Comprehensive evaluation of rare case:From diagnosis to treatment of a sigmoid Schwannoma:A case report

BACKGROUND Schwannomas are uncommon tumors originating from Schwann cells,forming the neural sheath.They account for approximately 2%-6%of all mesenchymal tumors and are most commonly identified in peripheral nerve trunks,with rarity in the gastrointestinal tract.Among gastrointestinal locations,the stomach harbors the majority of nerve sheath tumors,while such occurrences in the sigmoid colon are exceptionally infrequent.CASE SUMMARY This study presented a clinical case involving a 60-year-old female patient who,during colonoscopy,was diagnosed with a submucosal lesion that was later identified as a nerve sheath tumor.The patient underwent surgical resection,and the diagnosis was confirmed through immunohistochemistry.This study highlighted an exceptionally uncommon occurrence of a nerve sheath tumor in the sigmoid colon,which was effectively managed within our department.Additionally,a comprehensive review of relevant studies was conducted.CONCLUSION The preoperative diagnosis of nerve sheath tumors poses challenges,as the definitive diagnosis still relies on pathology and immunohistochemistry.Although categorized as benign,these tumors have the potential to demonstrate malignant behavior.Consequently,the optimal treatment approach entails the complete surgical excision of the tumor,ensuring the absence of residual lesions at the margins.

Global research trends and prospects of cellular metabolism in colorectal cancer

BACKGROUND An increasing number of studies have focused on the role of cellular metabolism in the development of colorectal cancer(CRC).However,no work is currently available to synthesize the field through bibliometrics.AIM To analyze the development in the field of“glucose metabolism”(GM),“amino acid metabolism”(AM),“lipid metabolism”(LM),and“nucleotide metabolism”(NM)in CRC by visualization.METHODS Articles within the abovementioned areas of GM,AM,LM and NM in CRC,which were published from January 1,1991,to December 31,2022,are retrieved from the Web of Science Core Collection and analyzed by CiteSpace 6.2.R4 and VOSviewer 1.6.19.RESULTS The field of LM in CRC presented the largest number of annual publications and the fastest increase in the last decade compared with the other three fields.Meanwhile,China and the United States were two of the most prominent contri-butors in these four areas.In addition,Gang Wang,Wei Jia,Maria Notar-nicola,and Cornelia Ulrich ranked first in publication numbers,while Jing-Yuan Fang,Senji Hirasawa,Wei Jia,and Charles Fuchs were the most cited authors on average in these four fields,respectively.“Gut microbiota”and“epithelial-mesenchymal transition”emerged as the newest burst words in GM,“gut microbiota”was the latest outburst word in AM,“metastasis”,“tumor microenvironment”,“fatty acid metabolism”,and“metabolic reprogramming”were the up-to-date outbreaking words in LM,while“epithelial-mesenchymal transition”and“apoptosis”were the most recently occurring words in NM.CONCLUSION Research in“cellular metabolism in CRC”is all the rage at the moment,and researchers are particularly interested in exploring the mechanism to explain the metabolic alterations in CRC.Targeting metabolic vulnerability appears to be a promising direction in CRC therapy.

Effectiveness of fecal DNA syndecan-2 methylation testing for detection of colorectal cancer in a high-risk Chinese population

BACKGROUND Colorectal cancer(CRC)is among the most prevalent and life-threatening malignancies worldwide.Syndecan-2 methylation(mSDC2)testing has emerged as a widely used biomarker for early detection of CRC in stool and serum samples.Cancer(CRC)is among the most prevalent and life-threatening malignancies worldwide.mSDC2 testing has emerged as a widely used biomarker for early detection of CRC in stool and serum samples.AIM To validate the effectiveness of fecal DNA mSDC2 testing in the detection of CRC among a high-risk Chinese population to provide evidence-based data for the development of diagnostic and/or screening guidelines for CRC in China.METHODS A high-risk Chinese cohort consisting of 1130 individuals aged 40-79 years was selected for evaluation via fecal mSDC2 testing.Sensitivity and specificity for CRC,advanced adenoma(AA)and advanced colorectal neoplasia(ACN)were determined.High-risk factors for the incidence of colorectal lesions were determined and a logistic regression model was constructed to reflect the efficacy of the test.RESULTS A total of 1035 high-risk individuals were included in this study according to established criteria.Among them,16 suffered from CRC(1.55%),65 from AA(6.28%)and 189 from non-AAs(18.26%);150 patients were diagnosed with polyps(14.49%).Diagnoses were established based upon colonoscopic and pathological examinations.Sensitivities of the mSDC2 test for CRC and AA were 87.50%and 40.00%,respectively;specificities were 95.61%for other groups.Positive predictive values of the mSDC2 test for CRC,AA and ACN were 16.09%,29.89%and 45.98%,respectively;the negative predictive value for CRC was 99.79%.After adjusting for other high-risk covariates,mSDC2 test positivity was found to be a significant risk factor for the occurrence of ACN(P<0.001).CONCLUSION Our findings confirmed that offering fecal mSDC2 testing and colonoscopy in combination for CRC screening is effective for earlier detection of malignant colorectal lesions in a high-risk Chinese population.

Crosslink among cyclin-dependent kinase 9,ATP binding cassette transporter G2 and Beclin 1 in colorectal cancer

Colorectal cancer(CRC)ranks third in the number of cancers mainly because of the inability to diagnose it at an early stage.The pathogenesis of CRC is complicated,which is the result of the complex interaction of multiple genetic and environmental factors.Currently,one of the main treatments for CRC is chemotherapy.But the primary cause of CRC treatment failure is drug resistance.The expression of cyclin-dependent kinase 9(CDK9)was correlated with elevated autophagy levels in colon cancer,and high expression of CDK9 indicates a poor prognosis in CRC.The incidence of autophagy and the expressions of Beclin 1 and ATP binding cassette transporter G2 are different in left and right colon cancer,and autophagy may be involved in the occurrence of chemotherapy resistance.In this article,the roles of CDK9,ATP binding cassette transporter G2 and Beclin 1 in CRC were elucidated,emphasizing the linkages among them and providing potential therapeutic targets of CRC.

Current guidelines in the surgical management of hereditary colorectal cancers

Incidence of colorectal cancer(CRC)is on rise.While approximately 70%of all CRC cases are sporadic in nature,20%-25%have familial aggregation and only<5%is hereditary in origin.Identification of individuals with hereditary predilection for CRC is critical,as it has an impact on their overall surgical management including surgical timing,approach&technique and determines the role of prophylactic surgery and outcome.This review highlights the concept of hereditary CRC,provides insight into its molecular basis,possibility of its application into clinical practice and emphasizes the current treatment strategies with surgical management,based on the available international guidelines.

E3 ubiquitin ligase TRIM55 promotes metastasis of gastric cancer cells by mediating epithelial-mesenchymal transition

BACKGROUND Gastric cancer(GC)is considered a major global health problem.The role of TRIM55,a member of the three-domain protein family,in GC is unknown.AIM To determine the expression of TRIM55 in GC tissues and its relationship with clinicopathological characteristics,and to investigate the effects of TRIM55 on the malignant biological behavior of GC cells.METHODS Differential expression of TRIM55 in GC and para-cancer tissues was detected by immunohistochemistry,and the relationship between TRIM55 level and clinicopathological characteristics and prognosis was analyzed.Gain-of-function,lossof-function,cell counting kit-8 assay,colony formation,transwell assay,wound healing assay,and western blot analysis were used to assess the potential role of TRIM55 in the development of GC.RESULTS TRIM55 expression was significantly increased in GC tissues compared with adjacent normal tissues.High expression of TRIM55 was associated with advanced pathological stage and poor prognosis.Overexpression of TRIM55 promoted invasion and metastasis of GC cells in vitro by regulating epithelial-mesenchymal transition(EMT),whereas knockdown of TRIM55 had the opposite effect.Our data showed that TRIM55 is highly expressed in GC tissues,and is associated with poor prognosis.TRIM55 plays the role of an oncogene in GC,and it promotes metastasis of GC through the regulation of EMT.CONCLUSION TRIM55 may be a possible target for the diagnosis and prognosis of GC patients.

Association and prognostic significance of alpha-L-fucosidase-1 and matrix metalloproteinase 9 expression in esophageal squamous cell carcinoma

BACKGROUND Alpha-L-fucosidase-1(FUCA1)has been demonstrated to play opposing regulatory roles in adenocarcinoma and non-adenocarcinoma.Moreover,recent studies reported that FUCA1 could decrease the invasion capability by downregulating matrix metalloproteinase 9(MMP-9)expression.However,the potential role and prognostic significance of FUCA1 in esophageal squamous cell carcinoma(ESCC)have not yet been explored.AIM To evaluate the status,association,and prognostic value of FUCA1 and MMP-9 expression in ESCC.METHODS Patients who underwent esophagectomy for ESCC between January 1,2014,and December 31,2014 at Sun Yat-Sen University Cancer Center were enrolled.The expression status of FUCA1 and MMP-9 in cancerous tissues was detected using immunohistochemistry.In addition,the expression profiles of the FUCA1 and MMP-9 genes in non-metastatic ESCC were extracted from The Cancer Genome Atlas(TCGA)database.RESULTS High expression of FUCA1 and MMP-9 was found in 90 patients(75.6%)and 62 patients(52.1%),respectively.In the high FUCA1 expression group,the constituent ratios of patients with stage III disease(61.1%vs 37.9%,P=0.029),lymphatic invasion(62.2%vs 31.0%,P=0.003),and high MMP-9 expression(60.0%vs 27.6%,P=0.002)were significantly higher than those in the low FUCA1 expression group.In Kaplan-Meier univariate analysis,advanced tumor-nodemetastasis stage(III,P=0.001),positive regional lymph node metastasis(N+,P=0.002),high FUCA1 expression(P=0.001),and high MMP-9 expression(P=0.002)were potential predictors of shorter overall survival(OS),which was similar to the results analyzed based on the TCGA database.Further Cox multivariate regression analyses still demonstrated that FUCA1 and MMP-9 expression levels were independent prognostic factors of OS[hazard ratio(HR):0.484,95%confidence interval(CI):0.239-0.979;P=0.044;and HR:0.591,95%CI:0.359-0.973,P=0.039,respectively].CONCLUSION FUCA1 cooperation with MMP-9 may have a major role in affecting the ESCC invasion and metastatic capability,and serve as a valuable prognostic biomarker in ESCC.

Surgical resection of gastric stump cancer following proximal gastrectomy for adenocarcinoma of the esophagogastric junction

BACKGROUND Proximal gastrectomy(PG) is performed widely as a function-preserving operation for early gastric cancer located in the upper third of the stomach and is an important function-preserving approach for esophagogastric junction(EGJ)adenocarcinoma. The incidence of gastric stump cancer(GSC) after PG is increasing. However, little is known about the GSC following PG because very few studies have been conducted on the disease.AIM To clarify clinicopathologic features, perioperative complications, and long-term survival rates after the resection of GSC following PG.METHODS Data for patients with GSC following PG for adenocarcinoma of the EGJ diagnosed between January 1998 and December 2016 were retrospectively reviewed. Multivariate analysis was performed to identify factors associated with overall survival(OS). GSC was defined in accordance with the Japanese Gastric Cancer Association.RESULTS A total of 35 patients were identified. The median interval between the initial PGand resection of GSC was 4.9(range 0.7-12) years. In 21 of the 35 patients, the tumor was located in a nonanastomotic site of the gastric stump. Total gastrectomy was performed in 27 patients; the other 8 underwent partial gastrectomy. Postoperative complications occurred in 6 patients(17.1%). The tumor stage according to the depth of tumor invasion was T1 in 6 patients, T2 in3 patients, T3 in 9 patients, and T4 in 17 patients. Lymph node metastasis was observed in 18 patients. Calculated 1-, 3-, and 5-year OS rates were 86.5%, 62.3%,and 54.2%, respectively. Multivariate analysis showed advanced T stage to be associated with OS.CONCLUSION This study reveals the characteristics of GSC following PG for adenocarcinoma of the EGJ and suggests that a surgical approach can lead to a satisfactory outcome.

Significance of HER2 protein expression and HER2 gene amplification in colorectal adenocarcinomas

BACKGROUND Human epidermal growth factor receptor 2(HER2) is an oncogenic driver, and a well-established therapeutic target in breast and gastric cancers. While the role of HER2 as a prognostic biomarker in colorectal adenocarcinomas(CRCs) remains uncertain, its relevance as a therapeutic target has been established. We undertook the present study to evaluate the frequency of HER2 expression in CRC and to correlate it with various clinicopathological variables.AIM To correlate HER2 protein expression and HER2 gene amplification with clinicopathological features and survival in surgically resected CRC.METHODS About 1195 consecutive surgically resected CRCs were analyzed by immunohistochemical staining(IHC) to assess HER2 protein expression, and 141 selected tumors were further evaluated by fluorescence in situ hybridization(FISH) to assess HER2 gene amplification. Follow-up information was availablefor 1058 patients, and using this information we investigated the prevalence of HER2 protein overexpression and gene amplification in a large series of surgically resected CRCs, and evaluated the relationship between overexpression and clinicopathological parameters and prognosis.RESULTS HER2 IHC scores of 3+, 2+, 1+, and 0 were seen in 31(2.6%), 105(8.8%), 475(39.7%), and 584(48.9%) tumors, respectively. HER2 gene amplification was seen in 24/29 tumors with an IHC score of 3+(82.8%; unreadable in 2/31), 12/102 tumors with an IHC score of 2+(11.8%; unreadable in 2/104), and 0 tumors with IHC score of 1+(0/10). HER2 gene amplification was seen in 36/1191 tumors(3.0%; unreadable in 4/1195). Among the tumors with HER2 IHC scores of 3+and 2+, the mean percentage of tumor cells with positive IHC staining was 90%(median 100%, range 40%-100%) and 67%(median 75%, range 5%-95%),respectively(P < 0.05). Among tumors with IHC scores of 2+, those with HER2 gene amplification had a higher number of tumors cells with positive IHC staining(n = 12, mean 93%, median 95%, range 90%-95%) than those without(n =90, mean 70%, median 50%, range 5%-95%)(P < 0.05). HER2 gene status was significantly associated with distant tumor metastasis and stage(P = 0.028 and0.025). HER2 protein overexpression as measured by IHC or HER2 gene amplification as measured by FISH was not associated with overall survival(OS)or disease-specific survival for the overall group of 1058 patients. However,further stratification revealed that among patients with tubular adenocarcinomas who were 65 years old or younger(n = 601), those exhibiting HER2 gene amplification had a shorter OS than those without(mean: 47.9 mo vs 65.1 mo, P =0.04). Among those patients with moderately to poorly differentiated tubular adenocarcinomas, those with positive HER2 tumor IHC scores(2+, 3+) had a shorter mean OS than those with negative HER2 IHC scores(0, 1+)(47.2 mo vs64.8 mo, P = 0.033). Moreover, among patients with T2 to T4 stage tumors, those with positive HER2 IHC scores also had a shorter mean OS than those with negative HER2 IHC scores(47.1 mo vs 64.8 mo, P = 0.031).CONCLUSION HER2 protein levels are correlated with clinical outcomes, and positive HER2 expression as measured by IHC confers a worse prognosis in those patients 65 years old or younger with tubular adenocarcinomas.

MicroRNA-320a suppresses tumor progression by targeting PBX3 in gastric cancer and is downregulated by DNA methylation

BACKGROUND Ectopic expression of miRNAs promotes tumor development and progression.miRNA(miR)-320a is downregulated in many cancers,including gastric cancer(GC).However,the mechanism underlying its downregulation and the role of miR-320a in GC are unknown.AIM To determine expression and biological functions of miR-320a in GC and investigate the underlying molecular mechanisms.METHODS Quantitative real-time polymerase chain reaction(PCR)was used to determine expression of miR-320a in GC cell lines and tissues.TargetScanHuman7.1,miRDB,and microRNA.org were used to predict the possible targets of miR-320a,and a dual luciferase assay was used to confirm the findings.Western blotting was used to detect the protein levels of pre-B-cell leukemia homeobox 3(PBX3)in GC cells and tissue samples.Cell Counting Kit-8 proliferation,Transwell,wound healing,and apoptosis assays were performed to analyze the biological functions of miR-320a in GC cells.Methylation-specific PCR was used to analyze the methylation level of the miR-320a promoter CpG islands.5-Aza-2’-deoxycytidine(5-Aza-CdR)and trichostatin A(TSA)were used to treat GC cells.RESULTS miR-320a expression was lower in GC cell lines and tissues than in the normal gastric mucosa cell line GES-1 and matched adjacent normal tissues.miR-320a overexpression suppressed GC cell proliferation,invasion and migration,and induced apoptosis.PBX3 was a target of miR-320a in GC.The methylation level of the miR-320a promoter CpG islands was elevated and this was partly reversed by 5-Aza-CdR and TSA.CONCLUSION miR-320a acts as a tumor suppressor and inhibits malignant behavior of GC cells,partly by targeting PBX3.DNA methylation is an important mechanism associated with low expression of miR-320a.

Histo-molecular oncogenesis of pancreatic cancer:From precancerous lesions to invasive ductal adenocarcinoma

Pancreatic cancer is a lethal malignancy,whose precursor lesions are pancreatic intraepithelial neoplasm,intraductal papillary mucinous neoplasm,intraductal tubulopapillary neoplasm,and mucinous cystic neoplasm.To better understand the biology of pancreatic cancer,it is fundamental to know its precursors and to study the mechanisms of carcinogenesis.Each of these precursors displays peculiar histological features,as well as specific molecular alterations.Starting from such pre-invasive lesions,this review aims at summarizing the most important aspects of carcinogenesis of pancreatic cancer,with a specific focus on the recent advances and the future perspectives of the research on this lethal tumor type.

Polymorphisms in mucin genes in the development of gastric cancer

Gastric cancer(GC) is the third leading cause of cancerrelated death worldwide.In areas of high prevalence,such as Japan,South Korea and China,most cases of GC are related to Helicobacter pylori(H.pylori),which involves well-characterized sequential stages,including infection,atrophic gastritis,intestinal metaplasia,dysplasia,and GC.Mucins are the most abundant highmolecular-weight glycoproteins in mucus,which is the first line of defense and plays a major role in blocking pathogenic factors.Normal gastric mucosa shows expression of MUC1,MUC5 AC and MUC6 that is specific to cell type.However,the specific pattern of MUC1,MUC5 AC and MUC6 expression is changed in gastric carcinogenesis,accompanied by de novo expression of secreted MUC2.Recent studies have provided evidence that variations in these mucin genes affect many steps of GC development,such as H.pylori infection,and gastric precancerous lesions.In this review,we focus on studies of the association between polymorphisms in mucin genes and development of GC.This information should be helpful for the early detection,surveillance,and treatment of GC.

Role of retinoids in the prevention and treatment of colorectal cancer

Vitamin A and its derivatives, retinoids, have been widely studied for their use as cancer chemotherapeutic agents. With respect to colorectal cancer(CRC), several critical mutations dysregulate pathways implicated in progression and metastasis, resulting in aberrant Wnt/β-catenin signaling, gain-of-function mutations in K-ras and phosphatidylinositol-3-kinase/Akt, cyclooxygenase-2 over-expression, reduction of peroxisome proliferatoractivated receptor γ activation, and loss of p53 function. Dysregulation leads to increased cellular proliferation and invasion and decreased cell-cell interaction and differentiation. Retinoids affect these pathways by various mechanisms, many involving retinoic acid receptors(RAR). RAR bind to all-trans-retinoic acid(ATRA) to induce the transcription of genes responsible for cellular differentiation. Although most research concerning the chemotherapeutic efficacy of retinoids focuses on the ability of ATRA to decrease cancer cell proliferation, increase differentiation, or promote apoptosis; as CRC progresses, RAR expression is often lost, rendering treatment of CRCs with ATRA ineffective. Our laboratory focuses on the ability of dietary vitamin A to decrease CRC cell proliferation and invasion via RAR-independent pathways. This review discusses our research and others concerning the ability of retinoids to ameliorate the defective signaling pathways listed above and decrease tumor cell proliferation and invasion through both RAR-dependent and RAR-independent mechanisms.

The role of antioxidants and pro-oxidants in colon cancer

This review focuses on the roles antioxidants and prooxidants in colorectal cancer(CRC).Considerable evidence suggests that environmental factors play key roles in the incidence of sporadic CRC.If pro-oxidant factors play an etiological role in CRC it is reasonable to expect causal interconnections between the wellcharacterized risk factors for CRC,oxidative stress and genotoxicity.Cigarette smoking,a high dietary consumption of n-6 polyunsaturated fatty acids and alcohol intake are all associated with increased CRC risk.These risk factors are all pro-oxidant stressors and their connections to oxidative stress,the intestinal microbiome,intestinal microfold cells,cyclooxygenase-2 and CRCare detailed in this review.While a strong case can be made for pro-oxidant stressors in causing CRC,the role of food antioxidants in preventing CRC is less certain.It is clear that not every micronutrient with antioxidant activity can prevent CRC.It is plausible,however,that the optimal food antioxidants for preventing CRC have not yet been critically evaluated.Increasing evidence suggests that RRR-gamma-tocopherol(the primary dietary form of vitamin E)or other"non-alpha-tocopherol"forms of vitamin E(e.g.,tocotrienols)might be effective.Aspirin is an antioxidant and its consumption is linked to a decreased risk of CRC.

Cholangiocarcinoma developed in a patient with IgG4-related disease

A 77-year-old man with jaundice and a pancreatic head tumor was referred to our hospital in August2006.The initial laboratory tests,computed tomography(CT)scan,magnetic resonance imaging(MRI),and endoscopic retrograde cholangiopancreatography suggested IgG4-related cholangitis and autoimmune pancreatitis.Oral prednisolone(PSL)was then administered.This treatment reduced the size of the pancreatic parenchyma,and the lower common bile duct(CBD)returned to its normal size.Thus,the oral PSL was gradually tapered to a maintenance dose.In February 2010,a CT scan and MRI showed segmental wall thickening and stenosis of the middle CBD,the progression of which led to extrahepatic obstructive jaundice.We suspected the emergence of a cholangiocarcinoma rather than the exacerbation of the IgG4-related sclerosing cholangitis because the stricture of the CBD was short and localized.Then,a percutaneous transhepatic biliary drainage was performed.The biopsy specimens obtained via the percutaneous transhepatic tract indicated an abnormal glandular formation,suggesting the presence of a moderate,well-differencated adenocarcinoma.The gross examination,microscopic examination and immunohistochemical analysis of the pancreaticoduodenectomy specimen suggested that a cholangiocarcinoma developed from the IgG4-related sclerosing cholangitis.

Management of afferent loop obstruction from recurrent metastatic pancreatic cancer using a venting gastrojejunostomy

Pancreatic cancer is an aggressive malignancy poten-tially curable with surgical intervention. Following pan-creaticoduodenectomy for suspected pancreatic head malignancy, patients have a high risk for both immedi-ate and delayed problems due to surgical complica-tions and recurrent disease. We report here a patient with pancreatic cancer treated with pancreaticoduode-nectomy who developed recurrent disease resulting in obstruction of the afferent limb. The patient developed biliary obstruction and cholangitis at presentation. Her biliary tree failed to dilate which precluded safe percu-taneous biliary decompression. During surgical explo-ration, she was found to have a dilated afferent limb at the level of the transverse mesocolon. The patient underwent decompression of the afferent limb as well as the biliary tree using a venting gastrojejunostomy to the blind loop. This represents a novel surgical ap-proach for management of this complicated and diffi-cult problem.

Era of universal testing of microsatellite instability in colorectal cancer

Colorectal cancer (CRC) incidence and mortality are constantly decreasing, but CRC still remains the third most prevalent cancer and the third most common cause of cancer death in both males and females in the United States. Recent rapid declines in CRC incidence rates have largely been attributed to increases in screening that can detect and remove precancerous polyps, and the decrease in death rates for CRC largely reflects improvements in early detection, treatment and the understanding of molecular/genetic basis of CRC. One of the important molecular/genetic findings is the presence of microsatellite instability (MSI) in CRCs. Many studies have shown the importance of MSI testing in diagnosing Lynch syndrome and predicting prognosis and response to chemotherapeutic agents in CRCs. Increased emphasis has been placed on the importance of MSI testing for all newly diagnosed individuals with CRCs. Both immunohistochemical staining (IHC) and polymerase chain reaction (PCR)-based MSI testing show high sensitivity and specificity in detecting MSI. The current clinical guidelines and histopathology features are indicative of, but not reliable in diagnosing Lynch syndrome and CRCs with MSI. Currently, there are evidences that universal testing for MSI starting with either IHC or PCR-based MSI testing is cost effective, sensitive, specific and is getting widely accepted.

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GENERAL INFORMATIONWorld Journal of Gastrointestinal Oncology(World J Gastrointest Oncol,WJGO,ISSN 1948-5204,DOI:10.4251),is a monthly,open-access(OA),

The issue of lymphadenectomy during laparoscopic gastrectomy for gastric carcinoma

Surgical resection remains the mainstay of treatment for gastric cancer.Laparoscopic assisted gastrectomy has failed to gain universal acceptance as an alternative to the open approach for a number of reasons,one of which includes the issue of oncological radicality in terms of lymph node dissection.Nodal status,which is one of the most crucial and independent predictors of patient survival,therefore has been examined both in single institutional trials and also in randomised controlled trials especially on early gastric cancer.The issue of oncological adequacy for laparoscopic lymph node harvesting for advanced gastric cancer remains a contentious issue because of the unique challenges it poses in terms of complexity,safety and time,and also the lack of randomised controlled trials in this area.It is thus imperative that good quality multicentre randomised controlled trials are designed to investigate the benef its of extended lymphadenectomy in the setting of laparoscopic surgery,especially for advanced gastric cancer and its impact on both short and long term survival.

Network pharmacology-based analysis of heat clearing and detoxifying drug JC724 on the treatment of colorectal cancer

BACKGROUND Heat-clearing and detoxifying drugs has protective effect on colorectal cancer(CRC).Given the complicated features of Traditional Chinese medicine formulas,network pharmacology is an effective approach for studying the multiple interactions between drugs and diseases.AIM To systematically explore the anticancer mechanism of heat-clearing and detoxifying drug JC724.METHODS This study obtained the active compounds and their targets in JC724 from Traditional Chinese Medicine System Pharmacology Database.In addition,the CRC targets were obtained from Drugbank,TTD,DisGeNET and GeneCards databases.We performed transcriptome analysis of differentially expressed genes in CRC treated with JC724.Venn diagram was used to screen the JC724-CRC intersection targets as candidate targets.Core targets were selected by proteinprotein interaction network and herb ingredient-target-disease network analysis.The functional and pathway of core targets were analysed by enrichment analysis.RESULTS We found 174 active ingredients and 283 compound targets from JC724.940 CRC-related targets were reserved from the four databases and 304 CRC differentially expressed genes were obtained by transcriptome analysis.We constructed the network and found that the five core ingredients were quercetin,βBeta sitosterol,wogonin,kaempferol and baicalein.The core JC724-CRC targets were CYP1A1,HMOX1,CXCL8,NQO1 and FOSL1.JC724 acts on multiple signaling pathways associated with CRC,including the Nrf2 signaling pathway,oxidative stress,and the IL-17 signaling pathway.CONCLUSION In this study,we systematically analyzed the active ingredients,core targets and main mechanisms of JC724 in the treatment of CRC.This study could bring a new perspective to the heat-clearing and detoxifying therapy of CRC.