Background:Breast cancer is the most common malignancy worldwide. Brain metastasis in breast cancer severely impacts prognosis, and the objective of this study is to develop a machine learning model for predicting the risk of brain metastasis in breast cancer patients to assist clinical management. Methods:Univariate and multivariate logistic regression analyses were employed to screen the final included variables, and eight machine learning algorithms were utilized for model construction. Model performance was evaluated using receiver operating characteristic curves, precision-recall curves, decision curve analysis (DCA), and calibration curves, with the optimal model selected based on these metrics. The model was trained on a cohort of 154,193 patients, internally validated on 66,084 patients, and externally validated on 765 real-world cases, incorporating metrics such as area under the curve (AUC), area under the precision-recall curve (AUPRC), decision curves, and calibration plots, while SHAP analysis was applied to enhance interpretability. A web-based calculator was developed based on the optimal model to facilitate clinical application. Results:Univariate logistic regression identified higher tumor grade, advanced T/N stage, advanced clinical stage, and PR positivity as risk factors, whereas radiotherapy, chemotherapy, surgery, HR + /HER2- subtype, and unilateral tumors served as protective factors (P < 0.001). Multivariate analysis confirmed independent risk factors, including poorer pathological grade, N3 lymph node status, later stage, and PR positivity, and protective factors, including radiotherapy, chemotherapy, surgery, non-HR-/HER2- subtypes, and HER2 positivity. The XGBoost model achieved an AUC of 0.98 in 10-fold cross-validation, with AUCs of 0.99 and 0.97 in the internal test set and external validation set, respectively; AUPRC values were 0.933, 0.864, and 0.648; decision curve analysis demonstrated superior net benefit compared to alternative models within the 0.1-0.8 threshold range; calibration curves showed high concordance between predicted and observed event rates. SHAP analysis highlighted surgery as the primary protective factor, followed by stage and T classification as risk enhancers, revealing interactions among treatment variables. Conclusion:This study developed an interpretable and clinically deployable XGB model, accompanied by a web-based calculator, thereby advancing personalized risk stratification, early screening, and resource optimization in the management of breast cancer brain metastasis.

BackgroundWith significant progress made in immunotherapy for locally advanced and metastatic gastroesophageal junction or gastric cancer (EGJ/GC), multiple studies have been initiated on neoadjuvant chemoradiotherapy (nCRT) combined with immune checkpoint inhibitors (nCRT+ICIs) for locally resectable EGJ/GC. Consequently, current clinical trials investigating nCRT+ICIs for locally advanced EGJ/GC were summarized within this study. A systematic review and meta-analysis were performed to evaluate the efficacy and safety of this combination therapy, with the objective of providing clinicians with robust, evidence-based treatment strategies and clinical references.Materials and methodsRelevant studies were retrieved from electronic databases including PubMed, Embase, the Cochrane Library, ClinicalTrials.gov, ASCO, ESMO, and CNKI. Efficacy was evaluated based on the pathological complete response (pCR) rate, major pathological response (MPR) rate, downstaging and the R0 resection rate. Safety was assessed by the incidence of grade ≥3 treatment-related adverse events (TRAESs) and grade ≥3 immune-related adverse events (irAEs). All statistical analyses were performed using Stata version 15.0.ResultsA total of 12 studies fulfilled the inclusion criteria for analysis. The pooled rates of pathological complete response (pCR), major pathological response (MPR), and R0 resection were found to be 29%, 52%, and 100%, respectively. The pooled T-stage downgrading rate was 51%. The N-stage downstaging rate was 73%, with all cases successfully downstaged to ypN0. The incidences of grade ≥3 TRAESs and irAEs were 47% and 6%, respectively. The pooled 2-year progression-free survival (PFS) rate was 65%, while the 1-year and 2-year overall survival (OS) rates were 91% and 74%, respectively. Subgroup analyses indicated pCR rates of 26% and 33% for the programmed death-ligand 1 (PD-L1) and programmed death-1 (PD-1) inhibitor subgroups, respectively. Comparable pCR rates of 29% were observed for both sequential and concurrent chemoradiotherapy combined with immunotherapy. Within the concurrent therapy subgroup, a higher pCR rate was achieved with PD-1 inhibitor-based regimens (36%) than with PD-L1 inhibitor-based regimens (25%), while a 29% pCR rate was demonstrated for PD-L1 inhibitor sequential therapy. Stratification by the PD-L1 combined positive score (CPS) yielded pCR rates of 22% for CPS <1, 23% for CPS 1–5, and 51% for CPS ≥5. Radiation dose stratification showed pooled pCR rates of 26% for doses <45Gy and 33% for doses ≥45Gy. Regional variations were observed, with Asian cohorts exhibiting a higher pCR rate (36%) than Western cohorts (26%).ConclusionIn locally advanced EGJ/GC, the combination of PD-1/PD-L1 inhibitors with nCRT demonstrates promising response rates and acceptable toxicity profiles. Notably, this regimen achieved pCR rate of 51% in patients with CPS ≥5. Furthermore, favorable outcomes were observed even in those with low CPS. This study is primarily based on phase II or single-arm data; therefore, these results remain preliminary. These findings require further validation in future large-scale randomized controlled trials (RCTs).Systematic review registrationhttps://www.crd.york.ac.uk/prospero/, identifier CRD42024590688.

The diagnosis and treatment of prostate cancer (PCa) continue to encounter numerous. The specific regulatory mechanism is not yet clear. Studies have shown that miRNA plays a role in the progression of PCa. This research was the first to systematically explore the regulatory mechanism of the miR-26b-5p/ADAM17 pathway in PCa. It reveals the role of the “miR-26b-5p/ADAM17” signaling axis in inhibiting the malignant phenotype of PCa cells and the tumor inflammatory microenvironment. This study recruited serum samples from 138 PCa patients and 138 healthy controls. RT-qPCR was employed to quantify mRNA expression. The interaction was validated using a dual-luciferase assay. Cell proliferation was assessed by the CCK-8 assay, while cell migration and invasion were evaluated via Transwell. Flow cytometry was utilized to measure cell apoptosis, and enzyme-linked immunosorbent assay (ELISA) was performed to determine inflammatory cytokines levels. miR-26b-5p was significantly downregulated in PCa. Its low expression was strongly correlated with poor prognosis, and it functioned as an independent protective prognostic factor. Functional experiments demonstrated that the overexpression of miR-26b-5p markedly suppressed proliferation, migration, and invasion while promoting apoptosis and inhibiting the secretion of tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6). Mechanistically, miR-26b-5p exerted its anti-tumor effects by directly targeting and suppressing ADAM17 expression. Furthermore, the overexpression of ADAM17 partially reversed the tumor-suppressive and anti-inflammatory effects mediated by miR-26b-5p. miR-26b-5p functioned in PCa by directly targeting ADAM17.

BackgroundBreast cancer continues to be a predominant cause of female mortality globally, characterized by limited therapeutic options and substantial adverse effects. Artesunate (ART), a traditional Chinese medicine approved by the FDA for malaria treatment, has demonstrated potential anticancer properties against breast cancer. However, the underlying molecular mechanisms remain incompletely elucidated. This study posits that the antitumor efficacy of artesunate may be mediated through the regulation of the lncRNA TUG1/miR-145-5p/HOXA5 axis.MethodsA comprehensive array of in vitro assays was employed to investigate the proposed molecular pathway, including CCK-8 proliferation assay, EdU incorporation assay, Transwell invasion assay, scratch wound healing assay, TUNEL apoptosis assay, and dual-luciferase reporter assay. Additionally, Western blot analysis, quantitative real-time PCR (qPCR), and plasmid transfection techniques were utilized to validate the findings.ResultsThe results revealed that artesunate exerted a dose-dependent inhibitory effect on breast cancer cell proliferation. This was accompanied by the down-regulation of HOXA5, WNT, β-catenin, Fizz1, and Arg-1, implicating the involvement of the WNT/β-catenin signaling pathway. Furthermore, artesunate significantly modulated the expression levels of lncRNA TUG1, miR-145-5p, and HOXA5, suggesting a mechanistic role of the lncRNA TUG1 pathway in its anticancer activity.ConclusionsThese findings indicate that artesunate may inhibit breast cancer progression through the lncRNA TUG1/miR-145-5p/HOXA5 axis, highlighting its potential as a promising therapeutic candidate for future clinical trials in cancer therapy.

[This retracts the article DOI: 10.3892/etm.2016.3992.].

Prostate cancer (PCa) remains a leading cause of cancer-related incidence and mortality in men. Disruptions in amino acid (AA) metabolism contribute to the disease progression, with brucine, a glycine antagonist, exhibiting antitumor effects. This study explores the antitumor impact of brucine on PCa and investigates its mechanisms in regulating AA metabolic pathways. The study employed the PCa cell line DU-145, characterized by high sarcosine (Sar) levels, for various assays including Cell Counting Kit-8 (CCK8), wound healing, Transwell, 5-Ethynyl-2’-deoxyuridine (EDU), TdT mediated dUTP Nick End Labeling (TUNEL), flow cytometry, Western blot, and ultra-high-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS). Network pharmacological analysis determined the anticancer mechanisms of brucine. Sar levels in DU-145 cells were significantly higher than in normal prostatic epithelial cells RWPE-1. Treatment with brucine resulted in a marked decrease in cell viability, proliferation, invasion, and migration, while promoting apoptosis in a dose-dependent manner. Sar levels decreased with increasing brucine concentration. Network pharmacology analysis linked brucine’s anticancer effect to the AA metabolism and glycine N-methyltransferase (GNMT) pathways. GNMT expression in prostate cancer tissues and The Cancer Genome Atlas database was significantly elevated compared to controls. Treatment with brucine led to downregulation of GNMT expression in DU-145 cells without significant effect on sarcosine dehydrogenase (SARDH). Addition of recombinant GNMT partially reversed the inhibitory effects of brucine on DU-145 cells. Treatment with brucine downregulates GNMT expression in DU-145 cells, reducing Sar accumulation and inhibiting tumor progression. These findings provide new insights into the antitumor mechanisms of brucine in PCa.

Epstein-Barr virus (EBV)-associated gastric cancer (EBVaGC) is a distinct molecular subtype of gastric cancer (GC). At present, the clinical characteristics and prognostic implications of EBV infection and the potential clinical benefits of immune checkpoint blockade in GC remain to be clarified. Hence, this study was designed to analyze the clinical and pathological characteristics of GC patients with varying EBV infection states and compare their overall survival (OS). A retrospective study was performed on 1031 consecutive GC patients who underwent gastrectomy at the Affiliated Hospital of Xuzhou Medical University from February 2018 to November 2022. EBV-encoded RNA (EBER) in situ hybridization (ISH) was used for EBV assessment, and immunohistochemical staining was used for evaluation of human epidermal growth factor receptor 2 (HER2), programmed death ligand 1 (PD-L1), and Ki67 expression. EBVaGC was defined as tumors with EBV positivity. In addition, EBV-negative GC (EBVnGC) patients were matched with EBVaGC patients based on seven clinicopathological parameters (age, gender, anatomic subsite, tumor size, Lauren classification, degree of differentiation, and tumor-node-metastasis [TNM] stage). The correlations of clinical features with HER2, PD-L1, and Ki67 expression were evaluated statistically. The survival of patients was assessed through medical records, telephone, or WeChat communication, and prognostic analysis was performed using the logrank test as well as univariable and multivariable regression analysis. Out of 1031 GC patients tested, 35 (3.4

Tumor infiltrating lymphocytes (TILs), especially CD8+ T cells, play an important role in the process of anti-tumor immune response and are significantly correlated with the prognosis of esophageal cancer (EC), but there are also inconsistent conclusions. This study aimed to comprehensively evaluate the relationship between invasive CD8+ T cells and the prognosis in patients with EC through meta-analysis, and to provide a basis for prognosis and immunotherapy for EC. Articles related to CD8+ T cells and EC prognosis in PubMed, Cochrane Library, Embase, and CNKI were searched. Cancer specific survival (CSS), overall survival (OS) and disease-free survival (DFS) served as endpoint events. Besides, Stata15.0 was adopted for meta-analysis, and hazard ratio (HR) and 95

Objective: To investigate the diagnostic value of magnetic diffusion tensor imaging（ DTI） combined with auditory brainstem response in autism spectrum disorder（ ASD）. Methods:A total of 60 children with ASD in hospital from January 2019 to January 2022were selected as the observation group,among them,40 cases were mild to moderate,20 cases were severe,and 60 normal children were selected as the control group. The differences of fractional anisotropy（ FA）,apparent diffusion coefficient（ ADC） and brainstem auditory evoked potential（ BAEP） were analyzed. Results:The FA of the corpus callosum in the observation group was significantly higher than that in the control group（ t=6.433,P＜0.05）,while the ADC was significantly lower than that in the control group（ t=8.468,P＜0.05）. The latency of wave Ⅰ in the observation group was significantly shorter than that in the control group（ t=3.417,P＜0.05）. The FA of the splenium of corpus callosum in severe children in the observation group was significantly higher than that in mild to moderate children（ t=2.457,P＜0.05）. The ADC and wave Ⅰ latency of the splenium of the corpus callosum were significantly lower than those of mild to moderate children（ t = 4. 564, P ＜ 0. 001; t = 3. 519, P ＜ 0. 05）. The area under the ROC curve of the FA of the corpus callosum,the ADC of the corpus callosum and the latency of the first wave in predicting severe ASD were 0.667,0.789 and 0.700,respectively（ all P＜0.05）.Conclusion:MRI quantitative parameters combined with auditory brainstem response have certain value in the diagnosis of ASD and the differentiation of disease severity in children.

目的 探讨结直肠癌(CRC)组织中整合素β2(ITGB2)和Kindlin-2的表达及其临床意义.方法 收集2021年6月至2022年2月徐州医科大学附属医院60例CRC患者手术切除的肿瘤组织标本及对应的癌旁(距肿瘤边缘≥5 cm)正常组织标本.采用免疫组化法检测组织中ITGB2和Kindlin-2的表达情况,并分析CRC组织中ITGB2和Kindlin-2的表达与临床病理特征的关系及两者的相关性.结果 CRC组织中ITGB2和Kindlin-2的阳性表达率均高于癌旁正常组织,差异均有统计学意义(均P＜0.05).分化程度差、浸润深度深、TNM分期晚、有淋巴结转移的CRC组织中ITGB2和Kindlin-2的阳性表达率分别高于分化程度好、浸润深度浅、TNM分期早、无淋巴结转移的CRC组织,差异均有统计学意义(均P＜0.05).CRC组织中ITGB2和Kindlin-2蛋白表达呈正相关(rs=0.356,P＜0.05).结论 ITGB2和Kindlin-2在CRC组织中高表达,且均与CRC的TNM分期、浸润深度、分化程度、淋巴结转移密切相关,推测其可能与CRC的发病机制密切相关.

Introduction: Melatonin (5-methoxy-N-acetyl-tryptamine) is a circadian hormone synthesized and secreted by the pineal gland. In addition to regulating circadian rhythms of many physiological functions, melatonin is involved in regulating autonomic nervous function and blood pressure. Hypothalamus paraventricular nucleus (PVN), receiving melatonin projections from the superchiasmatic nucleus, is a critical brain region to regulate neuroendocrine and cardiovascular function. Here, we determined the synaptic mechanisms involved in the effect of melatonin on the sympathetic outflow and blood pressure.Methods and Results: Microinjection of melatonin into the PVN produced a depressor effect and decreased renal sympathetic nerve activity (RSNA). While microinjection of luzindole, a non-selective melatonin receptor antagonist, into the PVN did not change melatonin-induced sympathoinhibition, GABAA receptor antagonist bicuculline eliminated melatonin-induced sympathoinhibition. Furthermore, melatonin decreased firing rate of retrogradely labeled PVN neurons which project to the rostral ventrolateral medulla (RVLM), an effect was not altered by luzindole but eliminated by bicuculline. Melatonin significantly increased the amplitude of spontaneous and evoked GABAergic inhibitory synaptic currents, as well as GABA-induced currents.Conclusion: These data suggest that melatonin in the PVN suppresses sympathetic vasomotor tone through enhancing GABAA receptor activity. This study provides novel information for understanding the cellular mechanisms involved in the effect of melatonin on regulating blood pressure and sympathetic output.

Objective:To study the effects of oncolytic adenovirus expressing LASP-1 gene siRNA (ZD55-LASP-1)on the growth of implanted human renal cancer in nude mice.Methods:The model of human renal carcinoma transplanted with 786-0 cells in nude mice was established. Thirty-two nude mice with tumor volume of 100-150 mm 3 were randomly divided into 4 groups, with 8 mice in each group, including replication-defective adenovirus (Ad-LASP-1 group), oncolytic adenovirus (ZD55-EGFP group, ZD55-LASP-1 group) and phosphate buffer solution (PBS group). The volumeThe volume of tumor was measured regularly, and the expression of LASP-1 protein in tumor tissue was detected by immunohistochemistry. The expression of adenovirus E1A gene in transplanted tumor was detected by immunofluorescence method. Apoptosis of tumor cells was detected by in situ end labeling (TUNEL). HE staining was performed on liver and lung tissues of nude mice to investigate liver damage and distant lung metastasis. Results:The volume of transplanted tumor in ZD55-LASP-1 group was lower than that in ZD55-EGFP group and Ad-LASP-1 group, and the difference was statistically significant (all P<0.05). There was no E1A protein expression in PBS group and Ad-LASP-1 group, but E1A expression was found in ZD55-LASP-1 group and ZD55-EGFP group. Immunohistochemical test results of LASP-1 protein showed that compared with ZD55-EGFP group, Ad-LASP-1 group and PBS group, ZD55-LASP-1 group could inhibit the expression of target gene LASP-1 protein (all P<0.05). TUNEL experimental results show that the The positive rate of apoptosis in ZD55-LASP-1 group was (45.9±4.6)%, and Ad-LASP-1group, ZD55-EGFP group and PBS group [(26.3±3.1)%、(34.9±3.2)% 、(13.8±1.6)%], difference was statistically significant (all P<0.05). Compared with Ad-LASP-1 group and ZD55-EGFP group, ZD55-LASP-1 could further promote apoptosis of renal carcinoma cells. ZD55-LASP-1, ZD55-EGFP and Ad-LASP-1 groups all showed tumor tissue growth inhibition, which was manifested by different degrees of nuclear deep staining, and the nucleoli were not obvious. Tumor lung metastasis was observed in 3 nude mice in PBS group and 1 nude mice in ZD55-EGFP group, while no metastasis was observed in ZD55-LASP-1 and Ad-LASP-1 groups and no significant liver tissue changes were observed. Conclusions:ZD55-LASP-1 can more effectively inhibit the growth of tumor, may be a novel tool for gene therapy of human renal carcinoma.

AbstractBackgroundBreast cancer (BC) has been studied more and more in modern medicine. Circ_0002496 has established a critical role in BC. MiR‐433‐3p can exert important activity in cancer. YWHAZ can participate in BC development, but the targeting relationship among the three variables and its influence on the related process of BC are not clear.MethodsRT‐qPCR was used to analyze circ_0002496, miR‐433‐3p, and YWHAZ expression. Immunoblotting was used to analyze YWHAZ, Bax, Bcl‐2, and PI3K/AKT‐related proteins. RNase R assay was used to verify the ring structure of circ_0002496. Cell phenotypes were tested by Cell Counting Kit 8, EdU, sphere formation, tube formation, and flow cytometry assays.ResultsCirc_0002496 was enhanced and MiR‐433‐3p was downregulated in BC, while the expression of YWHAZ was higher in BC. Circ_0002496 targeted miR‐433‐3p and miR‐433‐3p targeted YWHAZ in BC cells. Depletion of circ_0002496 influenced the BC process, but miR‐433‐3p inhibitor reversed the impact of si‐circ_0002496 on the BC process. Re‐expression of YWHAZ weakened the influence of miR‐433‐3p on the BC process. Depletion of circ_0002496 could astrict tumor growth in vivo. Moreover, the circ_0002496/miR‐433‐3p/YWHAZ axis mediated the activation of the PI3K/AKT signaling pathway.ConclusionCirc_0002496 participated in the malignant procession of BC by miR‐433‐3p/YWHAZ regulation cascade.

Objective:To investigate the effect of oncolytic adenovirus (ZD55-LAP-1) loaded with LASP-1 siRNA on the proliferation of human renal cancer cells.Methods:Human renal cancer cells (786-0 cell lines) infected with ZD55-LAP-1 and oncolytic adenovirus ZD55-EGFP were selected, and they were divided into ZD55-LAP-1 group and ZD55-EGFP group, respectively. PBS was used as a negative control (negative control group). Western blot was used to detect the effect of ZD55-LAP-1 on the expression of E1A and LASP-1 proteins in cells infected with ZD55-LAP-1, and CCK8 method was used to detect the effect of ZD55-LAP-1 on the proliferation of 786-0 cells. Cell migration and invasion experiments were conducted to detect the inhibitory effect of ZD55-LAP-1 on the migration and invasion of 786-0 cells. The effect of ZD55-LAP-1 on apoptosis of 786-0 cells was detected by flow cytometry.Results:The 786-0 cells infected with ZD55-LAP-1 and ZD55-EGFP expressed E1A pro-tein, while the HK-2 cells infected with ZD55-EGFP did not express E1A protein. After virus infection of 786-0 cells, the expression level of LASP-1 protein in ZD55-LAP-1 and ZD55-EGFP groups was significantly lower than that in the negative control group (all P<0.05). The cell survival rate, the number of 786-0 cells penetrating the membrane, and the number of invasive cells in the ZD55-LAP-1 group were lower than those in the ZD55-EGFP group and the negative control group (all P<0.05). The apoptosis rate of ZD55-LAP-1 group was higher than that of ZD55-EGFP group and negative control group (all P<0.05). The E-cadherin protein in the ZD55-LAP-1 group was significantly higher than that in the ZD55-EGFP group and the negative control group, with significant differences (all P<0.05). The expression levels of N-cadherin and Vimentin in the ZD55-LAP-1 group were lower than those in the ZD55-EGFP group and the negative control group, with significant differences (all P<0.05). Conclusions:ZD55-LAP-1 can inhibit the expression of LASP-1 gene in human renal cancer cells and induce apoptosis in human renal cancer cells.

目的 探讨肌内效贴对脑性瘫痪(脑瘫)合并流涎患儿的临床疗效.方法 选取2020年6-12月该院康复科收治的脑瘫合并流涎患儿48例,采用随机数字表法分为观察组和对照组,每组24例.对照组给予常规康复治疗,观察组在常规康复治疗基础上加肌内效贴贴扎治疗,共治疗4周.采用教师流涎分级法(TDS)评估2组患儿治疗前后流涎症状,采用口运动功能、反复唾液吞咽测试(RSST)评估2组患儿吞咽功能,评定总有效率.结果 2组患儿治疗后TDS分级、口运动功能、RSST均较治疗前明显改善,且观察组改善效果更明显,总有效率明显优于对照组,差异均有统计学意义(P<0.05).结论 肌内效贴可有效改善脑瘫患儿流涎症状,促进吞咽功能恢复.

Introduction: The objective of our study was to explore the expression pattern of circular ribonucleic acid (RNA)_0,007,331 (circ_0,007,331) in breast cancer (BC) and its functional association with cellular paclitaxel (PTX) resistance and proliferation, migration, invasion and apoptosis.Methods: Real-time quantitative polymerase chain reaction was applied to measure RNA expression. The PTX resistance of BC cells was analyzed by cell counting kit-8 assay. Flow cytometry was applied to assess cell cycle progression and cell apoptosis. Transwell assays were utilized to analyze cell migration and invasion abilities. Protein expression was determined by Western blot assay. The target relationship between microRNA-200b-3p (miR-200b-3p) and circ_0,007,331 or Anillin (ANLN) was verified by dual-luciferase re-porter assay and RNA-pull down assay. The in vivo role of circ_0,007,331 was analyzed using xenograft tumor model.Results: Circ_0,007,331 expression was elevated in PTX-resistant BC cell lines relative to parental BC cell lines. Circ_0,007,331 contributed to the PTX resistance, proliferation, migration, invasion and suppressed the apoptosis of BC cells. Circ_0,007,331 interacted with miR-200b-3p in BC cells. Circ_0,007,331 silencing-mediated effects in BC cells were largely overturned by the knockdown of miR-200b-3p. ANLN was a target of miR-200b-3p in BC cells. Circ_0,007,331 silencing reduced ANLN expression partly through upregulating miR-200b-3p in BC cells. miR-200b-3p overexpression-induced effects in BC cells were largely counteracted by the accumulation of ANLN. Circ_0,007,331 silencing aggravated PTX-mediated inhibitory effect on tumor growth in vivo.Conclusions: Circ_0,007,331 contributed to the PTX resistance, proliferation and motility and inhibited the apoptosis of BC cells through mediating miR-200b-3p/ANLN signaling.(c) 2022 Elsevier Inc. All rights reserved.

目的:探讨胃癌组织中miRNA-340(miR-340)和cyclin D1的表达水平,并分析二者与胃癌患者临床病理参数的关系.方法:选取2019年12月至2020年06月期间我院病理科胃癌手术切除组织及对应癌旁正常胃黏膜组织(距离肿瘤边缘≥5 cm)共60例.采用qRT-PCR检测组织中miR-340的表达水平,采用免疫组化染色检测cyclin D1蛋白表达水平,并分析二者与胃癌患者临床病理参数的关系.结果:胃癌组织中miR-340的表达水平(2.38±0.51)明显低于癌旁正常黏膜组织(2.70±0.54),差异具有统计学意义(P<0.05);胃癌组织中cyclin D1蛋白的表达水平(48.33％)明显高于癌旁正常黏膜组织(16.67％),差异具有统计学意义(P<0.05).胃癌组织中miR-340表达与cyclin D1蛋白表达呈负相关(r=-0.367,P<0.05).胃癌组织中miR-340的表达与肿瘤直径、肿瘤的分化程度、浸润深度、临床分期有关(P<0.05),cyclin D1蛋白的表达与肿瘤的分化程度、浸润深度、临床分期、神经侵犯及淋巴结转移有关(P<0.05).结论:胃癌组织中miR-340和cyclin D1蛋白表达异常,且与不良预后相关,二者联合有望成为胃癌诊疗的潜在生物标志物.

目的 探讨晚期肺癌炎症指数(advanced lung cancer inflammatory index,ALI)对晚期结肠癌(advanced colon cancer,ACC)患者预后的影响.方法 纳入2014年1月 ～2017年12月在笔者医院诊治的ACC患者共103例,收集患者临床及随访资料,应用受试者工作特征(receiver operating character istic,ROC)曲线确定ALI的最佳截断值,并根据截断值将患者分为高ALI组和低ALI组,采用Kaplan-Meier法绘制生存曲线,组间比较利用Log-rank检验,并应用COX风险回归模型进行影响晚期结肠癌患者预后的单因素及多因素分析.结果 ROC曲线确定ALI的最佳截断值为27.16.高ALI组和低ALI组患者的中位无进展生存期(progression free survival,PFS)分别为12.1个月和7.6个月,中位总生存期(overall survival,OS)分别为33.2个月和15.1个月,差异有统计学意义(P＜0.05).COX多因素因素回归分析结果显示,ALI是影响患者PFS的独立预后因素,ALI与肝转移与否是影响晚期结肠癌患者OS的独立预后因素,差异均有统计学意义(P＜0.05).结论 低ALI组的晚期结肠癌患者预后一般较差,ALI对于评估晚期结肠癌患者的预后具有重要意义.

目的 评估贫血及贫血程度对中晚期胃癌术后患者预后的影响.方法 选取163例首诊中晚期(Ⅲ、Ⅳ期)胃癌患者,将患者分为初始贫血组和非贫血组,回顾性分析各临床病理参数与贫血的关系;生存分析采用Kaplan-Meier法,生存有差异行Log-Rank检验.多因素分析采用COX风险比例回归模型.结果 163例患者中,女性,非高血压的患者贫血的发生率更高(P<0.05),贫血组的PLR高于非贫血组(P<0.05).两组患者在吸烟、饮酒、糖尿病、冠心病人数所占比例比较,差异无统计学意义(P>0.05).年龄、BMI、分化程度、原发病灶部位、NLR、CEA、CA724水平与贫血的发生无关(P>0.05).多因素分析显示,性别,初始贫血,治疗后出现贫血与中晚期胃癌预后相关.结论 女性、初始贫血及治疗后出现贫血的中晚期胃癌术后患者预后不佳,贫血程度与预后无关.