Search Results (4,889)

Background: Computed tomography-based body composition parameters are emerging prognostic markers in pancreatic cancer. While sarcopenia and myosteatosis have been widely studied, the prognostic significance of ectopic fat deposition within the psoas muscle remains unclear. We aimed to evaluate the prognostic impact of the fat ratio within the psoas muscle (FRPM) in patients with stage IV pancreatic cancer receiving first-line systemic chemotherapy. Methods: This retrospective cohort study included 99 patients with stage IV pancreatic cancer treated with first-line chemotherapy. Baseline CT images at the L3 level were analyzed, and FRPM was calculated as the proportion of intramuscular fat to total psoas muscle area. FRPM was analyzed primarily as a continuous variable. Exploratory low- and high-FRPM groups were defined using sex-specific medians for descriptive comparisons and Kaplan–Meier analyses. Overall survival (OS) and progression-free survival (PFS) were assessed using Kaplan–Meier and Cox regression analyses. Multivariable models were adjusted for age, sex, ECOG performance status, liver metastasis, and C-reactive protein (CRP). Results: Among 99 patients, 48 were categorized as having low FRPM and 51 as having high FRPM based on exploratory sex-specific median-based groups. Higher FRPM correlated with older age and higher BMI and inversely correlated with psoas muscle size and PMI. Median OS was 9.76 months in the low-FRPM group versus 5.78 months in the high-FRPM group, and median PFS was 5.29 versus 3.68 months. In the main multivariable Cox model, higher FRPM was associated with worse OS when analyzed as a continuous variable and reported per 1-standard deviation increase (adjusted HR: 1.43, 95% CI: 1.08–1.91, p = 0.014). After additional adjustment for first-line treatment-regimen category, the association remained directionally consistent but did not retain conventional statistical significance (adjusted HR: 1.32, 95% CI: 0.99–1.77, p = 0.060). Conclusions: Higher FRPM was associated with shorter OS and PFS in patients with stage IV pancreatic cancer receiving first-line systemic chemotherapy. These findings suggest that ectopic fat deposition within the psoas muscle may represent a potential CT-based muscle-quality marker associated with adverse prognosis. External validation and comparison with conventional adiposity parameters are required before clinical application. Full article

Background/Objectives: Allomyrinasin is a cationic antimicrobial peptide derived from Allomyrina dichotoma larvae with known antibacterial and anti-inflammatory properties; however, its effects on migration-related mechanisms in oral squamous cell carcinoma (OSCC) remain poorly understood. This study investigated the anti-migratory potential of allomyrinasin in OSCC cells, focusing on Na⁺/HCO₃⁻ cotransporter (NBC) activity as a key migratory module. Methods: NBC activity was assessed in YD-38 OSCC cells treated with allomyrinasin. Cell migration was evaluated by wound healing and Transwell assays, and MMP expression. Intracellular reactive oxygen species (ROS), apoptosis-related markers, and lamin A/C expression were analyzed using fluorescence-based assays and gene expression analysis. Results: Allomyrinasin inhibited NBC activity and suppressed cell migration without substantial loss of cell viability. MMP-13 was selectively downregulated among the tested MMPs. Lamin A/C expression was markedly upregulated, suggesting enhanced nuclear stiffness that may restrict confined cell migration. Intracellular ROS levels were elevated, and apoptotic progression was confirmed by increased Annexin V/PI positivity along with downregulation of B-cell lymphoma 2 (BCL2) and upregulation of BCL-2–associated X genes (BAX), through a p53-independent pathway consistent with the TP53-deleted status of YD-38 cells. Conclusions: Allomyrinasin suppresses OSCC cell migration by targeting NBC activity as a key component of the migratory machinery, accompanied by oxidative stress induction and pro-apoptotic signaling. These findings identify allomyrinasin as a potential anti-migratory therapeutic candidate and highlight NBC activity as a promising target for attenuating cancer metastasis. Full article

Background: Aging profoundly alters host immunity, yet how age-associated immune changes in the liver influence the growth of metastatic tumors remains incompletely understood. Liver metastasis is a major cause of cancer-related mortality, particularly in elderly patients, for whom aggressive treatments are often not feasible. This study aimed to clarify how aging reshapes the hepatic immune microenvironment and to identify age-associated host factors that influence liver metastasis growth. Methods: Tumor-naïve and tumor-bearing young and aged mice were analyzed using a syngeneic MC38 liver metastasis model. Immune cell composition in the liver was assessed by flow cytometry, and gene expression was evaluated by quantitative reverse transcription PCR (RT–qPCR). Public transcriptomic datasets were screened to identify age-associated inflammatory factors. The functional relevance of the S100A8/A9 axis was examined using the small-molecule inhibitor paquinimod. Results: Aging was associated with a distinct baseline immune cell composition in the liver. During liver metastasis, overall growth was comparable between young and aged mice; however, metastatic lesions in aged hosts showed increased expression of multiple inflammation-related genes and prominent accumulation of Ly6G⁺ cells. In silico screening identified S100a9 as one of the most highly upregulated inflammation-related genes in aged livers, which was confirmed in both tumor-naïve and metastatic liver tissues. Pharmacological modulation of the S100A8/A9 axis with paquinimod significantly reduced liver metastasis growth in aged, but not young, mice, and was accompanied by a shift in immune cell composition, including an increased representation of CD8⁺ T cells. Conclusions: These findings indicate that aging is associated with a distinct hepatic immune context that shapes the inflammatory and cellular composition of the tumor microenvironment during liver metastasis. S100A9 emerges as a key age-associated, host-derived factor that is functionally relevant to the growth of liver metastases in aged hosts, supporting the S100A8/A9 axis as a context-specific therapeutic target. Full article

Background/Objectives: Conventional assessments of lymphatic invasion in the primary tumor may fail to identify lymph node metastasis (LNM) in breast cancer. We evaluated periarterial or perivenous invasion (periA/V), using Elastica–van Gieson (EVG)-stained sections, as a histological marker associated with LNM in invasive breast carcinoma of no special type (IBC-NST), focusing on the impact of invasive tumor size. Methods: We retrospectively analyzed 213 IBC-NST cases. PeriA/V was defined as tumor nests in direct contact with perivascular elastic fibers on EVG-stained sections. Diagnostic performance was compared with that of conventional LI markers (hematoxylin and eosin and D2-40), with stratified analyses by pathological T category (pT1 vs. pT2–4) and pT1 subcategories (pT1a, pT1b, and pT1c). Results: LNM was observed in 87 cases (40.8%). Overall, periA/V demonstrated high sensitivity (97.7%) and negative predictive value (NPV; 93.5%). In pT1 tumors (n = 130), periA/V achieved 100% sensitivity and 100% NPV (27/27), and was consistently present in all node-positive pT1b–c tumors. In multivariate analyses, periA/V remained independently associated with LNM in the pT1 group (odds ratio [OR]: 16.08, p = 0.003) and pT1c subgroup (OR: 14.7, p = 0.010). In pT2–4 tumors, periA/V became frequent regardless of nodal status, indicating reduced discriminatory value. Conclusions: In this exploratory single-center cohort, EVG-based periA/V demonstrated high sensitivity for LNM in pT1 IBC-NSTs, with periA/V negativity consistently observed among node-negative cases. These preliminary findings suggest that periA/V may potentially contribute to LNM risk assessment in early-stage breast cancer. Full article

Background/Objectives: Sentinel lymph node biopsy is central to axillary staging in breast cancer, but conventional mapping often relies on radioisotopes and/or blue dye. Indocyanine green fluorescence has emerged as an alternative, although evidence for its use as a sole tracer in routine practice remains limited. This study evaluated the technical feasibility, lymph node yield, nodal metastasis detection, and short-term clinical outcomes of indocyanine green used as the only tracer for axillary staging in a consecutive single-centre cohort. Methods: This retrospective observational cohort study included 260 patients with histologically confirmed breast cancer who underwent axillary surgery at University Hospital Kaspela between 2024 and 2025 under an institutional protocol using indocyanine green as the sole tracer. Indocyanine green-guided mapping was attempted in all patients. For node-focused statistical analyses, a predefined complete-case–cohort of 230 patients was used. Descriptive analyses assessed axillary procedure distribution, lymph node yield, nodal metastasis, and postoperative outcomes. Exploratory multivariable logistic regression was performed to evaluate predictors of nodal metastasis. Results: Mapping was successful in 259/260 patients (99.6%). In the complete-case–cohort, sentinel lymph node biopsy was performed in 166/230 patients (72.2%), targeted axillary dissection in 4/230 (1.7%), and axillary lymph node dissection in 60/230 (26.1%). Median overall lymph node yield was 4 (IQR 3–7), but this pooled value reflected heterogeneous axillary procedures and should not be interpreted as sentinel node yield alone. In the clinically node-negative upfront SLNB subgroup, median lymph node yield was 4 (IQR 2.75–5), and nodal metastasis was identified in 22/112 patients (19.6%). Overall, nodal metastasis was identified in 58/230 patients (25.2%), with a median of 2 metastatic nodes (IQR 1–3) among nodal-positive cases. Reoperation for axillary lymph node dissection occurred in 14/230 patients (6.1%). In exploratory multivariable analysis, suspicious biopsied-positive nodes (OR 12.85, 95% CI 3.98–41.52), suspicious non-biopsied nodes (OR 15.58, 95% CI 3.44–70.59), and neoadjuvant therapy (OR 0.31, 95% CI 0.11–0.87) were associated with nodal metastasis; these findings should be interpreted cautiously given the expected clinical relationship between preoperative nodal suspicion and nodal positivity, and the limited number of nodal-positive events. Conclusions: Indocyanine green used as a sole tracer demonstrated high technical feasibility within a heterogeneous real-world axillary staging workflow in this single-centre cohort. These findings should be interpreted as implementation-focused feasibility data rather than formal diagnostic validation, given the retrospective design, heterogeneous case mix, and absence of an internal comparator. Full article

Background: Aspirin, initially recognized for its anti-inflammatory, antipyretic and analgesic properties, holds a prominent role in the treatment of cardiovascular disease. The utility of aspirin in cancer therapeutics has been explored and stratified into COX-dependent and -independent mechanisms. COX2 gene expression has been demonstrated to be significantly upregulated in colorectal cancer and various other gastrointestinal malignancies including pancreatic, esophageal, and gastric cancer. This study investigates the relationship of aspirin use and outcomes in patients with colorectal cancer. Methods: The Nationwide Inpatient Sample (NIS) database from 2017 to 2022 was analyzed for patients age > 18 who were hospitalized for colorectal cancer and its decompensations using ICD-10 diagnostic codes. These patients were further stratified based on the long-term use of aspirin. The principal outcome of this investigation are the odds of in-hospital mortality, with secondary outcomes including odds of pulmonary embolism, portal vein thrombosis, acute kidney injury, septic shock, requiring an ICU level of care and odds of hepatic, pulmonary, gastrointestinal and peritoneal or retroperitoneal metastatic disease. Multivariate logistic regression accounting for hospital and patient characteristics was implemented for analysis, with the Charlson Comorbidity Index used to adjust for coexisting comorbidity burden; a p-value (p) of <0.05 was considered statistically significant. Results: In our analysis of the NIS, 596,160 patients were identified with colorectal cancer and 11.7% (69,750) of this population were identified with long-term use of aspirin. Aspirin use was identified to have a significantly reduced odds of in-patient mortality (adjusted odds ratio) [aOR] 0.530, p value < 0.001 95% CI (confidence interval): 0.460–0.617. Patients with aspirin use also demonstrated significantly reduced odds of adverse outcomes and gastrointestinal, hepatic, pulmonary and retroperitoneal/peritoneal metastasis; (aOR 0.606, 95% CI: 0.564–0.653, p < 0.001), (aOR 0.628, 95% CI: 0.582–0.678, p < 0.001), (aOR 0.676, 95% CI: 0.605–0.755, p < 0.001) and (aOR 0.751, 95% CI: 0.685–0.825, p < 0.001) respectively. Conclusions: In recent years, there has been an alarming increase in incidence of colorectal cancer, particularly amongst younger individuals with increased associated mortality. This mortality increase, albeit alarming, is a driving force for treatment innovation with continual examination of our repertoire of medications for possible repurposed applications. COX2-mediated signaling serves as a key promotor of tumorigenic molecular signaling that directly contributes to tumor cell proliferation, angiogenesis and metastasis in colorectal cancer. Aspirin use and its inhibitory action on COX2 demonstrated a significantly reduced odds of in-hospital mortality. Aspirin use is also associated with significantly reduced odds of developing metastatic disease to the liver, gastrointestinal system, lungs and peritoneum in patients with colorectal cancer. These findings convey that aspirin use reduces the likelihood of in-hospital mortality, major comorbid conditions and of developing metastatic disease as compared to those who do not use aspirin. Full article

Background: Immune-related snoRNAs remain largely uncharacterized in cancer. Methods: We comprehensively investigated their functions and clinical relevance through an integrative pan-cancer analysis of The Cancer Genome Atlas (TCGA) datasets. We systematically identified immune-related snoRNAs via partial correlation with immune pathways and GSEA, validated their functions in vitro, and performed molecular subtyping in non-small-cell lung cancer (NSCLC) and head and neck squamous cell carcinoma (HNSC). Results: We established a comprehensive landscape of immune-related snoRNAs associated with core immune pathways, the majority of which were dysregulated across cancers and correlated with tumor immune cell infiltration. Functional screening revealed that numerous immune-related snoRNAs were aberrantly expressed in cancer stem cells; notably, SNORD116-19 potently suppressed breast cancer stemness and metastasis. Using a panel of immune-related snoRNAs, we classified NSCLC into three molecular subtypes with distinct molecular features and immune microenvironments, suggesting divergent immunotherapy response patterns. This classification framework was successfully extrapolated to HNSC. Conclusions: Our findings suggest that immune-related snoRNAs may serve as potential regulators linking tumor progression and immunity and could be explored as candidate biomarkers for molecular subtyping with the potential to inform personalized immunotherapy strategies. Full article

Background: Molecular classification has transformed risk stratification in endometrial cancer, providing prognostic information beyond traditional clinicopathologic features. However, the relationship between molecular subtype, nodal involvement, and recurrence risk remains incompletely defined. This study aimed to compare lymph node metastasis rates across molecular subgroups and evaluate survival outcomes and prognostic factors for recurrence. Methods: We conducted a retrospective study including 158 patients with a preoperative diagnosis of presumed early-stage endometrial carcinoma treated surgically between 2021 and 2024. Molecular classification was performed according to WHO criteria, including POLE-ultramutated, mismatch repair deficient (MMRd), p53-abnormal (p53-abn), and no specific molecular profile (NSMP). Sentinel lymph node biopsy (SLNB) was the primary method for nodal staging. Survival outcomes were assessed using a Kaplan–Meier analysis, and logistic regression was used to identify prognostic factors for recurrence. Results: NSMP was the most frequent molecular subtype (44.3%), followed by MMRd (29.1%), p53-abn (20.9%), and POLE-mutated tumors (5.7%). Overall, 11.4% of patients had nodal metastases, most commonly in the p53-abn subgroup, which showed significantly higher rates of positive sentinel lymph nodes (p = 0.010). Prognosis differed significantly across molecular subtypes. POLE-mutated and NSMP tumors demonstrated the most favorable outcomes, while p53-abn tumors showed the poorest overall survival and progression-free survival. In a univariate analysis, grade, lymphovascular space invasion (LVSI), myometrial invasion, FIGO stage, and molecular classification were associated with recurrence. Stratified analyses suggested LVSI as the most relevant prognostic factor within the MMRd subgroup. Conclusions: Molecular classification is strongly associated with nodal involvement and survival outcomes in early-stage endometrial cancer. Integrating molecular subtype with clinicopathologic factors may improve recurrence risk stratification and guide individualized surgical and adjuvant treatment strategies. Full article

Background and Objectives: Malignant ascites reflects the tumor microenvironment and provides valuable insights into peritoneal metastasis. This study aimed to assess soluble immune system-related molecules in the ascites fluid of advanced gastrointestinal cancer patients with peritoneal carcinomatosis and to explore potential therapeutic opportunities. Methods: This multicenter prospective cohort study included 48 patients with gastrointestinal adenocarcinoma (17 colorectal, 16 gastric, and 15 pancreatic) with malignant ascites and 15 patients for comparison who required benign ascites drainage for advanced heart failure. Blood samples for routine parameters and ascites fluid for cytokine and soluble immune checkpoint analysis were collected. Parameters were compared between cancer patients and the comparison group, across cancer subgroups, and in correlation with survival. Results: The mean age of participants was 60.2 ± 14.9 years, with a female-to-male ratio of 11:20. The median survival of cancer patients was 84.0 days. Compared with heart failure-associated transudative ascites, malignant ascites demonstrated higher levels of TNF-α, IL-6, IL-10, IL-12p70, IL-18, IL-23, s4-1BB, and TGF-β1, while albumin levels were lower. Significant intergroup differences were observed in TNF-α, IL-6, IL-8, IL-10, IL-12p70, IL-23, 4-1BB, TGF-β1, and PD-L1 levels. In exploratory multivariable analysis, IL-10 and soluble 4-1BB emerged as potential predictors of shorter survival, although these findings require validation in larger cohorts. Survival was negatively correlated with PD-L1, TNF-α, IL-6, and IL-10 in colorectal cancer; 4-1BB, TGF-β1, IL-8, and IL-10 in gastric cancer; and TGF-β1, IL-6, and IL-10 in pancreatic cancer. Conclusions: These exploratory findings indicate that the immunosuppressive milieu in malignant ascites in gastrointestinal cancers may be mediated by cancer subtype-specific pathways, warranting further mechanistic and translational investigation. Full article

Tamoxifen remains the standard treatment for estrogen receptor alpha (ER α) positive breast cancer (BC) cases. However, a significant proportion of patients develop chemoresistance, leading to disease recurrence. The Nuclear Factor Erythroid 2-Related Factor 2 (Nrf2), coded by NFE2L2 gene, has emerged as a key player in chemoresistance and tumoral progression across multiple cancer types, including BC. This study aimed to analyze the role of Nrf2 in metastasis-related processes in a tamoxifen-metabolite-resistant BC cell variant (MCF-7^Var-H) and to assess the impact of Nrf2 modulation. We analyzed Nrf2 expression and nuclear localization and observed that both were increased in endocrine-chemoresistant MCF-7^Var-H cells compared with MCF-7 parental cells. Critically, we assessed the effects of Nrf2 on migration, invasion, and metalloproteinase secretion capacity using wound-healing assays, Boyden chamber assays, and zymography, respectively. Our results suggest that Nrf2 actively promotes metastatic behaviors in the resistant variant. To further explore its pharmacological relevance, we designed and synthesized small interfering RNAs (siRNAs) targeting NFE2L2 mRNA in its coding region by heterogeneous-phase chemical synthesis. Transfection with these siRNAs significantly inhibited metastasis-related functions such as migration in MCF-7^Var-H cells. Overall, siRNAs targeting Nrf2 may be promising tools for treating chemoresistant and metastatic breast cancer. Full article

Background and Objectives: Papillary thyroid microcarcinoma (PTMC) is generally indolent; however, a subset exhibits aggressive features, reflecting biological heterogeneity. In the era of treatment de-escalation and active surveillance, accurate risk stratification is essential. We aimed to evaluate recurrence, identify factors associated with recurrence, determine predictors of lymph node metastasis (LNM) at diagnosis, and assess management strategies at our center. Materials and Methods: This retrospective study included 302 patients with PTMC. Associations between clinicopathological variables and outcomes were evaluated using chi-square test, Spearman correlation, and univariate and multivariate logistic regression analyses. Results: The cohort included 240 females (79.5%) and 62 males (20.5%), with a median age of 47 years. Total thyroidectomy was performed in 97.7%, and radioactive iodine (RAI) in 64.2%. LNM was identified in 26 patients (8.6%). Recurrence occurred in 4 patients (1.3%), and 98.0% were alive at last follow-up. Recurrence was associated with LNM at diagnosis, higher ATA risk categories, and positive surgical margins (p < 0.005). Younger age, larger tumor size, and vascular invasion independently predicted LNM (all p < 0.05), while autoimmune thyroiditis was associated with a reduced risk (p = 0.020). Conclusions: PTMC demonstrates clinically relevant heterogeneity, particularly in patients with LNM. However, given the limited number of recurrence events, recurrence-related findings should be interpreted cautiously and considered exploratory. These findings support risk-adapted management and careful patient selection in the era of treatment de-escalation. Full article

Background: Prognostic assessment in metastatic sarcoma remains challenging, and baseline variables may not adequately reflect outcome after metastatic onset. We investigated whether the 12-month landmark provides clinically relevant prognostic stratification for post-metastasis survival, while institution was examined as a contextual and adjustment variable rather than as the primary analytic focus. Methods: This retrospective observational study was based on prospectively collected real-world-time clinical data from two sarcoma centers. Overall survival (OS) and post-metastasis survival (PMS) were first analyzed descriptively across the two contributing centers using Kaplan–Meier methods. The principal analysis was a landmark-based prognostic stratification of PMS from 12 months after first metastatic documentation, with patients classified at the landmark as oligometastatic or polymetastatic. Univariable and multivariable Cox regression models were used to assess prognostic associations. Results: A total of 236 patients were included (135 at Institution A and 101 at Institution B). Crude OS was broadly comparable between institutions, whereas PMS showed a numerical separation. In the landmark analysis, metastatic state at 12 months clearly stratified subsequent PMS, with persistent oligometastatic disease associated with more favorable outcome than polymetastatic disease. In the reduced multivariable landmark model, polymetastatic state at 12 months remained the strongest independent predictor of inferior PMS (HR 3.09, 95% CI 1.87–5.09; p = 0.00001). High histologic grade also retained independent adverse prognostic significance (G3 vs. G1: HR 5.16, 95% CI 1.59–16.79; p = 0.006), whereas institution showed only a non-significant trend after adjustment (HR 0.67, 95% CI 0.42–1.07; p = 0.094). Conclusions: In metastatic sarcoma, realized metastatic state at 12 months provides stronger landmark-based prognostic stratification for post-metastasis survival than crude institutional comparison. These findings support a longitudinal state-based prognostic framework in which survival after metastatic onset is more informatively stratified by disease state at the 12-month landmark than by crude center attribution. Full article

Obesity has risen to the forefront of global public health challenges, particularly due to its association with several chronic diseases. Its association with cancer has attracted significant research interest. The relationship between obesity and cancer is complex and profoundly influences tumorigenesis, cancer progression, metastasis, and therapeutic efficacy. This review provides the molecular basis of these interactions, elucidating how obesity triggers changes in the tumor microenvironment, disrupts metabolic pathways, and promotes inflammation. These factors facilitate cancer development and reduce the efficacy of treatments. By unraveling these mechanisms, we aim to identify therapeutic strategies that could mitigate obesity’s detrimental effects on cancer outcomes and contribute to the development of more effective strategies for managing obesity-related cancers. Full article

Introduction: Breast cancer is one of the major killers among malignant conditions worldwide, affecting one out of 10 women in industrialized countries and being the leading cause of cancer-related morbidity and mortality in women. The relationships between risk factors and breast cancer development are not exactly known. The selection of the UBC9 gene and its c.73G>A polymorphism (rs11553473) in breast cancer studies is justified by the gene’s critical role in sumoylation, its impact on DNA repair, and its association with aggressive tumor characteristics. UBC9 (SUMO-conjugating enzyme) is frequently overexpressed in breast cancer, often 5–8-fold higher than in normal tissues, where it promotes tumor proliferation, invasion, and metastasis, often in a sumoylation-independent manner. Aim: In the present work, the association of polymorphism in the UBC9 genes c.73G>A with breast cancer risk was investigated. Materials and Methods: In the reported study, paraffin-embedded tumor tissue was collected from women with lymph node-negative (n = 59) and lymph node-positive (n = 41) ductal breast carcinoma. Samples from age-matched, cancer-free women (n = 100) served as controls. The genotypes of the UBC9 c.73G>A polymorphism were determined by ASO-PCR methods. Results: In the present work, a significant positive association between the UBC9 c.73G>A G/A genotype and breast cancer is demonstrated. The variant A allele of UBC9 increased breast cancer risk. Some correlation was observed between the genotypes of UBC9 polymorphism and breast cancer invasiveness. A statistically significant increase was observed regarding G/A heterozygote frequency in stage II patients, according to Bloom–Richardson classification. There were no significant differences in genotype distribution among subgroups defined by TNM stage, histological grade, hormone receptor status, or HER-2 expression. Conclusions: In conclusion, the reported study indicates that the polymorphisms of the UBC9 gene may be positively associated with the incidence of breast cancer. However, further research is needed on larger study populations. Full article

Alpha-enolase (ENO1) is a multifunctional protein best known for its canonical role in glycolysis, but growing evidence indicates that it also plays important roles in cancer development and progression. This review summarizes the current knowledge regarding the biological and clinical significance of ENO1 across multiple cancer types. We first outline the physiological characteristics of ENO1 and its distribution in normal tissues. Then, we discuss its aberrant expression patterns and genomic alterations in human cancers. We further examine the evidence linking ENO1 to major cancer-related processes, including proliferation, apoptosis resistance, cancer stemness, autophagy, metastasis, drug resistance, and angiogenesis. In addition, we review studies that evaluate the association between ENO1 expression and patient prognosis in pan-cancer datasets and individual malignancies. Collectively, the available literature indicates that ENO1 is closely associated with malignant progression through its involvement in metabolic reprogramming and broader tumor-promoting cellular functions. These findings suggest that ENO1 may serve as a context-dependent biomarker and a candidate therapeutic target in selected cancer settings; however, further mechanistic validation and clinically annotated studies are required before its translational value can be firmly established. Full article