Objective To identify and isolate the variant gene associated with gastric adenocarcinoma and clone the fragment of variant gene.Methods By arbitrarily primer polymerase chain reaction (AP-PCR), DNA samples from 5 matched gastric adenocarcinoma and non-tumor gastric tissues were analysed. Results The produced AP-PCR profiles were different in each matched gastric adenocarcinoma and non-tumor gastric tissue. One differentiated amplified DNA fragments PW2.2 from a matched gastric adenocarcinoma were cloned. The result of Southern blot hybridization with PW2.2 as a probe showing that this fragment was also found in some other gastric adenocarcinoma samples. Conclusion AP-PCR fingerprinting assay can be used to identify and clone the variant genes associated with gastric adenocarcinoma.
Objective To evaluate the effect of regiono-perfusional chemotherapy of pancreatic adenocarcinoma, and to seek the management of its complications. MethodsThirty-six patients with unresectable pancreatic adenocarcinoma received selectively intra-arterial catheterization and perfused with 5-Fu, ADM, DDP. Results Six patients had complete response, 15 partial response, and one underwent radical resection subsequently. Cmplications occurred in 14 patients with 2 patients died of complications.Conclusion Regiono-perfusional chemotherapy of pancreatic adenocarcinoma is effective, but the complications can not be neglected.
ObjectiveTo observe the effect of lncRNA-metastasis-associated lung adenocarcinoma transcript 1(MALAT1)on colorectal cancer cells-induced angiogenesis, and explore the potential underlying mechanism. MethodsMALAT1 was overexpressed in colorectal cancer cells SW48 by plasmids transfection, then SW48 cells were cultured at normoxia or hypoxia conditions. The culture media was collected, and the concentration of vascular endothelial growth factor (VEGF) in the media was measured by the enzyme-linked immuno sorbent assay (ELISA), and the human umbilical vein endothelial cells (HUVEC) were incubated with the media collected above. Meanwhile, the expression of hypoxia-inducible factor-1α(HIF-1α) in SW48 cells was detected by western blot. ResultsOverexpression of MALAT1 increased the VEGF level in the culture media, normoxia:the MALAT1 group (514±32) mg/L vs. the control group (110±14) mg/L, P < 0.05; hypoxia:the MALAT1 group (928±18) mg/L vs. the control group (230±21) mg/L, P < 0.05. Meanwhile, the tube formation activity of HUVEC was enhanced, and the expression of HIF-1αwas elevated in the MALAT1 group by western blot. ConclusionOverexpression of MALAT1 could promote colorectal cancer cells-mediated angiogenesis, it may be developed as a new drug target for colorectal cancer treatment.
ObjectiveTo summarize the remodeling of cholesterol metabolism in the occurrence and progression of pancreatic ductal adenocarcinoma (PDAC), and to review the research progress on targeted cholesterol metabolism in the treatment of PDAC. MethodRelevant literatures on cholesterol metabolism in the occurrence, development, and diagnosis and treatment of PDAC in recent years were searched and reviewed. ResultsMetabolites of PDAC tumor cells affected the expression of oncogenes or tumor suppressor genes. Signaling regulation within tumor cells affects cholesterol metabolism, characterized by increased de novo cholesterol synthesis and esterification, and reduced efflux. Tumor cells also regulated tumor immune microenvironment or tumor stroma formation through cholesterol metabolism. Inhibiting cholesterol metabolism could suppress the proliferation, invasion and migration of PDAC tumor cells, and combination therapy targeting cholesterol metabolism had a synergistic anti-PDAC effect. ConclusionsRemodeling of cholesterol metabolism occurs in both PDAC tumor cells and the tumor microenvironment, and is closely related to the occurrence, development, invasion, metastasis, and treatment response of PDAC. Targeting cholesterol metabolism or combined application with chemotherapy drugs can have anticancer effects. However, more research is needed to support the translation of cholesterol metabolism regulation into clinical treatment applications.
ObjectiveTo analyze the expression and clinical significance of cyclin-dependent kinase 1 (CDK1) in lung adenocarcinoma by bioinformatics.MethodsBased on the gene expression data of lung adenocarcinoma patients in The Cancer Genome Atlas (TCGA), the differential expression of CDK1 in lung adenocarcinoma tissues and normal lung tissues was analyzed. The expression of CDK1 gene in lung adenocarcinoma was analyzed by UALCAN at different angles. Survival analysis of different levels of CDK1 gene expression in lung adenocarcinoma was performed using Kaplan-Meier Plotter. Correlation Cox analysis of CDK1 expression and overall survival was based on clinical data of lung adenocarcinoma in TCGA. Gene set enrichment analysis was performed on gene sequences related to CDK1 expression in clinical cases. The protein interaction network of CDK1 from Homo sapiens was obtained by STRING. CDK1-related gene proteins were obtained and analyzed by the web server Gene Expression Profiling Interactive Analysis (GEPIA).ResultsBased on the analysis of TCGA gene expression data, CDK1 expression in lung adenocarcinoma was higher than that in normal lung tissues. UALCAN analysis showed that high CDK1 expression may be associated with smoking. Survival analysis indicated that when CDK1 gene was highly expressed, patients with lung adenocarcinoma had a poor prognosis. Univariate and multivariate Cox regression analysis of CDK1 expression and overall survival showed that high CDK1 expression was an independent risk factor for survival of patients with lung adenocarcinoma. Gene set enrichment analysis revealed that high CDK1 expression was closely related to DNA replication, cell cycle, cancer pathway and p53 signaling pathway.ConclusionCDK1 may be a potential molecular marker for prognosis of lung adenocarcinoma. In addition, CDK1 regulation may play an important role in DNA replication, cell cycle, cancer pathway and p53 signaling pathway in lung adenocarcinoma.
ObjectiveTo construct DPC4 gene recombinant expression vector and to study the inhibitory effect of DPC4 on the growth of human pancreatic adenocarcinoma cell line (PC3) cells.MethodsDPC4 cDNA was amplified from K562 cell line using RTPCR, and was cloned into the pcDNA3.1 vector to construct a recombinant expression vector plasmid pcDNA3.1DPC4. The recombinant expression plasmid was transferred into PC3 cells by liposome method. After G418 selection, cell cycle and apoptosis were assessed by flow cytometry, then the cell growth rate was estimated by cell count. The cells being not transferred plasmid and transferred pcDNA3.1 plasmid were used as controls.ResultsThe DPC4 gene recombinant expression vector was constructed. Wildtype DPC4 gene attributed to the increase of G1 phase cells and the decrease of S phase cells in PC3 cells,and could inhibit the growth of PC3 cells, the cell growth rates was reduced to 34.3%-41.1% of that of the controls, but cell apoptosis was not observed on all groups. ConclusionWildtype DPC4 gene could inhibit the proliferation of human pancreatic adenocarcinoma cells and could become one of the target genes of pancreas adenocarcinoma gene therapy
The incidence of esophagogastric junction adenocarcinoma is gradually increasing, and gastrointestinal surgery and thoracic surgery are paying more and more attention to its surgical treatment. “Chinese expert consensus on the surgical treatment of adenocarcinoma of esophagogastric junction (2018 edition)” discussed the core issues in the field of surgical treatment such as definition, classification, surgical approach, lymphadenectomy, digestive tract reconstruction, and neoadjuvant therapy for esophagogastric junction adenocarcinoma, and gave recommendations. However, there is still some controversy about these issues. The author discussed the consensus and controversial issues relevant to esophagogastric junction adenocarcinoma and related research progress in recent years.
Objective To identify the immune cell-related biomarkers in lung adenocarcinoma using weighted gene co-expression network. Methods In this study, based on TCGA database, gene co-expression network was constructed in TCGA-LUAD by WGCNA package, and different gene modules were formed by clustering. At the same time, ESTIMATE analysis was performed on lung adenocarcinoma tumor samples in the TCGA-LUAD dataset. Gene enrichment pathways in the most significant related modules were evaluated by GO and KEGG assays. Candidate hub genes in the selected key modules were used to construct protein-protein interaction (PPI) network for intersection to obtain hub genes. The prognostic properties of these hub genes and patient immune cell infiltration were verified by Kaplan-Meier curve and TIMER algorithm. Multivariate Cox regression analysis was performed on the acquired hub gene and a prognostic risk model was constructed. Results In the co-expression network, we observed that the brown module was closely related to ImmuneScore, StromalScore and ESTIMATE Score. Five immune-related hub genes CD53, PLEK, SPI1, IL10RA and C3AR1 were obtained. The enrichment analysis of brown module found that module genes were mainly enriched in GO items such as innate immune response regulation and KEGG pathways such as NF-kappa B signaling pathway. In addition, the results of this study also found that the expression levels of 5 hub genes were significantly positively correlated with the infiltration abundance of immune cells. IPS and TIDE validated the immune relevance of the model. At the same time, we found that the RiskScore we established has great potential in predicting immunotherapy. Conclusion In summary, the five key genes related to immune cells obtained may provide new and effective potential targets for the immunotherapy of lung adenocarcinoma, which is also beneficial to provide personalized diagnosis and treatment strategies for patients with lung adenocarcinoma in the later stage.
ObjectiveTo explore the predictive value of CT signs of mixed ground-glass nodules in the pathological subtype and differentiation of lung adenocarcinoma. MethodsThe clinical data of 66 patients with mixed ground-glass nodules pathologically diagnosed as invasive adenocarcinoma (IAC) in the Second Department of Thoracic Surgery, the First Affiliated Hospital of Xiamen University from May to December 2021 were retrospectively analyzed, including 20 males and 46 females, aged 35-75 years. The CT findings were analyzed before operation, and the lesion profile was cut after operation to distinguish the ground-glass and solid components, and the pathological results of different positions were obtained. According to the postoperative pathological results, the patients were divided into a low-risk group (containing adherent type and no components of micropapillary subtype and solid subtype, n=16), a medium-risk group (containing niple or acinar type and no components of micropapillary subtype and solid subtype, n=38), and a high-risk group (containing micropapillary or solid subtype, n=12). The relationships between CT features and the pathological subtype and degree of differentiation were analyzed and compared. ResultsIn 66 patients with IAC, the infiltration degree of solid components was greater than that of ground-glass components. When the solid component ratio (CTR) was≥25% (sensitivity 90.2%, specificity 64.0%, P=0.005), and the average CT value was＞−283.95 HU (sensitivity 82.9%, specificity 64.0%, P=0.000), the histological grade was more inclined to medium and low differentiation. The CTR, Ki-67, average CT value and histological grade of IAC in the medium- and high-risk groups were higher than those of nodules in the low-risk group. ConclusionThe infiltration degree of solid components is higher than that of ground-glass components in IAC mixed ground-glass nodules. The pathological subtype, Ki-67 expression and histological grade of lung adenocarcinoma can be predicted according to its CT characteristics, which has important clinical significance for determining the timing of surgery.
Objective To approach the inhibitory effect of Iodine-125 (125I) on moderately differentiated adenocarcinoma of colon by establishing the nude mice model bearing subcutaneous tumor of SW480 cell. Methods The moderately differentiated adenocarcinoma of colon cells (SW480) were implanted subcutaneously to the nude mice. The bearing tumor nude mice were randomly divided into study group (n=24) and control group (n=24) by using method of random sampling. One blank particle was implanted into the mouse of the control group, a 1.48×107 Bq dosage 125I particle was implanted into the mouse of the study group, then the growth of tumor was observed after implantation. Six bearing tumor nude mice were sacrificed and the tumors were obtained on day 7, 14, 21, and 28 after implantation, respectively. The expression of proliferating cell nuclear antigen (PCNA) was detected by immunohistochemistry SP method. The cell apoptosis was determined by TUNEL method. Results As the accumulation of radiation time, the volume of tumor in the study group was smaller than that in the control group on day 10 after implantation (Plt;0.05). The PCNA labeling index in the study group was lower than that in the control group on day 14 after implantation (Plt;0.05). The apoptotic index in the study group was higher than that in the control group on day 21 after implantation (Plt;0.05). Conclusion Persistent low dose 125I radiation could down-regulate the expression of PCNA, and induce the apoptosis of moderately differentiated adenocarcinoma of colon cell, which might be a mechanism of inhibiting the proliferation of moderately differentiated adenocarcinoma of colon.