The link between salt intake and the risk of gastric cancer remains uncertain, and a causal relationship has not been established. Therefore, clarifying the causal effect of salt intake on the risk of gastric cancer using reliable causal inference methods is necessary. The aim of this study was to assess the causal association between salt intake and cancer by integrating summary-level genome-wide association study (GWAS) data. Two-sample Mendelian randomization (MR) analyses were performed using summary statistics from a GWAS. Inverse-variance weighted (IVW) regression, Mendelian randomization-Egger (MR-Egger) regression, and weighted median analyses were used to evaluate the causal relationship between salt intake and gastric cancer. Moreover, Mendelian Randomization Pleiotropy RESidual Sum of Squares and Outliers and MR-Egger analyses were used to evaluate the level of multipotency, and "leave-one-out" sensitivity analysis was assessed. The IVW method estimate indicated that salt intake was not correlated with gastric cancer incidence. The IVW (β = 0.1008, standard error [SE] = 0.1510, odds ratio [OR] = 1.1061, 95% confidence interval [CI], 0.82-1.48, P = .5042), MR-Egger regression (β = 0.059, SE = 0.5318, OR = 1.0612, 95% CI, 0.37-3.01, P = .9111), and weighted median (β = 0.2639, SE = 0.2298, OR = 1.3020, 95% CI, 0.82-2.04, P = .2508) analyses revealed no causal relationship between salt intake and gastric cancer risk (P > .05). In addition, the funnel plot and MR-Egger analysis (P = .6694 > .05) did not indicate horizontal pleiotropy or heterogeneity. GWAS data from public databases were used in this study, and the causal relationship between salt intake and gastric cancer risk was analyzed via a two-sample MR method. The results revealed no genetic causal relationship between salt intake and gastric cancer.

This study aimed to investigate the enhanced tumor control in patients with non-small cell lung cancer (NSCLC) using intensity-modulated radiotherapy (IMRT) combined with microwave hyperthermia (MWD). We retrospectively analyzed the clinical data of 134 patients with NSCLC admitted to our hospital from March 2021 to February 2024. Among them, 66 patients received IMRT alone (IMRT group) and 68 patients received IMRT combined with MWD (combined group). Tumor control rates, serum tumor markers, immune function, and toxic side effects were evaluated. The tumor control rate was significantly higher in the combined group (82.35%) than in the IMRT group (69.70%; P < .05). After treatment, the combined group showed significantly lower levels of carbohydrate antigen 125 (CA125), cytokeratin 19-fragments (Cyfra21-1), and carcinoembryonic antigen (CEA) compared to the IMRT group (P < .05). Furthermore, the levels of CD3+, CD4+, and CD4+/CD8+ ratios in the combined group were significantly higher than those in the IMRT group (P < .05). No significant difference in toxic side effects was observed between the 2 groups (P > .05). IMRT combined with MWD for NSCLC can effectively downregulate tumor markers, restore immune function, and improve tumor control rates without increasing toxicity.

Perioperative catheterization is a well-known risk factor for developing postoperative catheter-associated urinary tract infection (CAUTI). The information about the effect of extended urinary catheterization after surgery for gastric cancer is still scarce. This is a retrospective study of 232 patients with gastric cancer who underwent surgery. Patients were divided into 2 groups based on the duration of their catheter placement: <72 hours and 72 hours or more. The primary outcome was CAUTI during the index hospitalization. Logistic regression was used to calculate odds ratios in unadjusted, adjusted, and sensitivity models. A dose-response analysis was conducted for ordered catheter duration categories. In patients with catheterization duration ≥72 hours versus those with catheterization <72 hours, CAUTI occurred significantly more frequently. In the unadjusted model, prolonged catheterization remained associated with increased odds of CAUTI, odds ratio = 5.66. The relationship was still significant, adjusting for age, diabetes, and operative time (longer operation time). After omitting patients with shock or severe complications, long-term catheterization was still independently associated with CAUTI, with an odds ratio of 3.99. A significant duration-related trend was observed with a steep increase in CAUTI after 72 hours of catheterization. Urinary catheterization for ≥72 hours was associated with an increased risk of CAUTI after gastric cancer surgery, which warrants the avoidance of unnecessary catheter prolongation if clinically possible.

This study examines the clinicopathological characteristics of patients with coexistent medullary thyroid carcinoma (MTC) and papillary thyroid carcinoma (PTC). A retrospective analysis was conducted on 169 patients who underwent surgical treatment for MTC at 2 medical centers between 2010 and 2019. The clinicopathological characteristics were documented, and associations between MTC/PTC and MTC were evaluated. Among the 169 MTC patients, 16 (9.5%) exhibited concomitant histological characteristics of both MTC and PTC. Three patterns of carcinoma distribution were identified: mixed carcinoma, tumors confined to the ipsilateral glandular lobe, and MTC/PTC lesions dispersed across both glandular lobes. Of these 16 patients, 9 were female and 7 were male, with a mean age of 50.6 years. The PTC lesions had a maximum diameter of 0.40 ± 0.21 cm, whereas the MTC lesions measured 1.73 ± 1.86 cm in maximum diameter. Additionally, 9 cases exhibited lymph node metastases, but no distant metastases were observed. Univariate analysis indicated no significant associations between MTC/PTC and MTC (P > .05), with no differences in survival or prognosis between the groups.

Liver metastases from colorectal cancer (CRC) are a primary cause of poor patient prognosis, closely linked to the liver's unique tumor microenvironment (TME). Compared to primary tumors, research on the TME of liver metastases remains insufficient. This review systematically summarizes recent advances in TME research concerning colorectal liver metastases (CRLM), emphasizing its organ-specific characteristics, pivotal role in tumor progression, and influence on treatment response. We delve into the intricate cellular components of the TME-including tumor-associated macrophages, cancer-associated fibroblasts, and myeloid-derived suppressor cells-and non-cellular constituents such as the extracellular matrix and soluble factors. Furthermore, we explore the multifaceted mechanisms which the TME drives CRLM progression through establishing pre-metastatic niches, facilitating cancer cell colonization, mediating immune evasion, and inducing drug resistance. Additionally, we evaluate therapeutic strategies targeting the TME, including opportunities and challenges in remodeling cellular components, modulating the extracellular matrix, and developing combination therapies. Ultimately, this review aims to provide theoretical foundations and novel insights for developing more effective anti-metastatic therapies, with the goal of improving the prognosis for CRLM patients.

The advent of immune checkpoint inhibitors (ICIs) targeting PD-1, PD-L1, and CTLA-4 has transformed the therapeutic landscape of advanced non-small cell lung cancer (NSCLC), and recent clinical trials have extended their application to resectable disease. Multiple randomized phase III trials have demonstrated that neoadjuvant and adjuvant immunotherapy, particularly when combined with platinum-based chemotherapy, significantly improves pathological complete response (pCR), major pathological response (MPR), event-free survival (EFS), disease-free survival (DFS), and overall survival (OS) compared to chemotherapy alone. Several key questions remain unresolved-including whether preoperative or postoperative immunotherapy yields superior outcomes, whether adjuvant therapy provides additional benefit after neoadjuvant immune checkpoint inhibitors plus chemotherapy (ICI-CT), and how best to identify the patients most likely to benefit from each strategy. This review will critically examine the current evidence, clinical trial landscape, and future directions for immunotherapy in resectable NSCLC.

The treatment of advanced hormone receptor-positive (HR+) breast cancer has seen relevant changes in last years. However, bevacizumab remains an option when combined with paclitaxel, but no certified pharmacogenetic profiles are now usable for the prediction of its response in breast cancer patients. This study aimed to explore the pharmacogenetic interactions among single nucleotide polymorphisms (SNPs) of genes involved in the angiogenic process and their impact on progression-free survival (PFS) and overall survival (OS) in hormone receptor-positive (HR+) metastatic breast cancer subjects administered with bevacizumab plus paclitaxel, or with paclitaxel alone (clinicaltrial.gov identifier NCT01935102).

Germline DNA extracted from blood samples was analyzed using real-time polymerase chain reaction to investigate SNPs. The multifactor dimensionality reduction (MDR) analysis was employed to assess interactions between these genetic variants. A total of 168 eligible patients were analyzed. Among these, 106 patients received both paclitaxel and bevacizumab, while 62 received paclitaxel alone.

In the combination therapy group, MDR analysis identified two pharmacogenetic interaction profiles involving specific genotypes of vascular endothelial growth factor-A(VEGF-A) rs833061 and vascular endothelial growth factor receptor-2 (VEGFR-2) rs1870377. Patients with a favorable genetic profile had a median PFS (mPFS) of 22.9 months, compared to 8.7 months in those with an unfavorable profile (p = 0.001). Cox proportional hazards analysis displayed an adjusted hazard ratio of 0.443 (95% CI: 0.284-0.691; p < 0.0001). The median OS (mOS) was 50.2 months for the favorable profile vs. 23.5 months for the unfavorable (p = 0.003), with an adjusted hazard ratio (HR) of 0.404 (95% CI: 0.249-0.657; p < 0.0001). In the 62 subjects administered with just paclitaxel, no significant differences in PFS (p = 0.820) or OS (p = 0.143) were observed between favorable and unfavorable genetic profiles.

The MDR analysis of VEGF-A rs833061 and VEGFR-2 rs1870377 genotypes can detect a subgroup of bevacizumab-administered+ metastatic breast cancer patients with improved PFS and OS.

Hepatocellular carcinoma (HCC) presents with poor treatment outcomes, creating an urgent need for novel biomarkers to improve diagnosis, prognosis, and precision medicine. While the MYB family of oncogenes is implicated in cancer, the role and regulatory mechanisms of its member, particularly MYB proto-oncogene like 2 (MYBL2), remain underexplored in HCC. Therefore, this study aimed to systematically validate the clinical significance of MYBL2, elucidate its functional role in tumor progression and drug sensitivity, and identify its upstream regulatory mechanisms using an integrative machine learning and experimental framework.

We applied an integrative pipeline combining LASSO-based feature selection on TCGA and GEO cohorts, single-cell transcriptomics, pharmacogenomic surveys, and CRISPR dependency screens. These computational approaches were complemented by in vitro HepG2 assays, luciferase reporter tests, iTRAQ proteomics, and an in vivo western diet/CCl₄ (WD/CCl₄) HCC model using miR-29a transgenic mice to investigate a putative regulatory axis.

MYBL2 robustly discriminated tumor from normal liver (AUC = 0.968), and high expression was associated with adverse features, including higher grade, microvascular invasion, HBV positivity, nonresponse to TACE, and worse survival. A nomogram combining MYBL2 with AJCC stage improved 1-, 3-, and 5-year AUCs versus stage alone. MYBL2 correlated with proliferative biomarkers (AFP, MKI67, PCNA, BIRC5) and CRISPR knockout inhibited growth in most HCC lines. High MYBL2 expression was associated with greater sensitivity to sorafenib in pharmacogenomic screens and was linked to an immunosuppressive microenvironment and higher MSI. Mechanistically, miR-29a was shown to suppress MYBL2 translation by directly binding to its 3^'-UTR; this was validated in vivo, where miR-29a transgenic mice were protected from WD/CCl₄-induced HCC, demonstrating reduced tumor burden, MYBL2 expression, and fibrosis. iTRAQ proteomics further confirmed MYBL2 as a top miR-29a-regulated protein.

MYBL2 is a potent diagnostic and prognostic biomarker in HCC that also predicts sorafenib sensitivity. Our findings establish a clear regulatory link where MYBL2 is a direct and functionally important target of the tumor-suppressive miR-29a. This positions MYBL2 as a tractable target for miR-29a-based therapeutic strategies, warranting clinical validation for patient stratification and treatment development in HCC.

Brain gliomas are among the tumors with the worst prognosis, and their incidence is increasing. Postoperative temozolomide-based chemoradiotherapy for grades 3 and 4 gliomas extended overall survival (OS) by approximately two months. An increasing number of clinical trials are investigating molecular-based therapy. Recent studies have demonstrated the involvement of Golgi apparatus proteins, including MYO18A (myosin-18A), in processes associated with abnormal proliferation, migration, apoptosis evasion, and angiogenesis promotion. The aim of this study was to investigate whether MYO18A has prognostic value in patients treated for brain gliomas.

The research material in the work included tumor samples taken during neurosurgery and blood samples from 45 patients treated for brain gliomas with grade of 1 to 4 according to WHO, which were used to determine the expression of MYO18A mRNA (messenger ribonucleic acid). Expression of MYO18A was presented as fold changes in RQ (relative quantification) mRNA levels.

This study showed higher MYO18A values in patients diagnosed with grade G4 glioma among those with a shorter progression-free survival (PFS) time and those living shorter than the group average. However, statistically significant differences were achieved only for PFS for the MYO18A RQ feature (PFS = 4.64, SD = 2.16 vs. PFS = 15.83 and SD = 7.27, p = 0.0231). Also, a positive correlation was demonstrated between tumor volume and MYO18A expression.

The level of expression of MYO18A can be considered a prognostic factor for PFS in patients treated for G4 gliomas, because higher MYO18A expression was associated with earlier recurrence.

Partial epithelial-mesenchymal transition (p-EMT) is a dynamic cellular state associated with metastasis and adverse outcomes in multiple cancers, but its prognostic significance in ovarian cancer remains unclear. This study aimed to develop and validate an ovarian cancer-specific transcriptomic signature based on p-EMT-related genes, and to determine whether this signature can improve prognostic stratification and overall survival prediction across independent cohorts.

A pan-cancer p-EMT gene set was curated from ten published studies. Using transcriptomic and clinical data from TCGA-OV (n = 488), a six-gene p-EMT signature was developed via LASSO regression to generate a patient-specific risk score. The score was integrated with clinical variables to construct a prognostic nomogram and validated in the external GEO cohort GSE140082 (n = 380) and GSE165808 (n = 51).

A six-gene p-EMT transcriptomic signature (ADAM9, ANXA8L1, FSTL3, RABAC1, TPM4, and TWIST1) was significantly associated with overall survival (OS) and stratified patients into high- and low-risk groups (adjusted HR = 1.74, p < 0.001). Incorporation with age and FIGO stage in a nomogram improved predictive performance, with AUCs of 0.727, 0.700, and 0.656 at 1-, 3-, and 5-year OS, respectively. External validation in GSE140082 and GSE165808 confirmed model robustness, yielding 3-year AUCs of 0.630 and 0.826, respectively, demonstrating preserved prognostic value across independent cohorts and disease stages.

This six-gene p-EMT transcriptomic signature demonstrates prognostic value in ovarian cancer and offers potential for individualized risk stratification and clinical decisionsupport.