Search Results (5,913)

Colorectal cancer (CRC) is one of the most common malignancies worldwide, and liver metastasis remains a major contributor to poor prognosis and treatment failure. Increasing evidence indicates that the gut–liver axis plays a critical role in colorectal cancer liver metastasis (CRLM) by linking intestinal microbial alterations with hepatic microenvironmental remodeling. Gut dysbiosis and intestinal barrier disruption facilitate the translocation of microbial components and metabolites through the portal circulation, contributing to hepatic immune remodeling, extracellular matrix alteration, and the establishment of a pre-metastatic niche favorable for tumor colonization. During metastatic progression, specific tumor-associated microorganisms may further promote circulating tumor cell (CTC) survival, immune evasion, and metastatic adaptation, while intratumoral microbiome alterations and metabolic reprogramming may influence tumor growth and therapeutic responses. This review summarizes the current understanding of gut–liver axis-mediated regulation of CRLM, focusing on intestinal barrier dysfunction, microbial translocation, hepatic pre-metastatic niche formation, tumor cell–microbiota interactions, and emerging clinical applications. Unlike previous reviews that have primarily focused on gut microbiota alterations in colorectal carcinogenesis, this review emphasizes the contribution of gut-derived microbial signals to liver-specific metastatic evolution. In addition, we discuss current challenges, including limited human causal evidence, technical issues in low-biomass microbiome analysis, and the need for longitudinal clinical validation. Future integration of spatial multiomics, prospective cohorts, and personalized microbiome-based interventions may provide new opportunities for early risk prediction and precision management of CRLM. Full article

Poly(ADP-ribose) polymerase inhibitors (PARPis) have transformed the treatment landscape of homologous recombination-deficient malignancies, particularly BRCA1/2-mutant breast, ovarian, pancreatic, and prostate cancers. In contrast, clinical studies evaluating PARPis in broadly selected colorectal cancer (CRC) patients have yielded disappointing outcomes despite evidence that a subset of CRCs harbor DNA damage response (DDR) defects and homologous recombination deficiency (HRD)-associated mutational signatures. These observations highlight the need for improved patient stratification and the development of strategies to enhance PARPi sensitivity in CRC. In this review, we integrate CRC-specific evidence with mechanistic and preclinical findings from other malignancies and discuss candidate biomarkers associated with PARPi responsiveness, including TP53, RAD51, and MRE11, and examine their potential utility in identifying CRC patient populations most likely to benefit from PARP inhibition. We further summarize therapeutic approaches aimed at inducing “BRCAness” and sensitizing CRC cells to PARPis through epigenetic modulation, targeting cell-cycle checkpoint regulators, inhibiting growth factor signaling pathways, and exploiting metabolic vulnerabilities. Emerging strategies involving polyamine inhibition and modulation of NAD+ metabolism have been specifically highlighted for their potential role in therapeutic response. Collectively, these approaches provide a framework for investigating mechanistically compelling opportunities to overcome intrinsic and acquired resistance to PARPis and expand the clinical utility of DDR-targeted therapies in CRC. A deeper mechanistic understanding of PARPi response and resistance, in addition to extensive investigations in CRC-specific models and molecularly selected clinical cohorts, will facilitate the development of biomarker-driven combination therapies and improve outcomes for patients with CRC. Full article

Background: Rising survival rates have created a growing population of childhood cancer survivors (CCSs) who have an increased risk of late effects and require long-term follow-up (LTFU) care. Existing services are often fragmented and may not reflect survivors’ priorities; optimizing such care requires understanding not only the self-reported burden of late effects and their impact on daily lives but also survivors’ information status and their preferences for future care. Methods: Survivor Deutschland e.V. conducted a nationwide cross-sectional online survey assessing the current late effects, daily-life impairments, subjective information statuses, current follow-up structures, and preferences for future LTFU care. A total of 339 CCSs were included, covering all childhood cancer entities, most frequently leukemia (30.7%), central nervous system tumors (18.3%), and lymphoma (16.5%). Data were analyzed descriptively and supplemented by paired non-parametric analyses. Results: Overall, 74.3% (252/339) reported at least one late effect. Self-rated limitations in daily life had a median of five (Q1–Q3 3–7) on a 1–10 scale, which increased with the number of reported late effects. The most frequently affected domains were endocrine (36.3%, n = 123), fertility (33.6%), psychological (30.4%, n = 103), neurocognitive (26.0%, n = 88), and orthopedic (24.8%, n = 84) problems. A majority (69.3%, n = 235) knew that late effects existed yet felt insufficiently informed, and 4.4% only learned of these through the survey. Among 172 survivors in adult follow-up care, only 26.8% (46/172) reported access to structured, specialized LTFU care, whereas 56.4% (97/172) preferred this model. Survivors rated the importance of LTFU care highly (median 9/10) but rated satisfaction with their current care as much lower (median 3/10). The most valued components were the coverage of follow-up costs, sufficient consultation time, a dedicated contact person, and clear communication of results. Psychological support was a notable gap (5.8%, 10/172 current access vs. 17.9% 31/172 preferred), and 84.1% were willing to travel up to two hours or more for high-quality care. Conclusions: German CCSs report a high late-effect burden, meaningful impairment of their daily lives, a pronounced information gap, and substantial unmet care needs. These patient-centered findings support structured, risk-adapted LTFU with proactive information, integrated psychological support, and sustainable financing at specialized LTFU centers. Full article

Repeated mixed-munition demolition may require explosive ordnance disposal personnel to re-enter a common demolition pit to inspect effects, recover debris and prepare subsequent stacks. Dinitrotoluene (DNT) is a recognised explosive ordnance occupational toxicant absorbed by inhalation, skin and ingestion. Urinary-tract malignancies and other adverse outcomes have been reported in highly exposed nitroaromatic-explosives workers. Recently, bladder-cancer incidence was documented as elevated among former British Army ammunition technicians. While these observations do not establish a causal relationship with DNT, they however provide a strong rationale for further investigation of credible exposure pathways. This study developed a scenario-based source-pathway-receptor model to examine whether residual DNT could constitute an occupational exposure source during these tasks. This model was applied to an explosive ordnance disposal operation involving 20 sequential demolitions and a documented aggregate TNT-equivalent basis of 1000 kg, used as a screening proxy because the operational inventory was predominantly TNT-filled. The model identified plausible primary inhalation from a blast-generated plume and secondary inhalation from resuspended residues, together with dermal and incidental-ingestion pathways. An important caveat is that it does not reconstruct individual dose or establish disease causation. Validation requires time-resolved post-blast and task-based personal air sampling, surface assessment, biomonitoring and detailed exposure reconstruction during representative demolition operations. As such, this study establishes crucial foundational hypotheses for future occupational hazard research into DNT exposure to explosive ordnance disposal personnel. Full article

Background: Racial and socioeconomic differences in prostate cancer outcomes are often described as survival disparities, but observed differences may also reflect healthcare access, treatment delivery, and resource allocation. Methods: NCDB and SEER–Medicare were treated as independent, complementary retrospective data sources without individual-level linkage. The analytic material comprised 111,396 database records from 2010 to 2020 across two independent source files; this is a cross-source record count, not a deduplicated count of unique persons. Harmonized descriptive analyses characterized stage, treatment, and treatment timing, while multivariable Cox proportional hazards modeling evaluated prostate cancer-specific survival (CSS) in outcome-eligible SEER–Medicare records. The CSS model denominator is therefore substantially smaller than the total record count, and the two should not be confused. Results: Records for non-Hispanic Black (NHB) men more often showed stage III–IV disease than records for non-Hispanic White (NHW) men (26.9% vs. 18.7%) and lower receipt of guideline-concordant first-course management initiated within 90 days, particularly in the low-SES subgroup (51.4% vs. 84.3% among high-SES NHW men). In the adjusted CSS model, NHB race was associated with higher mortality (HR = 1.32; 95% CI: 1.24–1.41). Uninsured status (HR = 1.47; 95% CI: 1.33–1.62), low income (HR = 1.28; 95% CI: 1.19–1.37), and rural residence (HR = 1.14; 95% CI: 1.06–1.22) were also associated with higher mortality. Conclusions: The findings support a healthcare-system interpretation of prostate cancer disparities and identify measurable targets for prospective evaluation, including EHR-enabled monitoring, nurse navigation, telehealth-supported follow-up, and facility-level treatment-concordance review. Full article

Hepatocellular carcinoma (HCC) is the most common primary liver malignancy and a leading cause of cancer-related mortality worldwide. Despite advances in diagnosis and therapy, the prognosis for advanced HCC remains poor due to late-stage diagnosis, high recurrence rates, therapeutic resistance, and pronounced molecular heterogeneity. HCC development is driven by complex somatic gene alterations, epigenetic reprogramming, dysregulated signaling pathways, metabolic changes, and an immunosuppressive tumor microenvironment. Molecular profiling studies have identified key oncogenic pathways involved in HCC progression, including MAPK/ERK (mitogen-activated protein kinase/extracellular signal-regulated kinase), Wnt/β-catenin, PI3K/AKT/mTOR (Phosphoinositide 3-kinase/Protein Kinase B/mechanistic Target of Rapamycin), Hippo-YAP/TAZ, (Yes-associated protein/transcriptional co-activator with PDZ-binding motif) cell cycle regulators, and p53-mediated tumor suppression. These pathways coordinate critical cellular processes such as proliferation, survival, metabolism, invasion, and genomic stability. Emerging mechanisms, including cancer stem cell plasticity, immune evasion, epigenetic dysregulation, and steroid receptor coactivator (SRC)-dependent transcriptional regulation, further contribute to tumor progression and therapeutic resistance. Additionally, recent bioinformatic analyses suggest a potential role for progesterone-mediated oocyte maturation pathways in HCC, although their functional relevance remains unclear. A thorough understanding of these interconnected mechanisms could lead to novel therapeutic targets and the development of more effective, personalized treatment strategies for HCC. This review discusses key signaling pathways and emerging mechanisms in HCC and their roles in disease development and treatment. Full article

Background: Cancer survivors are at increased risk for developing subsequent cancers, including HPV-associated cancers, compared to the general population. However, evidence regarding the receipt of HPV vaccination and cancer diagnosis status is limited. Methods: We analyzed 2019 and 2022 National Health Interview Survey data, focusing on adults aged 18–45 years who were eligible for HPV vaccination. We performed descriptive statistics and evaluated associations using survey-weighted bivariable and multivariable logistic regression to assess the association between a personal history of any cancer diagnosis and receipt of HPV vaccination, adjusting for sociodemographic and behavioral factors. Results: Among 20,917 participants (mean [SD] age (years): 31.41 [13.58]), 489 (2.0%) were cancer survivors; 99 (19.3%) received HPV vaccination. Among 20,423 adults without a cancer diagnosis, 5317 (27.8%) had received HPV vaccination. Five participants had missing data on cancer history. Cancer survivors had significantly lower odds of HPV vaccination compared to adults without a personal cancer history (Adjusted Odds Ratio [aOR]: 0.67, 95% CI: 0.52–0.87, p = 0.003). Living in non-metro areas (aOR: 0.77, 95% CI: 0.66–0.89, p < 0.001), smokers [current (aOR: 0.82, 95% CI: 0.71–0.94, p = 0.005), and former (aOR: 0.75, 95% CI: 0.67–0.84, p < 0.001)], non-US-born (aOR: 0.54, 95% CI: 0.47–0.61, p < 0.001), uninsured (aOR: 0.60, 95% CI: 0.52–0.69, p < 0.001) had significantly lower odds of receiving HPV vaccination. Those who were 18–26 years (aOR: 5.49, 95% CI: 4.73–6.37, p < 0.001), non-Hispanic others (aOR: 1.40, 95% CI: 1.11–1.75, p = 0.004), females (aOR: 3.18, 95% CI: 2.84–3.56, p < 0.001), higher education [some college/bachelor’s education (aOR: 1.57, 95% CI: 1.41–1.74, p < 0.001), and graduate degree/professional scholar (aOR: 1.91, 95% CI: 1.65–2.22, p < 0.001)], living in rented housing (aOR: 1.18, 95% CI: 1.08–1.29, p < 0.001) had significantly higher odds of receiving HPV vaccination. Conclusions: HPV vaccination uptake is low among cancer survivors. Targeted interventions such as strong oncologists’ recommendations, patient reminders, and care coordination between oncology and primary care professionals are needed to increase HPV vaccination uptake in this population. Full article

Surface-Enhanced Raman Spectroscopy (SERS) has emerged as a powerful analytical platform for breast cancer (BC) detection, offering ultrasensitive, multiplexed, and label-free molecular recognition. However, despite the rapid expansion of the field, no prior study has combined quantitative bibliometric mapping with a cluster-validated technical and translational synthesis, limiting a comprehensive understanding of the field’s structure, evolution and clinical projection. In this review, a PRISMA-guided bibliometric analysis was conducted; 199 articles on SERS-based BC detection (2016–2025) were retrieved from SCOPUS, Web of Science and Google Scholar, mapping publication trends, keyword co-occurrence networks (VOSviewer), and Multiple Correspondence Analysis (MCA) with hierarchical clustering on principal components. The results reveal sustained growth in scientific output, led by Asia, North America, and Europe. The 20 most-cited articles (271 citations maximum) showed a shift from substrate optimization toward AI-assisted liquid biopsy platforms. MCA identified five clusters, corroborated by the co-occurrence network: (1) nanostructured platforms for diagnosis; (2) biofunctionalization strategies; (3) liquid biopsy approaches targeting exosomes, circulating tumor cells, and alternative biofluids; (4) diagnostic interpretation based on chemometrics, machine learning (ML) and artificial intelligence (AI); and (5) translational achievements in preclinical and clinical studies. Each cluster was anchored by a technical sub-analysis of its landmark studies, an integration largely absent from prior SERS reviews. This framework clarifies the field’s trajectory and positions SERS as a key technology for non-invasive, personalized diagnostics in precision oncology. Full article

Background/Objectives: Circular RNAs (circRNAs) are emerging regulators of genetic information that share the spliceosome biogenesis pathway with messenger RNAs (mRNAs), influencing their expression. There is an increasing body of evidence supporting their role in colorectal cancer (CRC) tumorigenesis. This study explored circRNAs in two distinct CRC tumorigenesis pathways: microsatellite instability (MSI) and microsatellite stability (MSS). We investigated competition between mRNA and circRNAs from their host genes, which could potentially disrupt normal gene regulation, and examined specific patterns of alterations in MSS and MSI tumors. Methods: Circular (circ) and linear (lin) exon–exon junctions were quantified using exon-specific probes targeting 48 genes involved in CRC predisposition and tumorigenesis processes. RNA was extracted from colorectal FFPE samples (stage 1 to 4 adenocarcinomas and adenomas). MSS tumors (MSS-TTs) and adjacent normal tissue (MSS-NT) were selected from 21 patients with a severe personal or family history of cancer. MSI tumors (MSI-TTs) and adjacent normal tissue (MSI-NT) were selected from 16 patients. Muscle content was also investigated as a potential confounding factor. Results: Principal component analysis distinguished NT from TT samples based on the sums of circular and linear junctions. CircRNA abundance was higher in samples with an elevated muscle content (Kruskal–Wallis test p-value = 0.034). Linear regression, adjusted for muscle content, showed significantly reduced global circRNA levels in tumors compared to in healthy tissues (MSI and MSS combined, p-value = 0.00268). In the MSS group, significant differences were observed between MSS-NT and MSS-TT in terms of circ/lin ratios and linear and circular junction counts for specific genes. MSI analysis revealed distinct gene profiles, with significant differences only in linear junction counts. Conclusions: Our results do not suggest competition between the circRNAs and mRNAs of the key oncogenic genes that we investigated, but they do reveal differences in circRNA/mRNA expression patterns within normal and tumor tissues. Full article

Background/Objectives: A cancer diagnosis forces a rapid, often unwelcome reorganization of a patient’s sense of self, routines, and future plans, and patients vary considerably in how far they progress toward accepting that new reality. Personality is a candidate explanation for this variability, and although the Five-Factor Model has been linked to cancer-related distress and coping in several large cohorts, its relationship to illness acceptance specifically, alongside disease duration, treatment self-assessment, and perceived social support, has not been jointly examined in a single, diagnostically broad oncology sample. Methods: We surveyed 114 outpatients with a confirmed malignant tumor diagnosis, combining a study-specific questionnaire with the NEO-Five-Factor Inventory (NEO-FFI) and the Acceptance of Illness Scale (AIS). Because several study variables were non-normally distributed and the study-specific measures were ordinal, associations were examined using Spearman’s correlation, the Kruskal–Wallis H test, and the Mann–Whitney U test. Results: Illness acceptance was moderate on average (mean [M] = 26.55, standard deviation [SD] = 7.34); 22 patients (19.30%) were classified as having low acceptance, 76 (66.67%) as average acceptance, and 16 (14.04%) as high acceptance. All five personality domains correlated with acceptance, led by a strong negative association with neuroticism (ρ = −0.632, p < 0.001) and moderate positive associations with extraversion, agreeableness, conscientiousness, and openness to experience (all p < 0.001). Longer disease duration and a more favorable self-rated treatment outcome were both associated with higher acceptance, and patients who felt supported by close relatives scored higher than those who found support difficult to gauge. Conclusions: Personality traits, particularly neuroticism, were associated with illness acceptance. Brief psychosocial assessment may help identify patients reporting greater difficulties in psychological adjustment to cancer. Full article

Nutrition is an essential component of colorectal cancer (CRC) care, influencing treatment tolerance, functional status, and quality of life, yet it remains inconsistently integrated into practice. This study examined experiences with nutrition management and gaps in nutrition care among patients with CRC, caregivers, and healthcare professionals across Canada through a multi-center, cross-sectional survey conducted from July 2025 to February 2026. A total of 243 participants completed the survey, including 121 patients, 45 caregivers, and 77 healthcare professionals. Among patients, 51.2% reported that nutritional status was discussed or assessed during treatment, while 24.0% reported it was never discussed. More than half of patients (55.4%) said they did not receive adequate information regarding weight loss during treatment. Caregivers described substantial nutrition impact symptoms and identified a need for clearer guidance, emotional support, and improved access to dietitians. Healthcare professionals rated nutrition care as highly important yet reported barriers to effective delivery, including limited staffing, lack of standardized screening, and reactive care processes. Across groups, respondents emphasized the importance of timely, personalized, and culturally relevant nutrition care. Overall, nutrition remains insufficiently embedded in CRC care, highlighting the need for routine screening, standardized referral pathways, earlier intervention, and integrated patient-centered nutrition care models to improve CRC care. Full article

Immune checkpoints (ICPs) are essential regulators of immune homeostasis, maintaining the balance between effective immune responses and tolerance to self-antigens. Dysregulation of ICP signaling may contribute to impaired immune surveillance, immune evasion, chronic inflammation, autoimmunity, persistent infections, and tumor progression. Consequently, ICP molecules are increasingly recognized not only as therapeutic targets but also as potential diagnostic, prognostic, predictive, and treatment-monitoring biomarkers. This review provides a comprehensive overview of the biological functions, signaling mechanisms, and clinical significance of major co-inhibitory and co-stimulatory ICP pathways, including PD-1/PD-L1/PD-L2, CTLA-4/CD28/CD80/CD86, LAG-3, TIM-3, TIGIT, BTLA, VISTA, ICOS, OX40, 4-1BB, GITR, CD27, CD40, and CD2, together with their corresponding ligands. Particular emphasis is placed on their biomarker potential in cancer and immune-mediated diseases. In addition, the review presents a bioinformatic characterization of ICP receptors and ligands based primarily on data available in UniProtKB and complementary bioinformatic resources. The analysis includes protein sequence length, molecular weight, theoretical isoelectric point, amino acid composition, subcellular localization, conserved and functional domains, protein family classification, post-translational modifications, isoforms, and selected structural features. Collectively, the available evidence indicates that ICPs constitute a structurally and functionally diverse group of immunoregulatory molecules with substantial biomarker potential. Integrating their molecular, structural, functional, and bioinformatic characteristics may improve disease classification, prognosis, patient stratification, treatment selection, and therapeutic monitoring. Such an integrated approach may also support the identification of novel biomarkers and therapeutic targets and contribute to the further development of precision and personalized medicine. Full article

Background/Objectives: Molecular classification has reshaped risk assessment in endometrial cancer (EC), but the strength and clinical applicability of the evidence vary across molecular subgroups, assay platforms, patient populations, and treatment settings. This systematic review critically evaluated the prognostic and predictive value of TCGA-derived classifiers, additional biomarkers, multiple-classifier tumors, and molecularly informed therapeutic strategies. Methods: A protocol was developed a priori but was not prospectively registered. PubMed/MEDLINE, Embase, Scopus, Web of Science, and the Cochrane Library were searched for primary studies published from January 2013 through June 2026. Clinical guidelines were used only to provide clinical context and were not included in the formal evidence set. Because of substantial methodological heterogeneity, findings were synthesized narratively by study design and clinical question. Risk of bias was assessed using QUADAS-2, the Newcastle–Ottawa Scale, and RoB 2. Results: Seventy-four studies involving approximately 42,000 patients were included. POLE-mutated tumors showed the most favorable outcomes in most cohorts, whereas p53-abnormal tumors, defined by abnormal immunohistochemical patterns, generally had the poorest prognosis. Mismatch repair deficiency identified by immunohistochemistry and microsatellite instability-high status identified by PCR- or NGS-based testing were highly related but analytically distinct biomarkers and were not treated as exact synonyms. The NSMP group remained heterogeneous; integrated assessment of estrogen/progesterone receptor expression, CTNNB1, L1CAM, ARID1A, and chromosome 1q alterations may improve risk discrimination, although most of these markers remain investigational. In multiple-classifier tumors, available data support a practical hierarchy in which a pathogenic POLE mutation generally takes precedence, followed by MMR deficiency and then p53 abnormality. Across studies, molecular classification usually added prognostic information to clinicopathologic assessment, but the magnitude of benefit varied, and no overall certainty rating was assigned. Conclusions: Molecular classification is incorporated into contemporary guidelines and can support prognostic assessment and treatment selection when interpreted together with stage, histology, and other clinicopathologic factors. The strongest current clinical utility relates to POLE, MMR/MSI, p53 immunohistochemistry, and HER2 in selected settings; additional NSMP and multi-omics biomarkers require prospective validation, assay standardization, and demonstration of clinical utility before routine adoption. Full article

Background: Colorectal cancer is the third most commonly diagnosed cancer in the world. Liver metastases are frequent, adversely affecting patient prognosis. We compared progression-free survival and overall survival in colorectal cancer patients with liver metastasis treated with surgical resection or stereotactic body radiotherapy. No previous study had shown superiority of one treatment option over the other. Methods: We conducted a retrospective cohort study of 40 colorectal cancer patients with liver metastasis treated with surgical resection or stereotactic body radiotherapy at the Hebrew University-Hadassah Medical Center. Patient demographics, tumor characteristics, treatment details, and survival outcomes were analyzed. Kaplan–Meier curves and log-rank tests were used for survival analysis. Results: The median overall survival for the entire cohort was 44 months (95% CI 29–59 months). In patients treated with surgical resection, the median overall survival was 51 months (95% CI: 36–67 months), while in patients treated with stereotactic body radiotherapy the median overall survival was 32 months (95% CI: 21–43 months), a non-statistically significant result (p = 0.306). The number of lobes involved did not significantly impact overall survival (p = 0.214). Additionally, it did not significantly affect progression-free survival (p = 0.41). Liver metastases located in the left lobe led to considerably worse progression-free survival compared to other regions involved, specifically in the patients who underwent surgery. Conclusions: Our findings underscore the importance of personalized treatment strategies tailored to the distinct characteristics of colorectal cancer patients with liver metastasis. Currently, surgical resection remains the standard of care. Further research is warranted to address the possibility of extending SBRT to first-line treatment in selected unresectable patients. Full article

Persistent infection with high-risk human papillomavirus (hrHPV) is the principal cause of cervical cancer and initiates a complex process of immune evasion that enables malignant progression despite continuous expression of the viral oncoproteins E6 and E7. Effective antitumor immunity depends on coordinated antigen presentation through human leukocyte antigen class I (HLA-I) molecules, activation of CD8⁺ cytotoxic T lymphocytes, and balanced regulation of immune responses. During cervical carcinogenesis, these mechanisms are progressively disrupted through HLA-I downregulation, CD8⁺ T-cell exhaustion, expansion of FOXP3⁺ regulatory T cells, and activation of the PD-1/PD-L1 and CTLA-4 immune checkpoint pathways, ultimately establishing an immunosuppressive tumor microenvironment that promotes immune escape. This narrative review integrates current evidence on HLA-I-mediated antigen presentation, CD8⁺ cytotoxic T-cell function, FOXP3⁺ regulatory T cells, and immune checkpoint signaling into a unified model of immune escape during cervical carcinogenesis. In addition, it discusses the clinical implications of these interconnected mechanisms, including immune checkpoint inhibition, emerging therapeutic strategies, integrated immune profiling, and future directions in personalized immunotherapy. A comprehensive understanding of the interactions between antigen presentation, immune-cell function, and immune checkpoint regulation provides the biological foundation for current and future immunotherapeutic approaches. Integrating molecular, cellular, and spatial immune characteristics may improve patient stratification, optimize treatment selection, and facilitate the implementation of precision immuno-oncology in cervical cancer. Full article