Objective: This study aims to explore the minimum number of lymph nodes (LNs) necessary for assessing the postoperative staging of adenocarcinoma of esophagogastric junction (AEG).Methods: We extracted the data of patients from the Surveillance Epidemiology and End Results (SEER) database, who were pathologically diagnosed with AEG between 2000 and 2017. We explored the associations between the number of LNs and overall survival (OS) by univariate and multivariate analyses and determined the proper cutoff value of the number of LNs necessary for accurate postoperative staging.Results: Of the patients with AEG in the SEER database, 2668 met our inclusion criteria. The total number of regional LNs dissected was found to be significantly associated with survival in analyses stratified by T stage. Univariate and multivariate regression showed that age, grade, positive LNs, number of LNs examined, and T stage were independently associated with OS. For patients with T1-2 tumors, the 5-year survival rate was 58.7%, and patients with more than 11 LNs examined obtained a greater survival benefit. Among patients with T3-4 tumors, the 5-year survival rates were 28.9% and 39.7% for those with 1-16 LNs examined and for those with more than 17 LNs examined, respectively.Conclusion: To accurately determine the pathological stage of patients with AEG, no less than 11 LNs must be resected for patients with stage T1-2 disease, and no less than 16 LNs must be resected for patients with stage T3-4 disease.(c) 2023 Asian Surgical Association and Taiwan Robotic Surgery Association. Publishing services by Elsevier B.V. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/ licenses/by-nc-nd/4.0/).
Study reported that C-reactive protein (CRP) would peak at 48 h after the initiation of an acute inflammatory response. We proposed that the ratio of CRP level on postoperative day 3 to day 2 (POD3/2 CRP) can be used to early predict major postoperative complications (PCs) for patients who underwent laparoscopic radical gastrectomy. Patients were randomized into training cohort and validation cohort at a ratio of 7:3. PCs greater than grade II or more, according to Clavien-Dindo classification, were defined as major PCs. Three predictive models for major PCs based on CRP level were constructed, including POD3/2 CRP, the CRP level on POD3 (POD3 CRP), and the ratio of CRP level on POD3 to POD1 (POD3/1 CRP). The performances of three prediction models were assessed by AUC. Univariate and multivariate logistic regression analyses were performed to identify risk factors of major PCs. 344 patients were included. Major PCs were observed in 57 patients (16.6%). In the training cohort, POD3/2 CRP provided the best diagnostic accuracy with an AUC of 0.929 at an optimal cut-off value of 1.08, and the sensitivity and specificity were 0.902 and 0.880, respectively. In the validation cohort, the corresponding AUC was 0.917. BMI ≥ 25 kg/m2 and POD3/2 CRP > 1 were identified as risk factors for major PCs. POD3/2 CRP is a reliable marker to predict major PCs after laparoscopic radical gastrectomy. If CRP is higher on POD3 than on POD2, major PCs are highly likely.
Background Both tumor deposits (TD) and perineural invasion (PNI) have been identified as risk factors for poor survival in patients with non-metastatic colorectal adenocarcinoma (CRC). However, the adverse impacts of TD and PNI on the survival of patients with non-metastatic CRC have not been compared. Method Patients with non-metastatic CRC with known TD and PNI status were selected from the Surveillance, Epidemiology, and End Results (SEER) database. First, bivariate logistic regression analysis was utilized to identify the factors associated with TD and PNI status. Then, patients were divided into four groups, according to TD and PNI status. Propensity score matching (PSM) was performed to balance the baseline covariates. The impact of TD and PNI on survival was assessed by analyzing overall survival (OS) and cancer-specific mortality (CSM) rates. OS was calculated by the Kaplan–Meier method with log-rank analysis. CSM was estimated by competing risk analysis using the Fine and Gray model. Results A total of 70 689 patients with CRC met the inclusion and exclusion criteria. The positive rates of TD and PNI were 9.37% and 9.91%, respectively. For TD, the most important risk factor was N stage. With respect to PNI, the most significant factor was T stage. Tumor location, tumor size, differentiation grade, and serum CEA level were also correlated with TD and PNI status. After PSM, 1849 pairs were selected. Patients with TD + PNI + status had the worst 5 year CSM and 5 year OS. In addition, the long-term survival outcomes of patients with TD + PNI − and TD − PNI + status were comparable. Conclusion The adverse impacts of TD and PNI on the survival of patients with non-metastatic CRC were comparable. CRC patients with both TD and PNI positive had the worst survival outcome.
Backgroud: Esophagojejunal anastomotic leakage (EJAL) after laparoscopic gastrectomy with mediastinal lymph nodes resection for adenocarcinoma of esophagogastric junction (AEG) constituted the most common and serious postoperative complications (PCs). Early diagnosis of EJAL was of great importance. This retrospective study aimed to investigate whether the variation tendency of serum C-reactive protein can be used as an early marker to exclude EJAL after laparoscopic gastrectomy for AEG. Methods: Data for patients underwent laparoscopic gastrectomy for AEG, from January 2015 to March 2020, were retrospectively analyzed. Diagnostic accuracy was determined by the area under the receiver operating characteristic curve. Univariate and multivariate logistic regression analyses were performed to identify risk factors for PCs of grade II or more,according to the Clavien-Dindo classification. Results: A total of 114 patients were analyzed, of whom 21 (18.4%, 95% CI 11.4-25.4 %) developed major PCs, including anastomotic leakage in 13. The ratio of CRP level on postoperative day 3 to day 2 (POD3/2 CRP) provided the best diagnostic accuracy (AUC 0.903, 95% CI 0.814-0.993, p<0.001). Proximal gastrectomy (OR 8.224, 95% CI 1.976-34.234, p=0.004) and operation time ≥360 minutes (OR 6.753, 95% CI 2.037-22.395, p=0.002) were identified as significant independent risk factors for major postoperative complications. Conclusions: The POD3/2 CRP was the best marker to exclude anastomotic leakage after laparoscopic gastrectomy for AEG.
Background: Postoperative complications (PCs) after laparoscopic gastrectomy with mediastinal lymph nodes resection for adenocarcinoma of esophagogastric junction (AEG) prolonged the time of hospitalization and increased mortality rate. Early diagnosis of PCs was of great importance. This retrospective study aimed to investigate whether the variation tendency of serum C-reactive protein can be used as an early marker to predict major postoperative complications after laparoscopic gastrectomy for AEG. Methods: Data for patients underwent laparoscopic gastrectomy for AEG, from January 2015 to March 2020, were retrospectively analyzed. The area under the receiver operating characteristic (ROC) curve (AUC) was used to determine diagnostic accuracy of inflammatory markers. The optimal cutoff values were calculated by maximizing Youden’s index. Univariate and multivariate logistic regression analyses were performed to identify risk factors for PCs of grade III or more,according to the Clavien-Dindo classification. Results: A total of 114 patients were analyzed, of whom 21 (18.4%, 95% CI 11.4-25.4 %) developed major PCs, including anastomotic leakage in 13. The ratio of CRP level on postoperative day 3 to day 2 (POD3/2 CRP) provided the best diagnostic accuracy (AUC 0.903, 95% CI 0.814-0.993, p<0.001). Proximal gastrectomy (OR 8.224, 95% CI 1.976-34.234, p=0.004) and operation time ≥360 minutes (OR 6.753, 95% CI 2.037-22.395, p=0.002) were identified as significant independent risk factors for major PCs. Conclusions: The POD3/2 CRP was the best marker to predict PCs after laparoscopic gastrectomy for AEG.
Background Hypereosinophilic syndrome (HES) is a very rare disease and usually treated with corticosteroids. Gastrointestinal (GI) cytomegalovirus (CMV) infection is also rare but frequent in patients with immunocompromised status. These two related diseases present with similar manifestations, and may result in a life-threatening complication: perforation. However, the treatment strategies differ greatly. Here, we report a case of colon perforation due to cytomegalovirus infection in a patient with idiopathic HES. Case presentation A 41-year-old man with a history of HES was transferred to our hospital due to an acute onset of abdominal pain. During the treatment course of HES, this patient received CMV-DNA test with a result of < 2000 copies/ml. Computed tomography (CT) suggested colon perforation. An emergency surgery was performed immediately. Pathological diagnosis revealed CMV infection and infiltration of eosinophils. This patient received both anti-CMV therapy and immunosuppression therapy. Subsequently, the patient recovered and was discharged 25 days after the operation. Conclusion During the course of HES treatment, CMV infection should be reconsidered if digestive symptoms relapse.
MicroRNA-21-3p (miR-21-3p), the passenger strand of pre-mir-21, has been found to be high-expressing in various cancers and to be associated with tumour malignancy, which is proposed as a novel focus in malignant tumours. Colorectal cancer (CRC), currently known as one of the most prevalent malignancy, is a leading cause of cancer death. This study aimed to investigate the key role of miR-21-3p in CRC by inhibiting its expression using transfection with miR-21-3p inhibitors into human CRC HCT116 cells. Results showed that the expression of miR-21-3p was higher than other CRC cells used in the study including Lovo, HT29, Colo320 and SW480 cells, inhibition of which suppressed the proliferation and induced cell cycle arrest in HCT116 cells. Besides, transfection with miR-21-3p inhibitors also attenuated cell migration and invasion, and induced apoptosis as well. Moreover, luciferase assay confirmed RBPMS as a direct target of miR-21-3p in HCT116 cells. Further, miR-21-3p inhibitors increased the nuclear accumulation of Smad4 and reduced phosphorylation of ERK. Interestingly, we found that silence of RBPMS using RNA interference (siRNA) not only elevated the cell viability but also increased the phosphorylation of ERK and reversed the nuclear accumulation of Smad4 induced by miR-21-3p inhibitors in HCT116 cells. Data suggest that inhibition of miR-21-3p suppresses cell proliferation, invasion as well as migration and induces apoptosis by directly targeting RBPMS through Smad4/ERK signalling pathway in HCT116 cells. Our study demonstrates miR-21-3p as a potent target for suppressing tumour progression of CRC which may have implications in CRC therapy in the future.
Growing evidence has supported that long non-coding RNAs (lncRNAs) could play vital roles in the development, progression, and prognosis of colorectal cancer (CRC). However, little is known about the clinical significance of BRAF-activated non-coding RNA (BANCR) in CRC. The aim of this study is to explore the clinical value of lncRNA BANCR in CRC patients.
Helicobacter pylori infection is the strongest risk factor for development of gastric cancer. Host cellular stress responses, including inflammatory and immune responses, have been reported highly linked to H. pylori-induced carcinogenesis. However, whether mitochondrial regulation and metabolic reprogramming, which are potently associated with various cancers, play a role in H. pylori-induced gastric carcinogenesis is largely unknown. Here we revealed that Lon protease (Lonp1), which is a key inductive of mitochondrial unfolded protein response (UPRmt) and is required to maintain the mitochondrial quality, was greatly induced in H. pylori infected gastric epithelial cells. Importantly, we uncovered that knockdown of Lonp1 expression significantly diminished the metabolic switch to glycolysis and gastric cell proliferation associated with low multiplicity of H. pylori infection. In addition, Lonp1 overexpression in gastric epithelial cells also promoted glycolytic switch and cell overgrowth, suggesting H. pylori effect is Lonp1 dependent. We further demonstrated that H. pylori induced Lonp1 expression and cell overgrowth, at least partially, via HIF-1α regulation. Collectively, our results concluded the relevance of Lonp1 for cell proliferation and identified Lonp1 as a key regulator of metabolic reprogramming in H. pylori-induced gastric carcinogenesis.
LIN28B is involved in “stemness” and tumourigenesis by negatively regulating the maturation of let-7 microRNA family members. In this study, we showed that LIN28B expression promotes migration and recurrence of colon cancer. Immunohistochemistry and reverse-transcription polymerase chain reactions were performed to detect LIN28B expression in colon cancer tissue microarrays, paraffin-embedded surgical resected tissues and cancer cells. Loss-of-function, migration and proliferation analyses were performed to delineate the potential roles of LIN28B in colon cancer. LIN28B was upregulated in colon cancer tissue compared to normal mucosa, and its overexpression correlated with reduced patient survival and increased tumour recurrence. LIN28B suppression inhibited the migration of SW480 colon cancer cells and facilitated the cytotoxicity induced by oxaliplatin in SW480 and HCT116 colon cancer cells. In conclusion, LIN28B overexpression contributes to colon tumourigenesis, and LIN28B may serve as a diagnostic tool and therapeutic target for colon cancer.
Objective To study the relationship between the expression of EBV lytic genes and systemic lupus erythematosus (SLE). Methods The blood samples from 44 SLE patients and 43 matched normal controls were tested for BamHⅠ-W, the specific DNA fragment of EBV, by polymerase chain reaction(PCR)-Southern analysis. RT-PCR and Southern blotting were used to detect the EBV lytic genes (including immediate early genes BZLF1 and BRLF1, early genes BARF1, late genes BcLF1 and BLLF1) in EBV DNA-positive SLE patients. Results The EBV DNA was positive in 32 SLE patients and 3 controls. There was significant difference between the SLE patients and controls in the EBV DNA expression ( χ2 = 39.18, P 0.01), while no difference was observed between patients with active SLE and those with inactive SLE (q = 0.40, P 0.05). In the EBV DNA-positive SLE patients, 2 (both with active SLE) were positive for BARF1 mRNA; 14 (11 with active SLE and 3 with inactive SLE) were positive for BcLF1 mRNA; none was positive for BZLF1,BRLF1 or BLLF1 mRNA. No lytic genes were expressed in any of the 3 EBV DNA-positive controls. Conclusion EBV infection may be related to the development of SLE. EBV lytic infection exists in some SLE patients. EBV is at a low level of lytic activity in patients with SLE.