene signature for capturing tumor activities while introducing significant upgrades to its liquid biopsy transcriptomic profiling, digital scoring systems, and tracking capabilities. Results: The OncoMRD BREAST test processes inputs from multiple cutting-edge biomarkers—tumor and non-tumor microenvironment—to provide enhanced awareness of tumor activities in real time. By fusing data from these diverse intra- and inter-cellular networks, OncoMRD BREAST significantly improves the sensitivity and reliability of MRD detection and prognosis analysis, even under challenging and complex conditions. In a proof-of-concept real-world pilot trial, OncoMRD BREAST’s rapid quantification of potential tumor activity helped reduce the risk of incorrect treatment strategies, while advanced predictive analytics contributed to the overall benefits and improved outcomes of patients. Conclusions: By tailoring the assay to individual tumor profiles, we aimed to enhance early identification of residual disease and optimize therapeutic decision-making. OncoMRD BREAST is the world’s first and only gene signature-powered test for monitoring residual disease in solid tumors. Full article

Background: Clinical imaging is an important part of health care providing physicians with great assistance in patients treatment. In fact, segmentation and grading of tumors can help doctors assess the severity of the cancer at an early stage and increase the chances of cure. Despite that Deep Learning for cancer diagnosis has achieved clinically acceptable accuracy, there still remains challenging tasks, especially in the context of insufficient labeled data and the subsequent need for expensive computational ressources. Objective: This paper presents a lightweight classification and segmentation deep learning model to assist in the identification of cancerous tumors with high accuracy despite the scarcity of medical data. Methods: We propose a multi-task architecture for classification and segmentation of cancerous tumors in the Brain, Skin, Prostate and lungs. The model is based on the UNet architecture with different pre-trained deep learning models (VGG 16 and MobileNetv2) as a backbone. The multi-task model is validated on relatively small datasets (slightly exceed 1200 images) that are diverse in terms of modalities (IRM, X-Ray, Dermoscopic and Digital Histopathology), number of classes, shapes, and sizes of cancer pathologies using the accuracy and dice coefficient as statistical metrics. Results: Experiments show that the multi-task approach improve the learning efficiency and the prediction accuracy for the segmentation and classification tasks, compared to training the individual models separately. The multi-task architecture reached a classification accuracy of 86%, 90%, 88%, and 87% respectively for Skin Lesion, Brain Tumor, Prostate Cancer and Pneumothorax. For the segmentation tasks we were able to achieve high precisions respectively 95%, 98% for the Skin Lesion and Brain Tumor segmentation and a 99% precise segmentation for both Prostate cancer and Pneumothorax. Proving that the multi-task solution is more efficient than single-task networks. Full article

Gynecological malignancies (ovarian, endometrial, and cervical cancers), including disseminated intravascular coagulation (DIC), often provoke systemic coagulopathy. In recent years, tumor-derived, tissue factor–positive microparticles (TF⁺ MPs) have emerged as potent drivers of cancer-associated thrombosis and possibly DIC. These small (0.1–1 µm) membrane vesicles bud from cancer cell surfaces and carry procoagulant factors (phosphatidylserine and TF) on their surface. We review how TF⁺ MPs are generated by tumor cells and amplify the extrinsic coagulation cascade, potentially triggering DIC in patients with advanced gynecologic cancers. Clinical studies have linked el evated TF⁺ MP levels and activity to venous thromboembolism (VTE) in cancer, and small case series suggest dramatically high MP–TF activity in cancer-related DIC. We summarize evidence that TF⁺ MPs from ovarian tumors carry exceptionally high TF procoagulant activity (median ~80 pg/mL), and nearly all patients with cancer-associated VTE or DIC have MP–TF levels above normal. This review discusses diagnostic implications (e.g., measuring MP–TF activity as a biomarker) and treatment strategies (through the reduction in tumors, anticoagulation, and experimental TF inhibitors) in this setting. We also identify gaps in knowledge (standardized MP assays, prospective studies) and propose future directions (targeting MP formation or TF signaling). Two summary tables highlight recent studies of TF⁺ MPs in gynecologic cancer and their clinical outcomes. Illustrative figures depict the TF⁺ MP-triggered coagulation cascade and a conceptual framework for clinical management. Understanding TF⁺ MPs in gynecological cancer could improve the prediction and management of DIC and related thromboses. Full article

Conventional wisdom holds that nuclear oncogenes and tumor suppressors initiate malignant transformation. However, mounting research suggests that mitochondrial dysfunction—rooted in the unique evolutionary history and genetic autonomy of mitochondria—may serve as a more fundamental driver of oncogenesis. This paper proposes a “mitochondria-first” hypothesis of cancer, emphasizing the pivotal role of mitochondrial DNA (mtDNA) mutations, metabolic reprogramming, and immune evasion. By examining the evolutionary conflict between host and mitochondria, evaluating high mtDNA mutation rates, and highlighting the disruptive potential of mitochondrial transfer to immune cells, we outline robust mechanisms through which mitochondria could ignite cancer development. We also discuss emerging diagnostic and therapeutic approaches that target mitochondrial integrity, offering a potential paradigm shift in oncology. Full article

Background: Prostate cancer is a leading malignancy among men globally, with its incidence expected to rise due to aging populations and shifting lifestyles. While established risk factors include age, ethnicity, and genetics, the role of modifiable dietary factors, particularly sugar intake, remains less clear. Emerging evidence suggests that high sugar consumption may promote carcinogenesis through insulin resistance, chronic inflammation, and hormonal dysregulation. This systematic review aimed to evaluate the current evidence on the association between dietary sugar intake and prostate cancer risk. Methods: A systematic search was conducted across six databases for observational studies published between January 2005 and April 2025. Eligible studies assessed the associations between quantitative sugar intake and prostate cancer outcomes. Screening, data extraction, and a risk of bias assessment (using ROBINS-E) were performed independently by multiple reviewers. Results: Six studies met the inclusion criteria, comprising four prospective cohorts, one case–control study, and one cross-sectional study, with a combined sample of 11,583 men from the USA, Canada, Sweden, and France. Three studies reported a significant positive association between a high intake of dietary sugars and prostate cancer risk, two found no association, and one showed mixed findings depending on the type of sugar. Heterogeneity in the exposure assessments and confounder control limited the comparability. Conclusions: This review suggests a possible association between high dietary sugar intake and increased prostate cancer risk, especially from added sugars and sugar-sweetened beverages. However, inconsistent findings and methodological limitations highlight the need for robust, prospective studies with standardized assessments to understand this relationship better. Full article

Background: Hepatocellular carcinoma (HCC) remains a significant global health burden, particularly among vulnerable populations. This retrospective study investigates trends in HCC incidence and age at diagnosis within an urban medical center population, focusing on the impact of hepatitis C virus (HCV) treatment and racial disparities. Methods: The study includes 484 patients diagnosed with HCC between 2000 and 2023. Results: A significant decline in HCC incidence was observed with a peak in incidences between 2015 and 2017 (p < 0.02). The increase and subsequent decline were driven by a decline in HCV-related cases, particularly among the African American (AA) population. This trend was not seen for patients with other risk factors for HCC. An increase in age at diagnosis in HCV patients but not other risk patients was observed in AA (62 vs. 69 years p = 0.001) but not non-AA patients (66 vs. 67 p = 0.16). This increase in age for AA HCV patients could be due to an aging population, changing risk factor profiles, and/or limitations in surveillance and early detection of HCC. Conclusions: This study highlights the critical role of HCV treatment in reducing HCC incidence, particularly within the AA population. These findings emphasize the need for sustained efforts in surveillance, early detection, and targeted prevention strategies to address the evolving epidemiology of HCC and improve outcomes across all populations. Full article