Antibody–drug conjugates (ADCs) have reshaped the therapeutic landscape of advanced gastric cancer, with trastuzumab deruxtecan (T-DXd) and disitamab vedotin (RC48) establishing new standards for HER2-positive disease, and a wave of Claudin 18.2 (CLDN18.2)-directed ADCs demonstrating promising early efficacy. However, as the arsenal of effective ADCs expands, clinicians increasingly confront a question that existing guidelines leave unanswered: how should ADCs be sequenced after disease progression? This review synthesizes the emerging biology of ADC cross-resistance in gastric cancer, with particular attention to payload-specific resistance mediated by ABC transporters, the impact of linker technology on bystander killing, and the implications of target expression dynamics for sequencing decisions. We critically appraise the evidence for target switching from HER2 to CLDN18.2, highlighting the mutual exclusivity of these targets and the critical gap posed by the exclusion of HER2-positive patients from most CLDN18.2 ADC trials. We further evaluate the role of dynamic re-biopsy and circulating tumor DNA (ctDNA) in real-time monitoring of target evolution. We propose a three-pillar decision-making framework integrating cross-resistance risk stratification, target landscape reassessment, and patient-clinician shared decision-making, accompanied by four practical sequencing scenarios. This framework is intended as a conceptual scaffold to guide clinical reasoning while awaiting the prospective trials urgently needed to establish evidence-based sequencing strategies in gastric adenocarcinoma.
To synthesizes evidence on artificial intelligence (AI) performance in neuroblastoma (NB) diagnosis, risk stratification, prognosis, and genomic characterization. A systematic review and meta-analysis was conducted following PRISMA 2020 guidelines (PROSPERO: CRD42024539475) across five databases. Meta-analyses used random-effects models with logit-transformed Area Under the Curve (AUCs) and cluster-robust standard errors. AI models were classified as Machine Learning Models (MLM) or Hybrid Nomograms (HN) based on their construction methodology. Of 3,742 articles identified, 53 were included. MLMs demonstrated higher point estimates than radiologists in differential diagnosis (AUC: 0.87 vs. 0.83), though this difference was not statistically significant and carried substantial uncertainty. HNs achieved stronger performance in risk stratification (AUC: 0.87). AI-derived nomograms (AUC: 0.9) and gene signatures (AUC: 0.8) outperformed conventional prognostic markers descriptively. Chemotherapy response prediction remained below clinical utility thresholds across all model types. Only 33.9
Tele-health has evolved from a marginal tool confined to rural populations and selected follow-up programs into a structurally integrated component of modern cancer care. Prior to COVID-19, its adoption was constrained by regulatory fragmentation, non-uniform reimbursement, and licensure barriers. This narrative review evaluates the evolutionary integration of tele-health in oncology post-COVID-19, examines digital disparities across patient populations, and addresses the medico-legal implications of this integration, with the objective of providing a comprehensive and clinically actionable framework for the governance of virtual oncology care. The pandemic acted as a global catalyst, driving telehealth to over 50
Aberrant activation of the RAS-RAF-MEK-ERK signaling pathway contributes to numerous malignancies, congenital syndromes, and cardiovascular disorders, establishing MEK inhibitors (MEKi) as crucial therapeutic agents. MEKi demonstrate substantial clinical benefit as monotherapy (e.g., NF1-associated tumors) or combination therapy (e.g., melanoma, glioma, congenital RASopathies). Cardiovascular adverse events, primarily asymptomatic reductions in left ventricular ejection fraction (LVEF), have prompted intensive echocardiographic monitoring. Emerging evidence indicates that isolated mild LVEF decreases rarely progress to symptomatic heart failure, raising concerns about unnecessary treatment interruptions driven by overly rigorous imaging protocols. Integrating cardiac biomarkers into monitoring strategies could offer a more pragmatic approach, guiding echocardiographic evaluations based on biomarker elevation or symptoms. Expert recommendations advocate personalized, risk-adapted surveillance frameworks. High-risk patients include those with baseline cardiovascular conditions, abnormal biomarker profiles, or significant clinical symptoms. Normal-risk patients can be safely monitored clinically, reserving imaging for biomarker changes or symptom onset. Prospective studies should seek to validate these recommendations.
Despite major advances inimmunotherapy, pancreatic ductal adenocarcinoma (PDAC) remains one of the most immunotherapy-resistant solid tumors. This review aims to summarize the key biological mechanisms underlying immune resistance in PDAC and to evaluate established and emerging biomarkers that may guide immunotherapy strategies. Resistance to immunotherapy in PDAC arises from the interplay of tumor-intrinsic oncogenic signaling, low antigenicity, defective antigen presentation, and a profoundly immunosuppressive tumor microenvironment characterized by dense desmoplasia, hypovascularity, metabolic competition, and enrichment of regulatory T-cells, myeloid-derived suppressor cells, tumor-associated macrophages, and cancer-associated fibroblasts. While MSI-H/dMMR and high tumor mutational burden identify small subsets of patients who may benefit from immune checkpoint blockade, most other biomarkers, including PD-L1 expression, homologous recombination deficiency, KRAS-related immune phenotypes, and circulating markers such as ctDNA and exosomal PD-L1, remain investigational or primarily prognostic. Emerging data highlight the importance of transcriptomic, spatial, and composite biomarker approaches to better capture tumor–immune interactions. PDAC exhibits a complex and actively maintained state of immune resistance that cannot be overcome by checkpoint inhibition alone. Future progress will depend on biomarker-guided combination strategies targeting oncogenic pathways, stromal barriers, and innate immune suppression, along with prospective validation of integrated, multimodal biomarker models to advance precision immuno-oncology in PDAC.
Head and neck cancer (HNC) is characterized by profound genomic instability, therapeutic resistance, and suboptimal survival outcomes, particularly in advanced-stage disease. This review aims to critically examine the mechanistic interplay between DNA damage response (DDR) pathways, epigenetic dysregulation, and cytokine-driven inflammatory networks, and to evaluate their collective impact on HNC progression and therapeutic vulnerability. Recent studies have demonstrated that defects in DDR pathways contribute to genomic instability and activate cytosolic DNA sensing via the cGAS-STING pathway, leading to type I interferon production and modulation of the tumor microenvironment. In addition, epigenetic alterations influence DNA repair mechanisms and immune responses. Cytokine networks involving IL-6, TNF-α, and NF-κB/STAT3 signaling play a central role in tumor progression, immune evasion, and therapy resistance. Combination therapies, including PARP/ATR inhibitors with immune checkpoint blockade and cytokine-targeting agents, have shown promising results in preclinical and early clinical studies. The intricate crosstalk among DDR deficiency, epigenetic alterations, and inflammatory signaling constitutes a central axis in HNC pathobiology and therapeutic resistance. Targeting these interconnected pathways through rational combination strategies offers a promising avenue to enhance treatment efficacy and advance precision oncology. Continued integration of molecular profiling and biomarker-driven approaches will be essential to optimize patient stratification and improve clinical outcomes in HNC.
Gastrointestinal (GI) cancers are among the most common malignancies worldwide and impose a substantial symptom burden from diagnosis through survivorship. Despite advances in systemic therapies and surgical approaches, patients continue to experience undertreated symptoms, psychosocial distress, financial toxicity, and fragmented supportive care. This review examines how artificial intelligence (AI) may help transform GI supportive oncology from a reactive, episodic model to a proactive, continuous, and personalized approach. AI applications in GI supportive oncology are advancing along two related domains: (1) AI-enabled patient-reported outcome (PRO) tools, including real-time symptom monitoring, unsupervised symptom clustering, and AI-enhanced triage pathways; and (2) tumor-aware supportive care, including AI-driven radiomics for sarcopenia detection and multimodal prognostic models that inform supportive care needs. Systematic electronic PRO monitoring has been associated with improved survival and reduced acute care utilization, while AI-automated CT sarcopenia detection identifies muscle wasting that routine clinical documentation often misses. Important implementation challenges remain, including the black-box problem, algorithmic bias, privacy concerns, the digital divide, and regulatory uncertainty. Precision supportive oncology, integrating PRO-based symptom intelligence with imaging-derived risk stratification, has the potential to improve GI cancer care by making it more anticipatory and patient-centered. This review proposes a two-lane framework consisting of PRO-driven symptom intelligence and tumor-aware supportive care, unified by principles of privacy, explainability, and equity. Responsible adoption will require prospective validation, equitable design, and clinically interpretable systems.
Locoregional therapies have emerged as key components in the therapeutic arsenal against gastrointestinal cancers, offering minimally invasive options with curative potential. Beyond their direct cytotoxic effects, these interventions can remodel the tumour microenvironment by inducing immunogenic cell death and initiating local and systemic immune responses, including abscopal effects. This review aims to examine how these immunomodulatory properties may support locoregional therapies as an ideal platform for intratumoural immunotherapy, positioning their combination at the core of the evolving field of interventional immuno-oncology. Recent studies demonstrate that locoregional therapies can induce immune responses through modulation of the tumour microenvironment, creating conditions that may be exploited by intratumoural immunotherapy. This review provides a comprehensive overview of current locoregional modalities, including thermal and non-thermal ablative techniques, transarterial therapies, and minimally invasive radiation methods, detailing their mechanisms of action, clinical applications, and immune-related effects. Special attention is given to emerging evidence supporting the combination of these approaches with intratumoural delivery of immunomodulatory agents, to enhance anticancer immune responses. The convergence of locoregional intervention and targeted immunomodulation represents an emerging therapeutic concept in the treatment of gastrointestinal cancers, offering the prospect of personalised, tumour-directed immune activation. This approach holds the potential to extend the benefits of immunotherapy beyond genetically defined subgroups to a broader patient population.
The advent of anti-PD-1 therapy has transformed the treatment paradigm of advanced melanoma, enabling durable responses in a proportion of patients. However, the impact of both primary and acquired resistance remains a significant barrier to sustained disease control. This review explores the biological rationale and clinical progress of anti-PD-1 based combination strategies, with a particular emphasis on emerging triplet regimens and next-generation immunotherapeutic approaches designed to extend survival and overcome resistance. While dual checkpoint inhibition (anti-PD-1 plus anti-CTLA-4 or anti-LAG-3) has improved clinical outcomes, further therapeutic advances are needed to expand the depth and durability of responses. Triplet combinations have shown promising activity in early-phase trials, with acceptable safety profiles. Promising triplet strategies currently under investigation include combinations of BRAF and MEK inhibitors with anti-PD-1 agents in BRAF-mutant melanoma, as well as regimens pairing anti-PD-1 therapy with emerging immunomodulatory agents. Biomarkers and disease control prior to infusion appear to be key determinants of outcome. Anti-PD-1-based triplet therapies represent a promising frontier in melanoma treatment. Future trials should define optimal combinations, patient selection, and therapeutic sequencing to maximize benefit and minimize toxicity.
Sacizuzumab Tirumotecan is a novel antibody-drug conjugate targeting TROP2 glycoprotein, which is highly expressed across malignant cells. Sacizuzumab Tirumotecan has already demonstrated promising clinical activity in combating breast and lung cancer, and it is currently under evaluation for use against gynecologic malignancies. This review aims to highlight the therapeutic potential of Sacituzumab Govitecan in gynecologic malignancies and to summarize the most recent evidence supporting its clinical application. Ongoing phase III trials of Sacituzumab Tirumotecan include cervical, ovarian, and endometrial cancers. Preliminary safety data of Sacituzumab Tirumotecan indicates a manageable toxicity profile, with the most commonly reported adverse events including hematologic toxicity, oral mucositis, and alopecia. Mature data from Phase III trials are anticipated to clarify the impact of Sacituzumab Tirumotecan on overall survival, progression-free survival, and objective response rates. Additionally, biomarker analyses may enhance patient selection strategies and refine prognostic assessment in gynecologic oncology. Antibody-drug conjugates (ADCs) are an advent in the management of oncology patients. Sacituzumab Tirumotecan (sac-TMT/MK-2870/SKB264) is a promising new ADC undergoing clinical trials in solid tumors. Promising results have been published with the use of Sacituzumab Tirumotecan in gynecologic malignancies, mainly cervical, ovarian and endometrial cancers. More mature data from phase III trials are expected soon.
Head and neck squamous cell carcinoma (HNSCC) is a global malignancy characterised by extremely low survival rates, primarily contributed to by late diagnosis, tumour heterogeneity, and resistance to available therapies. Deciphering reliable biomarkers is crucial for early diagnosis, prognosis and personalized therapy. This review discusses the possibilities of clusterin (CLU) as an emerging biomarker in the field of HNSCC therapeutics by incorporating insights derived from preclinical, clinical and proteomic data. The expression of CLU in HNSCC cases has been found to be correlated with advanced stages of the tumour, metastatic potential higher histological grades and therapeutic resistance. Mechanistic studies demonstrate that CLU plays a dual role in enhancing tumour cell survival and facilitating apoptosis, contingent upon isoform and environmental context. Recent findings confirm the effectiveness of CLU as a biomarker for early diagnosis, risk evaluation, and forecasting therapeutic response. This review also focuses on the comparison of CLU to known HNSCC biomarkers and stresses the progress made in non-invasive screening and targeted therapies. In conclusion, CLU shows strong potential as a biomarker and therapeutic target, warranting further research for clinical application in HNSCC.
T-cell redirecting therapies have revolutionized the treatment of several hematologic malignancies. These include CAR T-cell therapy, an adoptive immunotherapy in which a patient’s T-cells are engineered to express synthetic receptors against tumor surface antigens, and bispecific T-cell engagers, antibodies simultaneously targeting CD3 and a tumor-specific antigen. Both approaches redirect T-cells toward tumor cells, thereby enhancing anti-tumor immunity independent of major histocompatibility complex class restriction. With expanding indications, their use is extending into older and less fit populations than those represented in pivotal trials, raising important questions regarding toxicity profiles in patients with greater comorbidity burden. Although cardiovascular toxicities of CAR T and bispecific T-cell engagers have been described, reported incidences are highly variable due to inconsistencies in adverse event definitions and surveillance across studies. Further, most studies have excluded patients with pre-existing heart failure or cardiomyopathy. Consequently, there is a lack of evidence-based guidance for risk stratification, peri-treatment management, or monitoring in this growing subgroup. Here, we briefly review the cardiovascular toxicities associated with T-cell redirecting therapies and highlight limitations in clinical trial inclusion criteria. We then emphasize the urgent need for uniformity in defining cardiovascular toxicities, as well as for dedicated studies in patients with pre-existing heart failure or cardiomyopathy as a distinct high-risk population.
Clonal hematopoiesis of indeterminate potential (CHIP) is characterized by the age-associated expansion of hematopoietic stem and progenitor cells (HSPCs) bearing somatic mutations in genes such as DNMT3A, TET2, ASXL1, and JAK2, without overt cytopenias or hematologic malignancy. CHIP is increasingly understood as a systemic inflammatory condition that influences extra-hematopoietic organs. Recent findings highlight its role in gastrointestinal (GI) pathology through immune dysregulation, chronic inflammation, and fibrogenic remodeling. In the liver, CHIP, particularly TET2 and DNMT3A mutations, enhances IL-6 and NLRP3 inflammasome signaling in Kupffer cells, promoting hepatic inflammation, fibrosis, and heightened risk for cirrhosis and hepatocellular carcinoma. In inflammatory bowel disease (IBD), persistent cytokine exposure may select for pro-inflammatory clones, with TET2-mutant CHIP linked to severe disease phenotypes. In colorectal cancer, mutant macrophage and monocyte populations derived from CHIP alter tumor immune microenvironments, affecting tumor progression and therapeutic responsiveness, including checkpoint blockade efficacy. Together, these findings suggest that hematopoietic clones harboring specific mutations may act as upstream regulators of chronic inflammation and carcinogenesis within the GI tract. This review consolidates gene-specific mechanisms, interactions with the gut-liver immune axis, and implications for targeted interventions linking CHIP with gastrointestinal inflammation, fibrosis, and malignancy.
Malignant pleural mesothelioma (MPM) remains a rare but highly aggressive malignancy with limited treatment options and poor prognosis. For nearly twenty years, platinum–pemetrexed chemotherapy has persisted as the unchanged standard treatment; although recent progress in immunotherapy has modestly disrupted this therapeutic plateau, survival outcomes remain disappointingly limited. This review aims to provide a comprehensive overview of the epigenetic landscape of MPM, focusing particularly on the oncogenic and therapeutic implications of enhancer of zeste homolog 2 (EZH2), and to discuss its potential as a target for novel therapeutic strategies and combination regimens. Epigenetic dysregulation has emerged as a central driver of mesothelioma pathogenesis. EZH2, the catalytic component of the polycomb repressive complex 2 (PRC2), mediates histone H3K27 trimethylation, silencing tumor suppressor genes and promoting malignant transformation. In addition to its canonical role, EZH2 has non-canonical oncogenic effects that modulate transcription, apoptosis, DNA repair, and immune evasion. High EZH2 expression correlates with BAP1 loss, which enhances chromatin remodeling defects and disease aggressiveness. Preclinical and early clinical data demonstrate that EZH2 inhibitors—including tazemetostat, valemetostat, GSK126, EPZ011989, tulmimetostat, and novel PROTAC-based degraders such as MS1943—can suppress tumor progression, modulate the tumor immune microenvironment, and restore therapeutic sensitivity. Furthermore, combination approaches integrating EZH2 inhibition with chemotherapy or immune checkpoint blockade show synergistic potential in overcoming resistance. EZH2 represents a pivotal epigenetic regulator and a promising therapeutic target in MPM. Further understanding the dual canonical and non-canonical roles of EZH2 in tumor biology will be key to optimizing targeted and combinatorial treatment strategies. Future research should focus on translating EZH2 inhibition into clinical benefit, identifying predictive biomarkers of response, and exploring rational combinations with chemotherapy, targeted drugs, or immunotherapy to improve survival outcomes in mesothelioma patients.
This review examines the limitations of conventional macroscopic approaches in detecting occult cervical lymph node metastasis (OCLNM). It also explores how multi-omics technologies and artificial intelligence (AI) driven cross-scale multimodal integration are reshaping precision diagnosis for patients with clinically node-negative (cN0) head and neck squamous cell carcinoma. Recent studies show that combining high-throughput omics data, such as genome-wide DNA methylation and spatial transcriptomics, with radiomics through deep learning models leads to markedly better performance than conventional imaging alone. New computational strategies, including habitat radiomics and cross-modal fusion networks, allow more detailed characterization of spatial tumor heterogeneity. They also provide insights into how the tumor microenvironment evolves during early metastatic spread. In addition to improving detection of microscopic disease, these approaches are beginning to support more reliable survival risk stratification. The integration of AI with multi-omics data is moving the field toward a noninvasive “panoramic virtual biopsy.” This framework offers a practical path to address a long-standing clinical challenge, balancing overtreatment against undertreatment in cN0 patients. With further validation, it may support safer surgical de-escalation and enable more personalized treatment strategies.
Radiotherapy remains a fundamental pillar of cancer treatment, however its efficacy is still often limited by tumor radioresistance and toxicity to surrounding healthy tissues. Poly(ADP-ribose) polymerase inhibitors (PARPi) have emerged as potent radiosensitizers by impairing DNA repair mechanisms, particularly base excision repair, thereby enhancing the cytotoxic effects of ionizing radiation (IR). This review provides a critical narrative synthesis, based on a structured literature search, consolidating current preclinical and clinical evidence on the therapeutic potential of combining PARPi with various IR modalities, including X-rays, γ-rays, α- and β-particles, protons, and carbon ions, across a broad spectrum of tumor types. The findings reveal that PARPi consistently enhance radiosensitivity, with the magnitude of effect influenced by radiation type, tumor-specific DNA repair capacity, and PARPi pharmacodynamics. Notably, combinations with high-LET radiation (e.g., carbon ions) demonstrate superior efficacy in certain contexts, while emerging data highlights the immunomodulatory potential of PARPi plus IR strategies via cGAS-STING pathway activation. Clinical trials confirm the feasibility of these combinations, although toxicity profiles vary by tumor type and treatment regimen. This review underscores the promise of PARPi plus radiotherapy combinations and identifies key avenues for future research, including biomarker-driven patient stratification and the development of triple-combination strategies to optimize therapeutic outcomes.
The FIGO staging system for endometrial cancer has evolved substantially over the past five decades, progressing from the original clinical classification in 1971, through the surgical refinements of 1988 and 2009, to the most recent 2023 revision that integrates both pathological and molecular determinants of disease behaviour, with the overarching aim of optimising adjuvant treatment selection to maximise therapeutic benefit while minimising unnecessary harm. This review aims to contextualise the rationale underlying these revisions and to clarify their clinical implications for contemporary staging and risk-adapted management. The 2023 FIGO update introduces refined anatomic criteria, including depth of myometrial invasion, cervical stromal involvement, lymphovascular space invasion, and improved discrimination between nodal micrometastases and macrometastases, while formally incorporating biologically defined molecular subgroups (POLEmut, p53abn, MMRd, and NSMP). Importantly, the 2025 ESGO–ESTRO–ESP recommendations further advance this framework by mandating estrogen receptor (ER) assessment within the NSMP category, demonstrating that ER negativity identifies early-stage disease with a significantly increased risk of recurrence and mortality and directly influences adjuvant treatment selection. Together, FIGO-2023 and ER-refined molecular stratification represent a clinically actionable precision-staging model. To support implementation, this review provides a uniquely integrated visual educational framework that combines a comprehensive schematic representation of FIGO-2023 staging pathways with corresponding high-resolution histopathological images and detailed interpretive guidance, facilitating accurate recognition of key pathological features and consistent application of the revised staging criteria in practice. The integration of refined anatomic staging with molecular and ER-informed risk stratification enhances prognostic precision, supports multidisciplinary communication, and enables more individualised therapeutic decision-making. Familiarity with this evolving framework is essential for improving consistency of staging across institutions and for optimising clinical outcomes through earlier and more accurate identification of dissemination and metastatic potential in endometrial cancer.
Gastric cancer remains a leading contributor to cancer-related mortality worldwide despite its declining incidence, with poor survival rates. Standard treatments, such as surgical resection, radiotherapy, chemotherapy, and immunotherapy, often achieve limited success, underscoring an urgent need for the development of novel and effective treatment strategies. Plant-derived diterpenoids demonstrate a wide range of bioactivities including antitumor activity. The aim of this review is to compile, integrate, and discuss the latest information concerning plant-derived diterpenoids with anti-gastric-cancer activities. In this review, we mainly summarize current knowledge on the anticancer effects of plant-derived diterpenoids against gastric cancer, with a focus on their underlying molecular mechanisms, such as induction of apoptosis, modulation of reactive oxygen species, inhibition of metastasis, and chemotherapy sensitization, based primarily on preclinical evidence from in vitro and in vivo experimental evidence, with human clinical data available only for paclitaxel. Among the diterpenoids reviewed, carnosol, triptolide, and paclitaxel demonstrate the most robust preclinical evidence, supported by patient-derived xenograft models, direct target identification, or clinical validation. We also analyze the realistic challenges in translating these plant-derived diterpenoids into clinical practice. We conclude from this review that plant-derived diterpenoids demonstrate anticancer activity against gastric cancer in preclinical models through various pharmacological mechanisms. This review highlights that these key mechanisms are mediated by distinct pharmacological pathways, that most evidence is derived from in vitro and animal studies, and that clinical relevance remains limited. These insights may inform future research aimed at therapeutic development.
Mucosal injury of the alimentary tract (mucositis) has been a consistent, markedly symptomatic, and clinically disruptive side effect of conventional cytotoxic chemotherapy and radiotherapy regimens since their inception. Despite its impact, mucositis remains a significant unmet clinical need as available treatment options are sparse. This review uses oral mucositis as a predicate regimen-related toxicity to provide a comparative discussion of the pathobiology, clinical features, and risk factors of regimen-related mucosal injury by therapy class. The alimentary tract, especially the mouth, has not escaped collateral damage from newer forms of cancer therapy including targeted agents, immunotherapy, and antibody-drug conjugates. A critical assessment of the field reveals persistent challenges that have hindered the development of effective, mechanistically-based treatments across both conventional and emerging therapy classes. Recognizing the consistent observation that regimen-related toxicities routinely occur in clusters, common pathobiological underpinnings are noted in support of unified, systemic mitigation strategies.
Liquid biopsy has emerged as a minimally invasive approach to overcome the limitations of tissue biopsy in oncology. This review aims to synthesize recent advances in its clinical applications, particularly in early cancer detection, therapeutic monitoring, and minimal residual disease (MRD), while discussing current challenges, regulatory perspectives, and future directions. Circulating tumor DNA (ctDNA), circulating tumor cells (CTCs), extracellular vesicles, and epigenetic markers are the most extensively studied biomarkers, in which clinical trials such as TRACERx and DYNAMIC have demonstrated that ctDNA monitoring enables earlier detection of recurrence and guides adjuvant therapy decisions more precisely than standard imaging. Commercially validated assays, including Guardant360 CDx, FoundationOne Liquid CDx, and Epi proColon, have received regulatory approval, reflecting growing clinical adoption; however, limitations persist, including reduced sensitivity in low-tumor burden settings, technical variability between platforms, and the risk of false positives from clonal hematopoiesis. Ongoing research highlights the promise of multi-omic approaches and the integration of artificial intelligence to improve sensitivity, capture tumor heterogeneity, and provide predictive insights into treatment response and resistance. Liquid biopsy represents a paradigm shift in precision oncology by enabling real-time, longitudinal tumor profiling. Although significant barriers remain, such as cost, accessibility, and lack of standardization, technological innovations and large-scale validation studies are paving the way for its routine clinical integration.
