FDX1 as a novel biomarker and treatment target for stomach adenocarcinoma

BACKGROUND Stomach adenocarcinoma(STAD)is one of the main reasons for cancer-related deaths worldwide.This investigation aimed to define the connection between STAD and Cuproptosis-related genes(CRGs).Cuproptosis is a newly identified form of mitochondrial cell death triggered by copper.AIM To explore the identification of potential biomarkers for STAD disease based on cuproptosis.METHODS A predictive model using Gene Ontology(GO),Least Absolute Shrinkage and Selection Operator(LASSO),Kyoto Encyclopedia of Genes and Genomes(KEGG),Gene Set Variation Analysis(GSVA),and Gene Set Enrichment Analysis analyzed gene interconnections,focusing on 3 copper-related genes and their expression in The Cancer Genome Atlas-STAD.Networks for mRNA-miRNA and mRNA-transcription factor interactions were constructed.The prognostic significance of CRG scores was evaluated using time-receiver operating characteristic,Kaplan-Meier curves,and COX regression analysis.Validation was conducted with datasets GSE26942,GSE54129,and GSE66229.Expression of copper-related differ-entially expressed genes was also analyzed in various human tissues and gastric cancer subpopulations using the human protein atlas.RESULTS Three significant genes(FDX1,LIAS,MTF1)were identified and selected via LASSO analysis to predict and classify individuals with STAD into high and low CRG score subgroups.These genes were down-regulated in both risk categories.GO and KEGG analyses highlighted their involvement mainly in the electron transport chain.After validating their differential expression,FDX1 emerged as the most accurate diagnostic marker for gastric cancer.Additionally,the RCircos package localized FDX1 on chromosome 11.CONCLUSION Our study revealed that FDX1 could be a potential biomarker and treatment target for gastric malignancy,providing new ideas for further scientific research.

Comprehensive bioinformatic analysis of mind bomb 1 gene in stomach adenocarcinoma

BACKGROUND The carcinogenesis of stomach adenocarcinoma(STAD)involves many different molecules and multiple pathways,including the NOTCH signaling pathway.As a key factor that functions as a critical link in the NOTCH pathway,mind bomb 1(MIB1)is upregulated in various tumors and has been reported to promote cell metastasis and invasion.However,studies on the role of MIB1 in STAD are limited.Here,we evaluated the prognostic value of MIB1 in STAD and its association with immune infiltration and copy number variation.AIM To elucidate the relationship between MIB1 gene and gastric cancer(GC)and provide a new idea for the treatment of GC.METHODS We identified mutations in the MIB1 gene by searching the cBioPortal database and then analyzed their relationship with the overall survival rate and diseasefree survival rate using the Kaplan-Meier method.The Cancer Genome Atlas(TCGA)database provided transcript levels for MIB1 in STADs and normal tissues.As a method of distinguishing the STAD tissues from adjacent normal tissues,a receiver operating characteristic(ROC)curve was generated.Kaplan-Meier plotter was used to determine the effect of MIB1 expression on survival.Based on the LinkedOmics database,we were able to identify the coexpressed genes of the MIB1 gene,the top 50 positively correlated genes,and the top 50 negatively correlated genes.STRING was used to construct protein-protein interaction networks related to the MIB1 gene.An analysis of functional enrichment was carried out using the R package“Cluster Profiler”.The relationships between mRNA expression of MIB1 and immune infiltrates were assessed by Tumor IMmune Estimation Resource(TIMER)and the“GSVA package”in R.RESULTS According to the cBioPortal database,the MIB1 mutation rate in 287 patients in the TCGA dataset was approximately 6%.Kaplan-Meier survival analysis showed that patients with STAD in the mutated group had a worse prognosis than those in the unmutated group(P=0.0156).There was a significant upregulation of MIB1 expression in STAD tissues compared to adjacent normal tissues.A high T stage was associated with increased MIB1 mRNA expression.The ROC curve analysis revealed 59.4%sensitivity and 85.6%specificity of MIB1 for differentiating STAD tissues from adjacent normal tissues at a truncation level of 2.248.Kaplan-Meier plotter indicated that patients with higher MIB1 levels had a worse prognosis than those with lower levels(26.4 mo vs 56.2 mo,P=0.0330).A correlation analysis demonstrated an association between immune infiltrates and MIB1 mRNA expression.CONCLUSION Upregulation of MIB1 expression is significantly associated with poor survival rate and immune infiltration in gastric adenocarcinoma.MIB1 may be a biomarker for the poor prognosis of STAD patients and a potential immunotherapeutic target.

Survival-associated alternative splicing events interact with the immune microenvironment in stomach adenocarcinoma

BACKGROUND Alternative splicing(AS)increases the diversity of mRNA during transcription;it might play a role in alteration of the immune microenvironment,which could influence the development of immunotherapeutic strategies against cancer.AIM To obtain the transcriptomic and clinical features and AS events in stomach adenocarcinoma(STAD)from the database.The overall survival data associated with AS events were used to construct a signature prognostic model for STAD.METHODS Differentially expressed immune-related genes were identified between subtypes on the basis of the prognostic model.In STAD,2042 overall-survival-related AS events were significantly enriched in various pathways and influenced several cellular functions.Furthermore,the network of splicing factors and overallsurvival-associated AS events indicated potential regulatory mechanisms underlying the AS events in STAD.RESULTS An eleven-AS-signature prognostic model(CD44|14986|ES,PPHLN1|21214|AT,RASSF4|11351|ES,KIAA1147|82046|AP,PPP2R5D|76200|ES,LOH12CR1|20507|ES,CDKN3|27569|AP,UBA52|48486|AD,CADPS|65499|AT,SRSF7|53276|RI,and WEE1|14328|AP)was constructed and significantly related to STAD overall survival,immune cells,and cancer-related pathways.The differentially expressed immune-related genes between the high-and low-risk score groups were significantly enriched in cancer-related pathways.CONCLUSION This study provided an AS-related prognostic model,potential mechanisms for AS,and alterations in the immune microenvironment(immune cells,genes,and pathways)for future research in STAD.

Bioinformatics Analysis Revealed Potential Tumor Suppressors (KLF4/CGN), Oncogenes (SHH/LIF) and Biomarkers of Asian Stomach Adenocarcinoma

Stomach adenocarcinoma (STAD) is the fifth most prevalent cancer and the third leading cause of cancer-related death in the world and is more common in Asia than in most Western countries. There is an urgent need to identify potential novel oncogenes and tumor suppressor genes, and biomarkers for STAD. 6652 differentially expressed genes were identified between STAD and normal samples based on the transcriptome data analysis of the TCGA and GEO databases. 13 key modules were identified in STAD by WGCNA analysis. 293 potential STAD associated genes were identified from intersection by Venn Diagram. The 293 intersected genes were enriched in cell cortex and infection by GO and KEGG analysis. 10 hub genes were identified from PPI and Cytoscape analyses of the intersected genes. KLF4/CGN low and SHH/LIF high expression were associated with short overall survival of Asian STAD patients. Bioinformatics analysis revealed potential novel tumor suppressors (KLF4/CGN), oncogenes (SHH/LIF) and biomarkers for diagnosis, therapy and prognosis of STAD, specifically for Asian patients.

Activation of STAT3 signaling in human stomach adenocarcinoma drug-resistant cell line and its relationship with expression of vascular endothelial growth factor

AIM: To investigate the difference in activation of STAT3signaling between two human stomach adenocarcinoma cell lines: 5-fluorouracil resistant cell line and its parental cell line, and to evaluate its relationship with the expression of vascular endothelial growth factor (VEGF).METHODS: Western blot and electrophoretic mobility shift assay (EMSA) were used to detect the expression of phospho-STAT3 protein and constitutive activation of STAT3in two human stomach adenocarcinoma cell lines, 5-fluorouracil resistant cell line SGC7901/R and its parental cell line SGC7901, respectively. The mRNA expression of VEGF was analysed by semi-quantitative RT-PCR. The expressive intensity of VEGF protein was measured by immunocytochemistry.RESULTS: The expressions of phospho-STAT3 protein and constitutive activation of ST AT3 between two human stomach adenocarcinoma cell lines were different.Compared with the parental cell line SGC7901, the STAT3-DNA binding activity and the expressive intensity of phospho-STAT3 protein were lower in the drug-resistant cell line SGC7901/R. The expression levels of VEGF mRNA and its encoded protein were also decreased in drugresistant cell line.CONCLUSION: Over-expression of VEGF may be correlated with elevated STAT3 activation in parental cell line. Lower VEGF expression may be correlated with decreased STAT3activation in resistant cell line, which may have resulted from negative feedback regulation of STAT signaling.

Prognostic value of sorting nexin 10 weak expression in stomach adenocarcinoma revealed by weighted gene coexpression network analysis

AIM To detect significant clusters of co-expressed genes associated with tumorigenesis that might help to predict stomach adenocarcinoma(SA) prognosis.METHODS The Cancer Genome Atlas database was used to obtain RNA sequences as well as complete clinical data of SA and adjacent normal tissues from patients. Weighted gene co-expression network analysis(WGCNA) was used to investigate the meaningful module along with hub genes. Expression of hub genes was analyzed in 362 paraffin-embedded SA biopsy tissues by immunohistochemical staining. Patients were classified into two groups(according to expression of hub genes): Weak expression and over-expression groups. Correlation of biomarkers with clinicopathological factors indicated patient survival.RESULTS Whole genome expression level screening identified 6,231 differentially expressed genes. Twenty-four coexpressed gene modules were identified using WGCNA. Pearson's correlation analysis showed that the tan module was the most relevant to tumor stage(r = 0.24, P = 7 × 10-6). In addition, we detected sorting nexin(SNX)10 as the hub gene of the tan module. SNX10 expression was linked to T category(P = 0.042, χ~2 = 8.708), N category(P = 0.000, χ~2 = 18.778), TNM stage(P = 0.001, χ~2 = 16.744) as well as tumor differentiation(P = 0.000, χ~2 = 251.930). Patients with high SNX10 expression tended to have longer diseasefree survival(DFS; 44.97 mo vs 33.85 mo, P = 0.000) as well as overall survival(OS; 49.95 vs 40.84 mo, P = 0.000) in univariate analysis. Multivariate analysis showed that dismal prognosis could be precisely predicted clinicopathologically using SNX10 [DFS: P = 0.014, hazard ratio(HR) = 0.698, 95% confidence interval(CI): 0.524-0.930, OS: P = 0.017, HR = 0.704, 95%CI: 0.528-0.940].CONCLUSION This study provides a new technique for screening prognostic biomarkers of SA. Weak expression of SNX10 is linked to poor prognosis, and is a suitable prognostic biomarker of SA.

Progress and current perspectives of diagnosis and treatment of hepatoid adenocarcinoma of the stomach

Hepatoid adenocarcinoma of the stomach(HAS)is a rare malignant gastric tumor exhibiting both hepatocellular and adenocarcinomatous differentiation.Patients are often diagnosed at an advanced stage,and their clinical symptoms closely resemble those of gastric adenocarcinoma.Because of its rarity,misdiagnosis and missed diagnoses are prevalent.Compared with gastric adenocarcinoma,HAS typically exhibits higher invasiveness and amore unfavorable prognosis.This review aimed to elaborate on the pathological features,potential mechanisms,clinical characteristics,diagnosis,and prognosis of HAS.The insights provided aimed to contribute robust guidance for the clinical management of patients with HAS.

Hepatoid adenocarcinoma of the stomach:Thirteen case reports and review of literature

BACKGROUND The aim of the present study was to examine the clinical characteristics of hepatoid adenocarcinoma of the stomach (HAS) and its diagnosis,treatment,and prognosis.CASE SUMMARY A retrospective analysis of 13 HAS cases was performed.The mean age of the 13patients was 66.08 years,and 10 of the 13 patients were male.Prior to treatment,the alpha-fetoprotein levels in the serum were elevated in 7 patients,the tumour was located in the distal or gastric body in 11 patients,and the gastroscopy pathological results showed that 3 patients had poorly differentiated tumours and that 8 patients had moderately/poorly differentiated tumours.Abdominal CT scans showed local stomach wall thickening,and enlarged lymph nodes were visible around the stomach in 8 patients.Of the 13 patients,11 underwent radical surgery.The clinical pathological staging was as follows:Stage Ⅱ in 2 cases;stage Ⅲ in 8 cases;and stage Ⅳ in 1 case.A total of 3 patients were lost to follow-up.Otherwise,as of the last follow-up,3 patients had survived for 56 mo,and the other 7 patients failed to achieve long-term survival (survival period of 1-56 mo).CONCLUSION HAS is a special type of gastric cancer,and the prognosis of HAS has improved compared with past prognoses.Measurement of alpha-fetoprotein,early diagnosis,active surgical treatment,and application of new diagnostic and treatment techniques are conducive to improving the prognosis of HAS.

Liver metastasis from hepatoid adenocarcinoma of the stomach mimicking hepatocellular carcinoma: Dynamic computed tomography findings

AIM: To evaluate the dynamic computed tomography(CT) findings of liver metastasis from hepatoid adenocarcinoma of the stomach(HAS) and compared them with hepatocellular carcinoma(HCC).METHODS: Between January 2000 and January 2015, 8 patients with pathologically proven HAS and liver metastases were enrolled. Basic tumor status was evaluated for the primary tumor location and metastatic sites. The CT findings of the liver metastases were analyzed for tumor number and size, presence of tumor necrosis, hemorrhage, venous tumor thrombosis, and dynamic enhancing pattern.RESULTS: The body and antrum were the most common site for primary HAS(n = 7), and observed metastatic sites included the liver(n = 8), lymph nodes(n = 7), peritoneum(n = 4), and lung(n = 2). Most of the liver metastases exhibited tumor necrosis regardless of tumor size. By contrast, tumor hemorrhage was observed only in liver lesions larger than 5 cm(n = 4). Three patterns of venous tumor thrombosis were identified: direct venous invasion by the primary HAS(n = 1), direct venous invasion by the liver metastases(n = 7), and isolated portal vein tumor thrombosis(n = 2). Dynamic CT revealed arterial hyperattenuation and late phase washout in all the liver metastases.CONCLUSION: On dynamic CT, liver metastasis from HAS shared many imaging similarities with HCC. For liver nodules, the presence of isolated portal vein tumor thrombosis and a tendency for tumor necrosis are imaging clues that suggest the diagnosis of HAS.

Hepatoid adenocarcinoma of the stomach: A report of three cases

Hepatoid adenocarcinoma of the stomach (HAS) is a rare form of gastric cancer that has unique clinicopathological features and an extremely poor prognosis. Here, we report on three patients with suspected gastric cancer who were referred to our hospital. Gastrointestinal fiberscopy on the three patients revealed two lesions in the antrum and a third lesion in the gastroesophageal junction. The alpha fetoprotein (AFP) serum levels were markedly elevated in all cases. At the time of diagnosis, two cases were advanced stages with lymph nodes and/or liver metastases. Two patients underwent exploratory laparotomy. A total gastrectomy was performed on the operable lesion, and an expanded gastrectomy was completed in the case with hepatic metastases. Histopathological analysis revealed that the tumors displayed two pathological changes:hepatoid-like foci and adenocarcinomatous. Furthermore, the tumor cells were immunohistochemically positive for AFP, alpha-1 antitrypsin, and alpha-1 antichymotrypsin. All three patients received chemotherapy. The follow-up duration ranged from 8-36 mo. Our experience and previous published studies have suggested that HAS is an aggressive type of adenocarcinoma. However, radical surgery and chemotherapy may positively impact clinical outcomes.

Extremely well-differentiated adenocarcinoma of the stomach: Clinicopathological and immunohistochemical features

瞄准：否则作为极其区分得好的腺癌(EWDA ) 知道，子宫的宫颈的最小的偏差癌被它的良性的显微镜的外观与它的好攻击的行为相对照描绘。以便阐明 clinicopathological 特征和 EWDA 的胃的对应物的生物行为，用免疫组织化学，我们为联系 oncogene 的产品的表型的表示，增生的活动，和表示分析了九损害。方法：包括外科手术前的活体检视诊断， Clinicopathological 特征被考察。用免疫组织化学，在胃的损害把 p53 和 c-erbB-2 蛋白质的索引和表示标记的 Ki-67 被检测。结果：在中间的地点或上面第三个胃和水虫息似的宏观的特征胃的 EWDA 是特征的。尽管 9 损害中的 4 个显示出仅仅焦点的淋巴或静脉的侵略，淋巴节点转移不是现在，任何一个都没损害死于病人(吝啬的后续时期， 56 瞬间) 。EWDA 的所有 9 个盒子能被分类进胃的显型(5 损害) 和肠的显型(4 损害) 。以前的类似于的胃的小凹的上皮，颈部粘液细胞或幽门的腺，而是他们的乳突的结构经常被伸长，肿瘤房间和他们的原子核稍微更大并且更亢奋与正常上皮相比色彩。后者与最小的原子非典型和不规则的腺类似于肠的组织变形；二这些损害表明了完全的肠的显型，当二表明了不完全的肠的显型时。把索引标记的 Ki-67 是低的，任何一个都没盒子揭示 p53 和 c-erbB-2 蛋白质的在表示上。结论：不同于宫颈的最小的偏差癌，这些调查结果建议胃的 EWDA 是低档恶意的损害。这有利生物行为被把索引和 p53 或 c-erbB-2 蛋白质在表示上的缺乏标记的低 Ki-67 的数据支持。因为它到有肠的组织变形的正常胃粘膜或粘膜的相似， EWDA 经常被误诊。阻止如此的损害的错误诊断，临床、病理学的特征应该被考虑。

STERIGMATOCYSTIN INDUCED ADENOCARCINOMA OF THE LUNG AND ATYPICAL HYPERPLASIA OF GLANDULAR STOMACH IN MICE

Aspergillus versicolor was isolated from the gastric juice of patients with chronic stomach diseases in high-risk area of gastric cancer. Mice fed with Aspergillus-inoculated corn flour developed adenocarcinoma of the lung in 15 of 35 mice (42.9%) and atypical hyperplasia of the glandular stomach in 13 of 35 mice (37.4%). Sterigmatocystin was identified by high performance liquid chromato-graphy (HPLC) and fluorescence spectrophotometry in the extract of Aspergillus-inoculated corn flour. The results suggest that the mycotoxin Sterigmatocystin may play a potential role in carcinogenesis in human.

胃肝样腺癌的CT特征

目的分析胃肝样腺癌的临床和CT特征,提高对本病的认识。资料与方法回顾性分析2012年9月—2023年4月苏州大学附属第一医院经病理证实的38例胃肝样腺癌患者的临床病理资料、实验室检查、CT资料,分析病灶大小、形态、密度、边界、强化方式、转移及侵犯等情况,总结其临床及CT特征。结果38例患者中,血清甲胎蛋白水平升高24例,免疫组化甲胎蛋白表达阳性32例。CT表现为胃壁增厚,门静脉期病变最大截面长径2.38~11.95cm,中位数为5.200(3.365,7.215)cm,23例伴溃疡,20例内见坏死,25例周围侵犯,14例出现肝脏转移,5例出现门静脉系统癌栓。结论胃肝样腺癌为罕见肿瘤,血清甲胎蛋白常增高,CT增强检查肿瘤常较大,可见坏死,渐进性或持续强化,易发生转移、侵犯门静脉,认识这些特征有助于提高诊断水平。

^(18)F-FDG PET/CT在胃肝样腺癌诊断中的价值

目的分析胃肝样腺癌的^(18)F-FDG PET/CT显像特征,结合血清AFP水平,两者联合提高对该病认识及诊断准确率。方法选取5例经病理学证实胃肝样腺癌患者的^(18)F-FDG PET/CT检查资料,分析患者的临床表现、原发病灶位置及形态、最大标准摄取值(SUVmax)、肿瘤标志物水平、预后情况。结果原发病灶位于胃窦3例,位于贲门-胃体处2例。5例病灶的SUVmax范围为7.58~23.6,平均值13.8±6.4。5例中位生存期为8个月。结论胃肝样腺癌是一种特殊类型癌,侵袭性强,临床表现无特异性,明确诊断有赖于影像学与病理结合,无肝脏病变时患者血清AFP升高具有重要的诊断提示意义。

CT动态容积灌注成像检出早期胃癌并评估其病理分型

目的 观察CT动态容积灌注(DVPCT)成像检出早期胃癌并鉴别其病理分型的价值。方法 回顾性分析127例经病理证实的早期胃癌患者,根据术前检查方式分为增强CT组(n=67)或DVPCT组(n=60);比较组间一般资料、CT资料,以及DVPCT组内胃印戒细胞癌(SRCC)与胃腺癌的强化程度、门静脉期与延迟期峰值期相及峰值时间;绘制受试者工作特征(ROC)曲线,计算曲线下面积,评估DVPCT时间-密度曲线(TDC)鉴别早期SRCC与腺癌的效能。结果 DVPCT组肿瘤检出率、剂量长度乘积及有效剂量均高于增强CT组(P均<0.05);2组患者年龄、性别、病理分型、肿瘤位置及肿瘤最大径差异均无统计学意义(P均>0.05)。52例(52/60,86.67%)经DVPCT检出早期胃癌的患者中,SRCC 12例、腺癌39例、黏液腺癌1例;其中,早期胃SRCC与早期胃腺癌患者肿瘤强化程度、门静脉期及延迟期峰值期相及峰值时间差异均有统计学意义(P均<0.05)。以峰值时间37.3 s为最佳截断值,DVPCT TDC鉴别早期胃SRCC与早期胃腺癌的敏感度、特异度、阳性预测值、阴性预测值、准确率及曲线下面积分别为83.33%、84.62%、62.50%、94.29%、84.31%及0.895。结论 DVPCT检出早期胃癌效果优于常规增强CT;TDC可有效鉴别早期胃SRCC与早期胃腺癌。

一种罕见的胃癌-胃肝样腺癌

胃肝样腺癌(hepatoid adenocarcinoma of the stomach,HAS)是一种表现在肝脏外的罕见的特殊胃恶性肿瘤,与一般的胃癌不同,HAS的恶性程度高、侵袭性高,容易出现肝转移、淋巴转移、预后差,但是HAS的诊断、临床病理特征和预后仍有较大的争论.为了帮助临床医生更了解这种胃癌,本文从甲胎蛋白的起源开始对HAS的诊断、临床病理特征及其预后等进行系统综述,从而为这种特殊胃癌的临床诊治提供建设性的意见及帮助.

ELF1负调控TRIM16促进胃腺癌上皮间质转化

目的探讨E74样因子1(ELF1)对胃腺癌细胞迁移、侵袭和上皮间充质转化(EMT)的影响及其机制。方法利用基因表达谱交互分析2(GEPIA2)数据库分析ELF1在胃腺癌组织中的表达情况。实时荧光定量PCR(RT-qPCR)和Western blot分析胃癌细胞和正常胃黏膜细胞中ELF1的表达水平。ELF1短发夹RNA(sh-ELF1)或其阴性对照短发夹RNA(sh-NC)转染AGS细胞,分别命名为sh-ELF1组和sh-NC组。划痕实验检测细胞迁移能力,Tranwell侵袭实验检测细胞侵袭能力,Western blot检测EMT相关分子Snail、E-cadherin、Vimentin及三重基序包含蛋白16(TRIM16)的表达情况。染色质免疫共沉淀-PCR(ChIP-PCR)实验检测ELF1与TRIM16启动子区的结合情况。选取AGS细胞进行挽救实验,分为sh-ELF1+si-TRIM16组(sh-ELF1和TRIM16小干扰RNA共同转染)和sh-ELF1+si-NC组(sh-ELF1和阴性对照小干扰RNA共同转染),Western blot检测TRIM16、Snail、E-cadherin及Vimentin的表达情况,划痕实验和Tranwell侵袭实验分别检测细胞迁移和侵袭能力。结果ELF1在胃腺癌组织和胃癌细胞中高表达(P<0.05)。与sh-NC组相比,sh-ELF1组细胞迁移能力和侵袭能力显著降低(P<0.05);与sh-NC组相比,sh-ELF1组Snail和Vimentin表达水平显著下降(P<0.05),而E-cadherin和TRIM16表达水平显著上升(P<0.05)。ChIP-PCR结果显示,ELF1与TRIM16的启动子区结合,进而抑制TRMI16的表达。挽救实验表明,与sh-ELF1+si-NC组相比,sh-ELF1+si-TRIM16组Snail、Vimentin的表达上调(P<0.05),而E-cadherin的表达下调(P<0.05),细胞迁移能力和侵袭能力均增加(P<0.05)。结论ELF1可通过靶向负调控TRIM16促进胃腺癌细胞的迁移、侵袭和EMT。

12例胃肝样腺癌临床病理特征及预后分析

目的总结12例胃肝样腺癌(HAS)患者临床资料,探讨胃肝样腺癌的临床病理特征及预后。方法回顾性分析2016年1月至2022年12月宁夏医科大学总医院收治的12例HAS患者的临床病理学资料,病理及免疫组化结果由两位病理科医师复阅肿瘤组织切片判定。通过描述性统计方法总结患者的人口统计学和肿瘤特征。运用COX单因素和多因素回归分析胃肝样腺癌患者预后。结果12例患者中男性9例、女性3例,男女比例为3∶1;疾病中位诊断年龄为60岁;最常见发病部位为胃窦(41.7%),病变类型以BorrmannⅢ型(溃疡型)为主(45.5%),Lauren分型以弥漫型为主(58.3%),肿瘤分化程度多呈低分化(83.3%);8例患者血清癌胚抗原(CEA)≥5 ng·mL^(-1),6例患者进行血清甲胎蛋白(AFP)检测,其中4例(66.7%)升高,1例(16.7%)AFP≥300 ng·mL^(-1)。11例患者进行了手术治疗,术前远处转移5例,其中4例同时发生肝脏、腹膜后淋巴结转移;1例仅发生腹膜后淋巴结转移。10例患者(83.3%)发生脉管浸润,7例患者(58.3%)发生神经侵犯。根据肝样分化区所占比例不同,4例患者(33.3%)为单纯型HAS、8例患者(66.7%)为混合型HAS。临床分期:Ⅰ期1例、Ⅱ期1例、Ⅲ期5例、Ⅳ期5例。12例患者中位生存期为16个月,1、3、5年存活率分别为83.0%、41.0%、20.0%。根据单因素分析结果,不排除CEA水平、临床分期、肝样腺癌类型、是否行根治性手术、是否存在远处转移、远处转移是否为肝转移HepPar-1是否表达与患者预后可能有关。结论HAS是一种罕见的异质性肿瘤,常伴血清AFP升高及部分肝细胞癌标记物表达,易发生脉管浸润、淋巴结及远处转移,预后极差。

甲胎蛋白阳性胃癌和胃肝样腺癌预后危险因素对比分析

目的 研究甲胎蛋白阳性胃癌(AFPGC)和胃肝样腺癌(HAS)临床病理特征异同及预后危险因素分析。方法 回顾性分析西京医院2015年1月至2020年12月胃癌手术患者信息,共筛选出AFPGC手术患者60例,HAS手术患者39例。从患者病历中检索临床数据并通过电话和短信获得随访数据。采用χ^(2)检验和Fisher精确检验进行统计分析。基于Kaplan-Meier检验方法进行生存分析并使用GraphPad Prism 9绘制变量的生存曲线。所有检验均以α=0.05作为检验标准。结果 HE染色显示HAS具有独特的组织结构,正常胃上皮、肝细胞样分化胃腺癌区和普通胃腺癌区常共存于同一肿瘤组织中。相关性分析显示AFPGC患者肿瘤组织尾型同源盒基因转录因子2免疫组化染色阳性率高于HAS患者(85.0%vs 66.7%,P=0.032),HAS患者肿瘤组织肝细胞样分化标志物甲胎蛋白(AFP)、谷氨酰胺合成酶和人类婆罗双树样基因-4的阳性率均为41.0%,肝细胞石蜡抗原、磷脂酰肌醇蛋白聚糖3的阳性率均为64.1%。AFPGC和HAS的术后3年生存分析无显著性差异,但HAS的术后5年预后差于AFPGC(P=0.062)。血清AFP≥60.4μg/L的AFPGC组3年(P=0.030)及5年(P=0.022)预后均明显差于血清AFP<60.4μg/L组。血清AFP<20μg/L的HAS组3年(P=0.050)和5年(P=0.084)预后均明显差于血清AFP升高的HAS组。结论 HAS目前诊断依赖病理学检查,极易漏诊。HAS术后长期预后差于AFPGC,血清AFP≥60.4μg/L是AFPGC的预后危险因素,血清AFP低表达是HAS的预后危险因素。

食管胃结合部腺癌外科治疗中国专家共识(2024年版)

《食管胃结合部腺癌外科治疗中国专家共识(2018版)》自颁布以来,很大程度上促进了我国食管胃结合部腺癌(AEG)的规范化、同质化诊疗,提升了我国AEG的外科治疗水平。经过5年的临床实践,该共识普适性和可行性已得到广泛证实。鉴于AEG发病率持续上升的趋势及其解剖部位、临床病理特征和分子生物学特征的特殊性,AEG成为近5年来外科临床研究的热点之一,并不断有新的临床研究证据发表。但是,对于AEG的定义、分型、分期、手术路径、切除范围、淋巴结清扫规范和消化道重建等外科问题,仍旧存在争议。鉴于此,有必要对2018版的共识进行更新。《食管胃结合部腺癌外科治疗中国专家共识(2024版)》在前一版的基础上,整合并分析5年来新的最佳临床证据,参考最新国际指南与共识,结合我国外科专家组意见,针对AEG外科治疗关键环节,包括AEG的定义和分型、手术径路、手术方式、淋巴结清扫范围、消化道重建方式及外科围手术期治疗等存在争议的问题,提出相关推荐建议,以期更好地规范AEG的外科治疗方式。在本共识中未解决的相关问题,尚需积极开展高质量的临床研究,以逐步探索和解决。