Search Results (44)

The expansion of neoadjuvant immune checkpoint blockade, chemoimmunotherapy, and targeted therapies in oncogene-driven tumors is reshaping the management of resectable non-small cell lung cancer (NSCLC). Major pathologic response (MPR) and pathologic complete response (pCR), defined respectively as 10% or less residual viable tumor (RVT) within the primary tumor bed and the complete absence of viable tumor in both the resected primary tumor and sampled regional lymph nodes, have become widely adopted early efficacy endpoints. Both are consistently associated with favorable survival outcomes at the patient level, although their validity as trial-level surrogates for long-term outcomes remains incompletely established. Accurate pathologic response assessment requires rigorous standardization of gross specimen handling, tumor bed sampling, and microscopic quantification of viable tumor, necrosis, and stroma. International recommendations have improved methodological harmonization, and reproducibility studies have demonstrated good interobserver agreement when standardized protocols are applied. Increasing evidence also indicates that RVT behaves as a continuous prognostic variable and that integration of primary-tumor and nodal response may improve postoperative risk stratification. Beyond quantification of RVT alone, additional histologic characteristics of the residual tumor, together with stromal and immune therapy-related features, may provide complementary prognostic information. Digital pathology and artificial intelligence may support more reproducible quantitative assessment, whereas circulating tumor DNA-based molecular residual disease evaluation may capture systemic risk not represented by the resection specimen. These emerging approaches remain investigational and require prospective validation. This review critically examines the methodological standardization, biological interpretation, and prognostic validation of pathologic response in resectable NSCLC, and discusses future strategies integrating histopathologic, digital, and molecular variables into post-neoadjuvant risk assessment. Full article

Testicular germ cell tumors (TGCTs) are highly curable malignancies, yet their clinical management still relies heavily on conventional serum tumor markers, including alpha-fetoprotein, beta-human chorionic gonadotropin, and lactate dehydrogenase, which have limited sensitivity and specificity in several clinically relevant settings. Circulating microRNAs, particularly miR-371a-3p, have emerged as promising liquid biopsy biomarkers with potential applications across the TGCT disease continuum. This narrative review summarizes the current evidence on the biological basis, diagnostic performance, clinical utility, and limitations of circulating microRNAs in TGCTs. MiR-371a-3p demonstrates high diagnostic accuracy for viable non-teratomatous TGCTs and consistently outperforms classical serum tumor markers in primary diagnosis. Its rapid decline after effective treatment and its association with tumor burden support potential roles in chemotherapy monitoring, early relapse detection during surveillance, and the assessment of selected post-chemotherapy residual masses. However, its inability to detect teratoma remains a major biological limitation, particularly in non-seminomatous residual disease and surveillance settings. Additional barriers to implementation include assay heterogeneity, the lack of universally accepted cutoffs, the variable use of serum versus plasma, and the absence of broad regulatory approval. Emerging translational data suggest that miR-371a-3p may also contribute to tumor–microenvironment communication and cisplatin resistance, although these findings remain preclinical. Overall, miR-371a-3p represents one of the most promising biomarkers in TGCT management, but its routine clinical integration will require standardized analytical protocols and prospective validation in marker-guided decision pathways. Full article

Colorectal cancer (CRC) kills approximately 850,000 people annually and is the second leading cause of cancer mortality worldwide. After curative-intent surgical resection, recurrence rates of 15–20% in stage II and 30–40% in stage III diseases highlight the fundamental limitations of pathological staging as the sole basis for adjuvant treatment decision-making. Circulating tumor DNA (ctDNA), which comprises tumor-derived cell-free DNA fragments shed into the bloodstream by dying cancer cells, offers a direct and dynamic readout of molecular residual disease (MRD) in the postoperative period. Because ctDNA clears within hours of macroscopically complete surgery, any persistently detectable postoperative signal reflects viable microscopic disease rather than surgical contamination. Over the past decade, evidence has matured rapidly from proof-of-concept observational studies to completed randomized clinical trials, culminating in the recent publication of DYNAMIC-III and ALTAIR in 2025–2026. The DYNAMIC trial established that ctDNA-guided management reduced adjuvant chemotherapy use from 27.9% to 15.3% in stage II colon cancer while maintaining an equivalent five-year recurrence-free survival (88% vs. 87%; difference 1.1%, 95% CI 5.8% to 8.0%). The GALAXY study confirmed ctDNA as the most powerful prognostic biomarker in resected CRC, with a disease-free survival hazard ratio of 11.99. Critically, DYNAMIC-III demonstrated that escalating chemotherapy intensity in ctDNA-positive stage III patients did not improve recurrence-free survival (HR 1.11, p = 0.6), and the phase III ALTAIR trial showed that trifluridine/tipiracil failed to significantly improve disease-free survival at the point of molecular recurrence (HR 0.79, p = 0.107). This review critically synthesizes the current evidence for ctDNA-guided treatment decisions in resected CRC across three therapeutic strategies: de-escalation in ctDNA-negative patients, escalation in ctDNA-positive patients, and post-adjuvant therapy at the point of molecular recurrence. Future progress requires biomarker-matched escalation strategies, adaptive trial designs, and formal validation of ctDNA clearance as a surrogate endpoint for predicting patient outcomes. Full article

Neoadjuvant immunochemotherapy (NICT), mainly anti-PD-1/PD-L1 therapy combined with cytotoxic chemotherapy, significantly improved perioperative outcomes for resectable solid tumors such as lung cancer and breast cancer. But a large number of patients still had residual lesions and eventually relapsed. Residual tumor cells are not simply unremoved cellular debris, but represent a therapy-selected and therapy-amplified subset of a pre-existing heterogeneous and plastic tumor ecosystem. To avoid implying that therapy generates a new form of tumor plasticity de novo, we use the term “plasticity of non-apoptotic residual tumor cells” to describe the plastic behavior of viable malignant cells that survive treatment-induced cytotoxicity rather than entering apoptosis. In this review, we define the plasticity of non-apoptotic residual tumor cells as the capacity of residual malignant cells to preserve, switch, or re-enter phenotypic states such as dormancy, hybrid EMT, stem-like regeneration, and immune evasion under the combined influence of intrinsic tumor heterogeneity, systemic therapy pressure, and microenvironmental protection. Before the NICT-specific discussion, we outline general theoretical frameworks including therapeutic stress response, apoptosis-induced regeneration, genetic and non-genetic heterogeneity, as well as spatial heterogeneity of involved lymph nodes, so as to provide a more robust interpretation of residual lesion biology under NICT. Also, this review proposes that residual disease may be reconceptualized as a treatment-shaped plastic niche, whose biological behavior is jointly shaped by clonal selection, reversible phenotypic transformation, and microenvironmental ecological protection. We summarize several key states of residual tumor cells: persistent-like/resting state, hybrid EMT/invasive plasticity state, stem-like/regenerative state, and immune escape state, and elucidate the underlying epigenetic basis, including DNA methylation, histone modification, chromatin remodeling, and non-coding RNA network reprogramming. Meanwhile, niche factors such as immune stress, CAF/TAM enrichment, fibrotic matrix, hypoxia, and metabolic stress can further stabilize these states and promote the survival of relapse seeds. Based on this, we propose that future postoperative assessments should be upgraded from residual volume to a stratified residual state, and dynamically identified by combining single-cell omics, spatial pathology, and ctDNA/MRD monitoring. Furthermore, treatment strategies should shift from simply shrinking tumors to plasticity-locking therapy, that is, identifying, classifying, and blocking the plasticity escape pathways of residual lesions before they evolve into recurrence. Full article

Background: In the immunotherapy era, cytoreductive nephrectomy (CN) for metastatic renal cell carcinoma (mRCC) is increasingly performed after neoadjuvant immune checkpoint inhibitor (ICI)-based therapy. Examination of the nephrectomy specimen may capture the depth of treatment-induced tumor clearance more accurately than size-based radiological criteria alone. However, pathological reporting is highly heterogeneous across studies: residual viable tumor (RVT), necrosis, pT stage, and binary downstaging have all been used, limiting reproducible cross-study comparison. We aimed to characterize this heterogeneity, assess its implications for evidence synthesis, and propose a pragmatic framework for qualitative interpretation. Methods: PRISMA-compliant systematic review of studies reporting pathological response and oncological outcomes in mRCC patients undergoing CN after neoadjuvant systemic therapy (PROSPERO CRD420251154068). A qualitative synthesis was performed. A three-category Pathological Response Category (PRC) framework is proposed to harmonize heterogeneous metrics. Results: Seven retrospective studies (n = 408) were included. Pathological reporting metrics were inconsistent across all studies, preventing formal meta-analysis. Nevertheless, across cohorts reporting survival outcomes, deeper pathological response was directionally associated with more favorable oncologic outcomes. A discordance between radiological and pathological response was observed, including near-complete tumor clearance in patients classified as radiologically stable, reflecting the non-size-based mechanisms of ICI-induced tumor killing. Conclusions: The central finding of this review is not that pathological response predicts survival—which is expected—but that current pathological reporting in the mRCC surgical setting is too heterogeneous to quantify the frequency, depth, or prognostic significance of that response in a reproducible way. Prospective adoption of standardized pathological reporting protocols is the most critical next step for this field. Full article

Background/Objectives: Atezolizumab plus bevacizumab (Atez/Bev) is a standard treatment for unresectable hepatocellular carcinoma (HCC), but its anti-tumor efficacy remains limited. Combining intrahepatic locoregional treatment (IHLRT) with Atez/Bev has been explored as a strategy to overcome this limitation. This study aimed to clarify the significance of IHLRT in Atez/Bev treatment for unresectable HCC. Methods: Eighty consecutive patients with unresectable HCC treated with Atez/Bev were retrospectively analyzed. IHLRT was performed in patients with residual viable hepatic lesions amenable to locoregional treatment during Atez/Bev therapy. Anti-tumor response was evaluated by RECIST; and progression-free survival (PFS), overall survival (OS), potential biomarkers, and contributing factors to OS were also assessed. Results: IHLRT was selectively performed in 20 patients based on individual clinical conditions. Pretreatment characteristics were comparable between patients who did and did not receive IHLRT. Both best and initial tumor responses were superior in the IHLRT group, and PFS was significantly longer (16.2 vs. 8.4 months, p = 0.019), with comparable rates of severe treatment-related adverse events. On multivariate analysis, hepatic reserve function, objective response, neutrophil-to-lymphocyte ratio (NLR) and IHLRT were independent predictors of OS (HR: 2.17, 3.13, 0.58, and 1.62; p = 0.02, <0.01, 0.03 and 0.03, respectively). Although high NLR was a negative predictive factor, IHLRT appeared to mitigate the negative prognostic impact of an elevated NLR. Conclusions: On-demand, selective IHLRT during Atez/Bev treatment is well tolerated and provides superior and more durable tumor control, particularly in patients achieving an initial objective response. Full article

Neoadjuvant strategies in head and neck squamous cell carcinoma (HNSCC) are reshaping therapeutic paradigms by shifting emphasis from anatomical staging toward biology-driven response stratification. The transition from induction chemotherapy to immune checkpoint–based and combination regimens has transformed the perioperative setting into a translational platform that enables interrogation of tumor–immune interactions and clonal selection under therapeutic pressure prior to surgery. In this context, pathological response assessment has emerged as a robust surrogate endpoint, overcoming the limitations of radiologic evaluation, which often fails to capture immune-mediated pseudoprogression and spatially heterogeneous regression. Quantification of residual viable tumor (RVT) provides a reproducible metric of therapeutic efficacy, while characterization of immune-related regression beds, tertiary lymphoid structures, macrophage polarization states, and compartment-specific nodal responses offers mechanistic insight into tumor clearance and resistance evolution. Evidence from phase II trials, single-cell sequencing, spatial transcriptomics, and multiplex immune profiling supports the prognostic relevance of pathology-driven endpoints. Integration of digital pathology and artificial intelligence–assisted image analysis further enhances reproducibility and enables high-resolution mapping of residual disease and immune architecture. Within this modern oncologic framework, the neoadjuvant-treated specimen functions as a dynamic biomarker platform guiding response-adapted surgical strategies and biomarker-driven clinical trial design. This study was designed as a narrative review. A structured literature search was performed using PubMed and major oncology journals to identify relevant studies on pathology-driven response assessment in neoadjuvant-treated head and neck squamous cell carcinoma. The review focused on publications addressing histopathological response criteria, immune microenvironment remodeling, spatial profiling technologies, and computational pathology approaches. Full article

Background: Neoadjuvant immunochemotherapy improves pathological response in resectable non-small cell lung cancer (NSCLC), but the need and intensity of postoperative adjuvant therapy across different pathological response rate (PRR) strata remain uncertain. Methods: In this single-center retrospective cohort, 105 patients with resectable NSCLC received neoadjuvant platinum-based chemotherapy with or without PD-1/PD-L1 inhibitors followed by R0 resection. PRR was defined as 1—residual viable tumor fraction and categorized as 0–60%, 60–90%, and ≥90% (major pathological response, MPR). Postoperative strategies included no further therapy, chemotherapy alone, or immunotherapy ± chemotherapy. Event-free survival (EFS) was analyzed using Kaplan–Meier estimates, multivariable Cox models, and restricted cubic spline-based treatment × PRR interaction. Results: Deeper PRR was associated with lower ypT/ypN stage and improved EFS. In the PRR 0–60% subgroup, immunotherapy-containing adjuvant regimens were associated with better EFS, whereas chemotherapy alone did not outperform observation. In the PRR 60–90% and MPR strata, EFS curves for different postoperative strategies largely overlapped, and in MPR patients, hazard ratios were close to 1. Interaction modeling suggested that the absolute 3-year EFS benefit of immunochemotherapy peaked at intermediate PRR (≈60–80%) and diminished as PRR approached ≥90%. Conclusions: The robustness of these findings was further confirmed through a sensitivity analysis focusing on a homogeneous cohort of clinical stage II-III patients receiving adjuvant therapy. Among NSCLC patients treated with neoadjuvant systemic therapy, PRR is a strong prognostic marker and modulates the benefit of postoperative immunotherapy. These data support a response-adapted strategy, with adjuvant immunotherapy intensification in low-PRR patients and potential de-escalation or surveillance alone in MPR patients, warranting validation in prospective PRR-stratified trials. Full article

Surgical resection of liver and lung metastases in breast cancer is increasingly considered a viable option for select patients with oligometastatic disease. Historically regarded as palliative, surgery is now supported by retrospective data suggesting potential survival benefits, particularly in patients with hormone receptor-positive or HER2-positive tumors, long disease-free intervals, and limited metastatic burden. This narrative review summarizes recent evidence on the surgical management of breast cancer metastases to the liver and lung, with a focus on patient selection, perioperative outcomes, and long-term survival. Liver metastasectomy has shown 5-year overall survival rates of up to 60% in well-selected patients, while pulmonary metastasectomy is associated with comparable outcomes when resection is complete and nodal involvement is absent. Minimally invasive techniques and non-surgical approaches, such as microwave ablation and stereotactic radiotherapy, expand treatment options for patients unfit for surgery. The review also explores emerging tools influencing surgical decision-making, including circulating tumor DNA for minimal residual disease detection, transcriptomic profiling to predict organotropism, and artificial intelligence (AI)-driven platforms that assist with surgical planning and multidisciplinary case evaluation. While prospective validation remains limited, these technologies may help redefine surgical candidacy through biologically informed algorithms. Ultimately, the integration of surgery within a multimodal, personalized treatment strategy—guided by systemic control, tumor biology, and evolving digital tools—represents an evolving and biologically informed direction for rigorously selected patients with visceral breast cancer metastases. Full article

Residual microcalcifications after neoadjuvant chemotherapy (NAC) in breast cancer remain a complex diagnostic and therapeutic challenge. Although NAC has significantly improved pathologic complete response (pCR) rates and transformed surgical approaches, the persistence or evolution of microcalcifications may not accurately reflect residual disease. This discrepancy complicates radiologic interpretation, impacts surgical decision-making, and may lead to overtreatment or unnecessary mastectomies. This review synthesizes current evidence on the radiologic–pathologic correlation of post-NAC microcalcifications, their prognostic value, and their relevance to guiding surgical management in contemporary precision oncology. A narrative review of the literature was performed, focusing on imaging evolution after NAC, pathologic correlations, predictive and prognostic implications, and the role of microcalcifications in defining optimal surgical strategies, ranging from breast-conserving surgery to mastectomy. Emerging contributions from digital breast tomosynthesis, contrast-enhanced mammography (CEM), Magnetic Resonance (MR) and radiomics are also examined. Studies consistently demonstrate that residual microcalcifications are often poor predictors of viable tumor tissue after NAC. Up to half of cases with persistent calcifications may reflect minimal or absent residual invasive cancer, whereas calcifications may also persist in areas of treatment-induced necrosis or fibrosis. Reliance on calcifications alone may therefore lead to unnecessary extensive resections. Conversely, specific morphologic patterns, especially fine pleomorphic or branching calcifications, are more strongly associated with residual malignancy. Advanced imaging and radiomics show promise in improving predictive accuracy. Residual microcalcifications after NAC should not be interpreted as a direct surrogate of residual disease. A multimodal assessment integrating imaging evolution, tumor biology, and treatment response is essential to optimize surgical planning and avoid overtreatment. Precision surgery in the NAC era increasingly requires individualized decision-making supported by advanced imaging and robust radiologic–pathologic correlation. Full article

Background and Objectives: Radiomics and artificial intelligence (AI) offer emerging quantitative tools for enhancing the diagnostic evaluation of testicular cancer. Conventional imaging—ultrasound (US), magnetic resonance imaging (MRI), and computed tomography (CT)—remains central to management but has limited ability to characterize tumor subtypes, detect occult nodal disease, or differentiate necrosis, teratoma, and viable tumor in post-chemotherapy residual masses. This systematic review summarizes current advances in radiomics and AI for both primary tumors and retroperitoneal disease. Materials and Methods: A systematic search of PubMed, Scopus, and Web of Science identified studies applying radiomics or AI to testicular tumors, retroperitoneal lymph nodes and post-chemotherapy residual masses. Eligible studies included quantitative imaging analyses performed on ultrasound, MRI, and CT, with optional integration of clinical or molecular biomarkers. Eighteen studies met inclusion criteria and were evaluated with respect to methodological design, diagnostic performance, and translational readiness. Results: Across modalities, radiomics demonstrated encouraging discriminatory capacity, with accuracies of 74–82% for ultrasound, 80.7–97.9% for MRI, and 71.7–85.3% for CT. CT-based radiomics for post-chemotherapy residual masses showed moderate ability to distinguish necrosis/fibrosis, teratoma, and viable germ-cell tumor, though heterogeneous methodologies and limited external validation constrained generalizability. The strongest performance was observed in multimodal approaches: integrating radiomics with clinical variables or circulating microRNAs improved accuracy by up to 12% and 15%, respectively, mirroring gains reported in other oncologic radiomics applications. Persisting variability in segmentation practices, acquisition protocols, feature extraction, and machine-learning methods highlights ongoing barriers to reproducibility. Conclusions: Radiomics and AI-enhanced frameworks represent promising adjuncts for improving the noninvasive evaluation of testicular cancer, particularly when combined with clinical or molecular biomarkers. Future progress will depend on standardized imaging protocols, harmonized radiomics pipelines, and multicenter prospective validation. With continued methodological refinement and clinical integration, radiomics may support more precise risk stratification and reduce unnecessary interventions in testicular cancer. Full article

PRMT5, a type II methyltransferase catalyzing symmetric dimethylation of arginine residues, has emerged as a promising therapeutic target in various cancers. However, the precise mechanism by which PRMT5 mediated the tumor immune microenvironment, particularly CD8⁺ T cell recruitment in cervical cancer remains elusive. Analysis of data from The Cancer Genome Atlas (TCGA) revealed elevated PRMT5 mRNA levels in cervical cancer tissues, which correlated with reduced immune cell infiltration and poorer patient prognosis. To further investigate the role of PRMT5 in tumor development, a CD8 knockout (KO) mouse tumor model was utilized. Significant inhibition of tumor growth was observed in cervical cancer using a mouse model lacking PRMT5. Notably, this antitumor effect was attenuated in CD8 KO mice lacking functional CD8⁺ T cells. Mechanistically, RNA sequencing (RNA-seq) analysis was conducted to explore how PRMT5 regulates immune cell recruitment. Disruption of PRMT5 was found to increase the secretion of chemokine CXCL10 by tumor cells. CXCL10 binds to its receptor CXCR3, thereby recruiting T cells to the tumor. Furthermore, in CXCR3 KO mice, PRMT5 knockdown failed to enhance T cell infiltration into tumors. These findings indicate that PRMT5 knockdown promotes CD8⁺ T cell recruitment to the tumor microenvironment via CXCL10 signaling. Furthermore, the therapeutic efficacy of the selective PRMT5 inhibitor EPZ015666 was evaluated in a cervical cancer xenograft mouse model. Treatment with EPZ015666 effectively suppressed tumor growth. In summary, these findings elucidate a novel mechanism whereby PRMT5 depletion in cervical cancer cells triggers a CXCL10-mediated chemotactic response, enhancing CD8⁺ T cell infiltration and restricting tumor progression. Thus, our study provides compelling evidence supporting the potential targeting of PRMT5 as a viable immunotherapeutic strategy for cervical cancer. Full article

Background/Objectives: Glioblastoma multiforme (GBM) is an aggressive primary brain tumor with limited therapeutic options. Neoantigen-based immunotherapy offers a promising avenue, but its efficacy primarily depends on the ability of somatic mutations to generate immunogenic peptides effectively presented by HLA class I molecules and recognized by cytotoxic T cells, in concert with innate immune mechanisms such as NK-cell activation and DAMP/PAMP signaling. This study aimed to characterize the MHC-I binding diversity of peptides derived from GBM-associated somatic variants, with a particular focus on interactions involving HLA-A68:01 and HLA-B15:01 alleles. These alleles were selected based on their ethnic prevalence and potential structural compatibility with neoepitopes. Methods: Somatic missense variants from TCGA-GBM were filtered using high-confidence genomic databases, including dbSNP, COSMIC, and MANE. Neoepitope prediction was performed across multiple HLA class I alleles using binding affinity algorithms (MHCflurry2). Peptide–HLA interactions were characterized through motif analysis and anchor residue enrichment. Structural modeling of peptide–HLA complexes was conducted using ColabFold (AlphaFold2-multimer v3) to evaluate conformational stability. The population frequency of selected HLA alleles was examined through epidemiological comparisons. Results: Canonical GBM driver mutations (e.g., EGFR, TP53, PIK3R1) are recurrent and biologically relevant, although pharmacological inhibition of EGFR alone has not consistently improved patient outcomes, underscoring the complex signaling redundancy in glioblastoma. HLA-A68:01 exhibited high binding affinity and favorable motif compatibility, supporting its potential for effective neoantigen presentation. HLA-B15:01 was identified as a viable presenter for the EGFR p.Arg108Lys variant. Structural modeling confirmed stable peptide insertion into the MHC-I binding groove, with high-confidence folding and preserved interface integrity. Ethnic distribution analysis revealed varying GBM incidence across populations expressing these alleles. Conclusions: This integrative analysis identified structurally validated, immunogenically promising neoantigens derived from GBM mutations, particularly for HLA-A68:01 and HLA-B15:01. These findings support allele-informed neoepitope prioritization in personalized immunotherapy, especially for patient populations with corresponding HLA genotypes and MHC-I presentation capacity. Full article

Esophageal cancer (EC) continues to pose a major global health burden, ranking as the ninth most common malignancy and sixth leading cause of cancer mortality, with over 600,000 new cases and 500,000 deaths annually as of 2025. While esophagectomy has long been the standard for curative intent in resectable disease, organ preservation strategies have advanced significantly, offering viable alternatives for patients with locally advanced esophageal squamous cell carcinoma (ESCC) or those unsuitable for surgery due to comorbidities. These approaches encompass definitive chemoradiotherapy (dCRT), neoadjuvant chemoradiotherapy (nCRT) followed by active surveillance (“watch-and-wait”), and innovative integrations of immunotherapy and targeted therapies. This narrative review synthesizes evidence from recent clinical trials, systematic reviews, and international guidelines up to 2025, demonstrating that organ-sparing protocols can achieve comparable overall survival (OS) rates—often exceeding 50% at 5 years in selected cohorts-while substantially enhancing quality of life (QoL) by preserving esophageal function. For instance, the SANO trial (2025) confirmed non-inferiority of active surveillance post-nCRT, with 2-year OS of 74% versus 71% for standard surgery. Key challenges include imprecise response assessment, locoregional recurrences (20–30%), and treatment-related toxicities such as esophageal strictures. Emerging trials like ESOSTRATE and PALACE3 are evaluating immunotherapy-enhanced regimens, potentially expanding organ preservation to esophageal adenocarcinoma (EAC). With genomic biomarkers and novel modalities like proton therapy, personalized organ preservation promises to broaden applicability, reduce morbidity, and improve outcomes across histological subtypes. Additionally, recent studies emphasize the role of liquid biopsies, such as circulating tumor DNA (ctDNA), in monitoring treatment response and guiding surveillance, potentially reducing the need for invasive procedures and improving detection of minimal residual disease. The aim of this review is not only to summarize recent trials but to synthesize them into an operational framework that clinicians and researchers can apply: a decision algorithm for selecting organ preservation candidates. This is the novel element that distinguishes this work from prior narrative reviews. Full article

Background: There is little evidence available regarding the long-term tumor response after transarterial radioembolization (TARE) for hepatocellular carcinoma (HCC). Aim: To identify preprocedural predictive factors for achieving a 5-year complete response (CR) following TARE in patients with HCC. Methods: This retrospective study included 37 patients with treatment-naïve HCC who underwent TARE between January 2016 and December 2019 and were followed for at least 5 years. Tumor characteristics—including maximum diameter, number of main lesions, presence of satellite nodules, and portal vein thrombosis—were evaluated using preprocedural liver dynamic magnetic resonance imaging. Treatment response was assessed according to the modified Response Evaluation Criteria in Solid Tumors. Multivariate logistic regression analyses were performed to identify factors associated with tumor response following TARE. Results: Thirty-seven patients (median age, 64 years) were categorized into two groups: (1) the CR group (n = 9), consisting of patients without tumor recurrence for 5 years and without additional treatment; and (2) the non-CR group (n = 28), consisting of patients who required additional treatment because of residual or recurrent viable tumors. Tumors in the non-CR group had significantly larger diameters compared with those in the CR group (9.8 cm vs. 5.9 cm, p = 0.006). In multivariable analysis, a tumor diameter > 7 cm was the only factor significantly associated with tumor recurrence (odds ratio = 21.277, p = 0.010). Portal vein thrombosis did not reach statistical significance (odds ratio = 9.779, p = 0.063). Conclusions: Tumor diameter > 7 cm is a significant predictor of tumor recurrence within 5 years after TARE for HCC. This finding may support a more individualized post-TARE management approach, potentially allowing clinicians to avoid overtreatment and adopt a watchful waiting strategy for selected patients. Full article