Digestive Tumors Research Articles

A Case of Double Primary Carcinoma was Accidentally Found During Operation: Hepatocellular Carcinoma and Appendiceal Mucinous Adenocarcinomas

Background: Synchronous double primary cancer of hepatocellular carcinoma (HCC) and appendiceal mucinous adenocarcinomas has not been reported. Liver metastasis of digestive tract tumors is so common that it is easy to ignore the existence of double primary cancer in the digestive system. The appendiceal malignant tumor itself is easy to be misdiagnosed or missed. For a better understanding of HCC and appendiceal mucinous adenocarcinomas, the information on our recent case has been summarized. Case Presentation: A 58-year-old man was admitted with repeated upper abdominal pain for one week. Imaging examination and liver biopsy pathology were diagnosed as hepatocellular carcinoma. Colonoscopy showed no obvious organic lesions in the terminal ileum and the whole large intestine. We had anatomical resection of the S5 and S6 segments of the liver. At the same time, two suspicious lesions in the right liver were ablated by microwave. But at the end of the operation, we accidentally found a hard mass about 3 cm × 3 cm in size at the end of the appendix. And the rapid pathological results showed appendiceal adenocarcinoma, so we had a right hemicolectomy. So far, the diagnosis of the patient was changed to synchronous double primary cancer consisting of HCC and appendiceal mucinous adenocarcinomas. Conclusion: It is the first time we have reported a case of synchronous double primary hepatic cancer consisting of HCC and appendiceal mucinous adenocarcinomas in the world. Due to the rarity and unspecific clinical features, it is extremely challenging to be diagnosed preoperatively. It requires a more comprehensive understanding of the patient's medical history, careful physical examination, and comprehensive exploration of the abdominal cavity during the operation to avoid missed diagnosis. Patients with HCC and appendiceal mucinous adenocarcinomas are generally associated with poor prognosis. It needs we put forward new countermeasures for the new question.

GK921, a transglutaminase inhibitor, strengthens the antitumor effect of cisplatin on pancreatic cancer cells by inhibiting epithelial-to-mesenchymal transition

Pancreatic adenocarcinoma (PAAD), a common digestive malignant tumor, presents high mortality rates and limited treatment methods. Currently, chemotherapy remains the main therapy method for patients with PAAD. As a classical chemotherapy drug, cisplatin (DDP) is limited by dose-related toxicity in patients with PAAD. In this study, we demonstrated that TGM2 may be a treatment and prognosis marker in pancreatic cancer patients. Co-treatment of low dose of DDP and GK921, a transglutaminase (TGM2) inhibitor, is capable of synergistically inhibiting the PAAD cell viability and proliferation in vitro and in vivo. Based on in vitro study, GK921 inhibited the epithelial-to-mesenchymal transition (EMT) induced by TGM2 as well as aggravated cell cycle arrest and apoptosis resulted from DDP, making pancreatic cancer cells more sensible to DDP. Our results showed that GK921 increased the protein levels regarding E-cadherin as well as decreased the protein level regarding Snail2, N-cadherin, which indicated that GK921 inhibited EMT in pancreatic cancer cells. Snail2 overexpression inhibited GK921/DDP-induced cell apoptosis, as well as mitigated the GK921/DDP-caused cell death and the EMT inhibition. In vivo studies also found GK921/DDP combination can further inhibit the growth of PAAD without significantly side effects. To sum up, we showed that GK921 increased PAAD cells sensitivity to DDP via inhibiting EMT. As revealed, DDP/GK921 co-treatment could promisingly serve for treating PAAD patients.

Analysis of textbook outcomes for ampullary carcinoma patients following pancreaticoduodenectomy.

Textbook outcomes (TOs) have been used to assess the quality of surgical treatment for many digestive tumours but not ampullary carcinoma (AC). To discuss the factors associated with achieving a TO and further explore the prognostic value of a TO for AC patients undergoing curative pancreaticoduodenectomy (PD). Patients who underwent PD at the China National Cancer Center between 1998 and 2020 were identified. A TO was defined by R0 resection, examination of ≥ 12 Lymph nodes, no prolonged hospitalization, no intensive care unit treatment, no postoperative complications, and no 30-day readmission or mortality. Cox regression analysis was used to identify the prognostic value of a TO for overall survival (OS) and recurrence-free survival (RFS). Logistic regression was used to identify predictors of a TO. The rate of a TO and of each indicator were compared in patients who underwent surgery before and after 2010. Ultimately, only 24.3% of 272 AC patients achieved a TO. A TO was independently associated with improved OS [hazard ratio (HR): 0.443, 95% confidence interval (95%CI): 0.276-0.711, P = 0.001] and RFS (HR: 0.379, 95%CI: 0.228-0.629, P < 0.001) in the Cox regression analysis. Factors independently associated with a TO included a year of surgery between 2010 and 2020 (OR: 4.549, 95%CI: 2.064-10.028, P < 0.001) and N1 stage disease (OR: 2.251, 95%CI: 1.023-4.954, P = 0.044). In addition, the TO rate was significantly higher in patients who underwent surgery after 2010 (P < 0.001) than in those who underwent surgery before 2010. Only approximately a quarter (24.3%) of AC patients achieved a TO following PD. A TO was independently related to favourable oncological outcomes in AC and should be considered as an outcome measure for the quality of surgery. Further multicentre research is warranted to better elucidate its impact.

Quality of life after prophylactic surgery for colorectal adenomatous polyposis.

Colorectal adenomatous polyposis is characterized by the onset of tens to thousands of adenomas in the colorectal epithelium and, if not treated, leads to a lifetime increased risk of developing colorectal cancer compared to the general population. Thus, prophylactic surgery is recommended. This study aims to investigate the quality of life of colorectal adenomatous polyposis patients following prophylactic surgery and indirectly compares these findings with those of healthy adults of the normative sample. All patients who underwent prophylactic surgery for polyposis and were in follow-up at the hereditary digestive tract tumors outpatient department of our institute were eligible for the study. The Short Form-36 questionnaire and 21 ad hoc items were used at the time of clinical evaluation. A total of 102 patients were enrolled. For the SF-36 domains, mean values ranged from 64.18 for vitality to 88.49 for physical functioning, with the highest variability for role-physical limitations; the minimum value of functioning was reached for role-physical limitations, role-emotional limitations, and social functioning. The maximum value of functioning was reached for role-emotional limitations (73.96%) and role-physical limitations (60.42%). In total, 48.96% and 90.63% of patients reported no fecal or urinary incontinence episodes, respectively; 69.79% of patients did not have problems in work/school resumption or the personal sexual sphere. Quality of life following prophylactic surgery for these patients seems to be good when indirectly compared to HP-normative samples'. Young adult patients appear to quickly manage and adapt to changes in bowel functioning. A minority of patients may experience social and sexual issues.

Interdisciplinary Spanish consensus on a watch-and-wait approach for rectal cancer.

Watch-and-wait has emerged as a new strategy for the management of rectal cancer when a complete clinical response is achieved after neoadjuvant therapy. In an attempt to standardize this new clinical approach, initiated by the Spanish Cooperative Group for the Treatment of Digestive Tumors (TTD), and with the participation of the Spanish Association of Coloproctology (AECP), the Spanish Society of Pathology (SEAP), the Spanish Society of Gastrointestinal Endoscopy (SEED), the Spanish Society of Radiation Oncology (SEOR), and the Spanish Society of Medical Radiology (SERAM), we present herein a consensus on a watch-and-wait approach for the management of rectal cancer. We have focused on patient selection, the treatment schemes evaluated, the optimal timing for evaluating the clinical complete response, the oncologic outcomes after the implementation of this strategy, and a protocol for surveillance of these patients.

Prediction of quality markers and medicinal value of sea buckthorn leaves based on network pharmacology, content determination, and activity evaluation

The leaves of sea buckthorn(Hippophae rhamnoides), considered as common food raw materials, have records of medicinal use and diverse pharmacological activities, showing a potential medicinal value. However, the active substances in the sea buckthorn leaves and their mechanisms of action remain unclear. In addition, due to the extensive source and large variety variations, the quality evaluation criteria of sea buckthorn leaves remain to be developed. To solve the problems, this study predicted the main active components, core targets, key pathways, and potential pharmacological effects of sea buckthorn leaves by network pharmacology and molecular docking. Furthermore, ultra-performance liquid chromatography with diode-array detection(UPLC-DAD) was employed to determine the content of active components and establish the chemical fingerprint, on the basis of which the quality markers of sea buckthorn leaves were predicted and then verified by the enzyme activity inhibition method. The results indicated that sea buckthorn leaves had potential therapeutic effects on a variety of digestive tract diseases, metabolic diseases, tumors, and autoimmune diseases, which were consistent with the ancient records and the results of modern pharmacological studies. The core targets of sea buckthorn leaves included PTPN11, AKT1, PIK3R1, ESR1, and SRC, which were mainly involved in the PI3K-AKT, MAPK, and HIF-1 signaling pathways. In conclusion, the active components of sea buckthorn leaves are associated with the rich flavonoids and tannins, among which quercitrin, narcissoside, and ellagic acid can be used as the quality markers of sea buckthorn leaves. The findings provide a reference for the quality control and further development and utilization of sea buckthorn leaves as medicinal materials.

The Tetraspanin Tspan8 Associates with Endothelin Converting Enzyme ECE1 and Regulates Its Activity.

Tspan8 is a member of the tetraspanins family of cell surface molecules. The ability of tetraspanins to organize membrane microdomains with other membrane molecules and interfere with their function suggests that they could act as surface integrators of external or internal signals. Among the first identified tetraspanins, Tspan8 promotes tumor progression and metastasis, presumably by stimulating angiogenesis and cell motility. In patients, its expression on digestive tract tumors seems to be associated with a bad prognosis. We showed previously that Tspan8 associates with E-cadherin and EGFR and modulates their effects on cell motility. Using Mass spectrometry and western blot, we found a new partner, the endothelin converting enzyme ECE1, and showed that Tspan8 amplifies its activity of conversion of the endothelin-1 precursor bigET1 to endothelin. This was observed by transduction of the colon carcinoma cell line Isreco1, which does not express Tspan8, and on ileum tissue fragments of tspan8ko mice versus wild type mice. Given these results, Tspan8 appears to be a modulator of the endothelin axis, which could possibly be targeted in case of over-activity of endothelins in biological processes of tissues expressing Tspan8.

CircEIF3I facilitates the recruitment of SMAD3 to early endosomes to promote TGF-β signalling pathway-mediated activation of MMPs in pancreatic cancer

BackgroundAmong digestive tract tumours, pancreatic ductal adenocarcinoma (PDAC) shows the highest mortality trend. Moreover, although PDAC metastasis remains a leading cause of cancer-related deaths, the biological mechanism is poorly understood. Recent evidence demonstrates that circular RNAs (circRNAs) play important roles in PDAC progression.MethodsDifferentially expressed circRNAs in normal and PDAC tissues were screened via bioinformatics analysis. Sanger sequencing, RNase R and actinomycin D assays were performed to confirm the loop structure of circEIF3I. In vitro and in vivo functional experiments were conducted to assess the role of circEIF3I in PDAC. MS2-tagged RNA affinity purification, mass spectrometry, RNA immunoprecipitation, RNA pull-down assay, fluorescence in situ hybridization, immunofluorescence and RNA–protein interaction simulation and analysis were performed to identify circEIF3I-interacting proteins. The effects of circEIF3I on the interactions of SMAD3 with TGFβRI or AP2A1 were measured through co-immunoprecipitation and western blotting.ResultsA microarray data analysis showed that circEIF3I was highly expressed in PDAC cells and correlated with TNM stage and poor prognosis. Functional experiments in vitro and in vivo revealed that circEIF3I accelerated PDAC cells migration, invasion and metastasis by increasing MMPs expression and activity. Mechanistic research indicated that circEIF3I binds to the MH2 domain of SMAD3 and increases SMAD3 phosphorylation by strengthening the interactions between SMAD3 and TGFβRI on early endosomes. Moreover, AP2A1 binds with circEIF3I directly and promotes circEIF3I-bound SMAD3 recruitment to TGFβRI on early endosomes. Finally, we found that circEif3i exerts biological functions in mice similar to those of circEIF3I in humans PDAC.ConclusionsOur study reveals that circEIF3I promotes pancreatic cancer progression. circEIF3I is a molecular scaffold that interacts with SMAD3 and AP2A1 to form a ternary complex, that facilitates the recruitment of SMAD3 to early endosomes and then activates the TGF-β signalling pathway. Hence, circEIF3I is a potential prognostic biomarker and therapeutic target in PDAC.

Research progress on drug delivery systems for curcumin in the treatment of gastrointestinal tumors.

Curcumin is a natural compound with a diketone structure, which can control the growth, metastasis, recurrence, neovascularization, invasion, and drug resistance of gastrointestinal tumors by inhibiting nuclear factor κB, overexpression of tumor cells, vascular endothelial growth factor, etc. However, due to the low bioavailability of curcumin formulation, it did not fully exert its pharmacological effects, and its application and development in the treatment of various malignant tumors are still limited. This review summarizes the research on drug delivery systems of curcumin combating digestive tract tumors in order to further reduce the toxic side effects of curcumin-containing drugs and fully exert their pharmacological activities, and improve their bioavailability and clinical value.

Inhibition of FNDC1 suppresses gastric cancer progression by interfering with Gβγ-VEGFR2 complex formation

Gastric cancer (GC) is a prevalent digestive tract malignant tumor characterized by an insidious onset, ease of metastasis, rapid growth, and poor prognosis. Here, we report that fibronectin type III domain containing 1 (FNDC1) has high expression in GC and indicates poor outcomes in patients with GC. FNDC1 over-expression or knockdown promotes or inhibits tumorigenesis and metastasis, respectively. The expression of FNDC1 is upregulated by TWIST1, strengthening its interaction with Gβγ and VEGFR2. The formation of the trimers, TWIST1 plus Gβγ and VEGFR2, increases VEGFR2 phosphorylation and Gβγ trafficking, which activates RAS-MAPK and PI3K-AKT signaling, benefiting GC progression. In this study, we demonstrated that arsenite can efficiently suppress FNDC1 expression, attenuating the formation of the trimers and downstream pathways. Altogether, our results indicate that FNDC1 might be a promising target for clinical treatment and prognostic judgment, while FNDC1 inhibition by arsenite provides a new opportunity for overcoming this fatal disease.

Application of serum gastric function markers and digestive tumor indices to the diagnosis of early gastric cancer and precancerous lesions.

To study the levels of carcinoembryonic antigen (CEA), carbohydrate antigen (CA) 199, CA724, CA242, pepsinogen (PG) I, PGII, gastrin-17 (G-17), the PGI/PGII ratio (PGR), as well as the expression of p27 and Ki67, in patients suffering from early gastric cancer and intraepithelial neoplasia and to provide new markers for the diagnosis of early gastric cancer and precancerous lesions. A retrospective study where the blood serum concentration of CEA, CA199, CA724, CA242, PGI, PGII, G-17 and PGR were tested and also the protein expression of p27 and Ki67 was detected in patients tissues by immunohistochemistry in the Gastrointestinal Endoscopy Center of the Affiliated Hospital of Xuzhou Medical University, Xuzhou, China, from March 2018 to March 2021. Carbohydrate antigen 242 and CA199 levels in tumor tissue significantly differed among the groups. Pepsinogen I levels decreased with increasing disease severity, G-17 levels increased with the aggravation of severity, and p27 expression decreased with the severity. The combination of serum gastric function markers (PGI and G-17) and p27 digestive tumor indices can serve as markers for the diagnosis of early gastric cancer and intraepithelial neoplasia.

Serpin Family A Member 1 Is Prognostic and Involved in Immunological Regulation in Human Cancers.

Serpin family A member 1 (SERPINA1) encodes a protease inhibitor participating in many human diseases, but its value in immunoregulation and prognosis of human cancers remains unclear. In this study, through comprehensive analysis of data from The Cancer Genome Atlas (TCGA) datasets, we found that SERPINA1 was dysregulated in many cancers compared with normal tissues. SERPINA1 expression was significantly associated with prognosis, immune subtype, molecular subtype, immune checkpoint (ICP) genes, tumor mutational burden (TMB), microsatellite instability (MSI), and the estimation of stromal and immune cells in malignant tumor tissues using expression data (ESTIMATE) score. There was a strong connection between SERPINA1 expression and tumor-infiltrating lymphocytes, and SERPINA1 showed significant relation to gene markers of immune cells in digestive tumors. Fluorescence-based multiplex immunohistochemistry confirmed that SERPINA1 protein expression was related to clinicopathologic features and immune infiltrates in hepatic cancer. This study suggests that SERPINA can potentially serve as a novel biomarker for cancer prognosis and immunotherapy.

Baicalin suppresses colorectal cancer cell proliferation, potentially via ARRDC4: Bioinformatics and experimental analysis

Colorectal cancer (CRC) is a malignant digestive tumor mostly prevalent among adolescents and has great proliferation potential. Baicalin is a flavonoid derived from the dried root of Scutellaria baicalensis, it has tumor-suppressing effects on various kinds of tumors. Although baicalin has been shown to regulate genes associated with CRC, its role in cancer proliferation remains poorly illustrated. In this work, we evaluated the effect of baicalin on the proliferative ability of three CRC cell lines using a cell counting kit-8 assay. Furthermore, we screened for differentially expressed genes in HCT-116 cells using baicalin-treated samples and control samples on a gene expression profile microarray. We identified 19 genes were identified significantly downregulated by baicalin, which may potentially play an indispensable role in the proliferation of HCT-116 cells. High-content screening evaluated whether silencing the 19 genes affected HCT-116 cell growth. The results showed that knocking down ARRDC4 exhibited the most potent inhibition of cell proliferation. ARRDC4 expression was knocked down by transfecting CRC cells with lentiviral shRNA. MTT assay, Caspase-Glo 3/7 assay and immunohistochemistry analysis were performed to explore the effects of baicalin on proliferation and apoptosis of CRC cells. Besides, RT-PCR showed that the expression levels of ARRDC4 mRNA decreased significantly in HCT-116 cells after baicalin treatment. In conclusion, these findings indicated that baicalin may attenuated the expression of ARRDC4 via regulating the levels of LCN2, Claudin-2 and GSTA4 to inhibit HCT-116 cell proliferation. The theoretical underpinnings for the investigation of the pharmacological effects of baicalin in the treatment of human CRC were also established in this study.

Amifostine attenuates bleomycin-induced pulmonary fibrosis in mice through inhibition of the PI3K/Akt/mTOR signaling pathway

Amifostine is a normal cell protection agent, not only used in the adjuvant therapy of lung cancer, ovarian cancer, breast cancer, nasopharyngeal cancer, bone tumor, digestive tract tumor, blood system tumor and other cancers in order to reduce the toxicity of chemotherapy drugs, and recent studies have reported that the drug can also reduce lung tissue damage in patients with pulmonary fibrosis, but its mechanism of action is not yet fully understood. In this study, we explored the potential therapeutic effects and molecular mechanisms of AMI on bleomycin (BLM)-induced pulmonary fibrosis in mice. A mouse model of pulmonary fibrosis was established using BLM. We then assessed histopathological changes, inflammatory factors, oxidative indicators, apoptosis, epithelial-mesenchymal transition, extracellular matrix changes, and levels of phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signaling pathway-related proteins in the BLM-treated mice to determine the effect of AMI treatment on these factors. BLM-treated mice had substantial lung inflammation and abnormal extracellular matrix deposition. Overall, treatment with AMI significantly improved BLM-induced lung injury and pulmonary fibrosis. More specifically, AMI alleviated BLM-induced oxidative stress, inflammation, alveolar cell apoptosis, epithelial-mesenchymal transition, and extracellular matrix deposition by regulating the PI3K/Akt/mTOR signaling pathway. This finding that AMI can alleviate pulmonary fibrosis in a mouse model by inhibiting activation of the PI3K/Akt/mTOR signaling pathway lays a foundation for potential future clinical application of this agent in patients with pulmonary fibrosis.

Analysis of influencing factors of self-care self-efficacy among patients with digestive tract tumors

Analysis of influencing factors of self-care self-efficacy among patients with digestive tract tumors

Clinical Characteristics and Responses to Immune Checkpoint Inhibitors in RET-Aberrant Digestive Tract Tumours.

RET plays an oncogenic role, and its aberrations are potentially actionable. However, they have seldom been reported in tumours other than lung or thyroid cancers. The correlation of RET aberrations with clinical characteristics, co-occurring aberrations, and responses to immune checkpoint inhibitors (ICPi) have not been explored in digestive tract tumours. The aim of the study was to elucidate the clinical characteristics, frequently co-altered genes, and treatment responses in RET-aberrant digestive tract tumours. We retrospectively evaluated patients with digestive tract cancers for RET-aberrant tumours via FoundationOne CDx tumour-based selected genome sequencing from Jan 2016 to Jan 2021. In a median follow-up time of 51 months, a total of 453 patients were analysed. RET-aberrant tumours accounted for 4.4% in the studied population (n=20), and 1.1% had an oncogenic fusion (n=5). APC, KRAS, TP53, MSH6 and STK11 were the differentiallyco-altered genes (all false discovery rates <0.05). The presence of RET aberrations alone was not a significant prognostic factor. Eleven patients with RET-aberrant tumours received ICPi-based treatment and none achieved an objective response. In contrast, 47 patients with non-aberrant tumours received ICPi treatment and had an objective response rate of 27.7% and a significantly longer treatment duration (6.2 vs 2.8 months, p=0.0008). Albeit rarely, RET aberrations can be found in digestive tract tumours. Patients with RET-aberrant tumours have a blunted response to ICPi and a comparable prognosis as compared with RET-wild type tumours. Together, these results provide insights into this rare but potentially actionable target in digestive tract tumours.

Construction and validation of a SEER-based prognostic nomogram for young and middle-aged males patients with hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) is the most common digestive tumor, and we aimed to develop and validate nomogram models, predicting the overall survival (OS) of young and middle-aged male patients with HCC. We extracted eligible data from relevant patients between 2000 and 2017 from the Surveillance, Epidemiology, and End Results (SEER) database. In addition, randomly divided all patients into two groups (training and validation = 7:3). The nomogram was established using effective risk factors based on univariate and multivariate analysis. The area under the time-dependent curve, calibration plots, and decision curve analysis (DCA) were used to evaluate the effective performance of the nomogram. The risk stratifications of the nomogram and the AJCC criteria-based tumor stage were compared. 11 variables were selected by univariate and multivariate analysis to establish the nomogram of HCC. The AUC values of 3, 4, and 5 years of the time-ROC curve are 0.858, 0.862 and 0.859 for the training cohort, and 0.858, 0.877 and 0.869 for the validation cohort, respectively, indicating that the nomogram has a good ability of discrimination. The calibration plots showed favorable consistency between the prediction of the nomogram and actual observations in both the training and validation cohorts. In addition, the decision curve DCA showed that the nomogram was clinically useful and had better discriminative ability to recognize patients at high risk than the AJCC criteria-based tumor stage. Prognostic nomogram of young and middle-aged male patients with HCC was developed and validated to help clinicians evaluate the prognosis of patients.

Incidence patterns and clinical implications of venous thromboembolisms (VTE) in patients (p) with neuroendocrine tumors (NET).

e24155 Background: Venous Thromboembolisms (VTE) is a common complication in cancer patients (p) and one of the lead causes of cancer-related death. Digestive neoplasms have specific characteristics in VTE incidence and treatment. There is a lack of data regarding VTE impact in p with neuroendocrine tumors (NET). Currently few studies have addressed VTE in NET, with an estimated incidence of 7.5%. Nevertheless, there is no evidence from large datasets to address specific implications of thrombosis in NET p. In the present study, we review incidence and treatment of VTE in NET in a large unicentric cohort. Methods: Consecutive p with gastroenteropancreatic (GEP) and thoracic NET treated in our institution were reviewed to study incidence of VTE including deep vein thrombosis (DVT), pulmonary embolisms (PE) and splanchnic venous thrombosis (SVT). Information regarding clinical characteristics and VTE treatment were collected. Results: 212 p were included in the analysis (38% Female; 42% Pancreatic, 35% Small Intestine, 6.5% lung). 50p presented any kind of thrombotic event (23.5%), and 23 were directly related to TNE (10.8%). Considering 23p with TNE-related VTE (82.3% Male; 82.3% Pancreatic), main origins included: SVT 11p (47.8%) and PE 7p (30.4%). Leading cause of SVT was splenic vein thrombosis. 80.9% of VTE cases received anticoagulant therapy, most of them with low-molecular weight heparin (82.6%) and indefinitely duration (58.8%). All cases that did not started anticoagulant therapy were splenic vein thrombosis due to physician decision. Any complication related to anticoagulant therapy was described in 5p (26.3%). No cases of VTE-related death were found. Conclusions: Patients with NET have a moderate risk of VTE events. Splenic thrombosis is the most common location but need of anticoagulant therapy in those cases remains controversial. Specific studies regarding VTE in NET population are needed.

What developments in the management of digestive tumours?

What developments in the management of digestive tumours?

The Diagnostic Value of Circulating miR-29 Family for Digestive System Malignancies: A Meta-Analysis.

To evaluate the diagnostic value of circulating microRNA-29 (miR-29) in digestive system malignant neoplasms by meta-analysis. We searched the PubMed, Embase, Cochrane Library, and Web of Science to collect studies, published through September 2022, on the diagnostic value of miR-29 in digestive system tumors. We included 7 studies in this meta-analysis, including colorectal cancer, esophageal squamous cell carcinomas, and cholangiocarcinoma. The pooled sensitivity, specificity, positive likelihood ratio, negative likelihood ratio, and diagnostic odds ratio were 0.64 (95% CI, 0.53-0.74), 0.83 (0.60-0.94), 3.75 (1.42-9.91), 0.44 (0.31-0.61), and 8.63 (2.54-29.26), respectively. The area under the summary receiver operating characteristic curve was 0.75. The sensitivity of miR-29 derived from serum was higher than that of miR-29 derived from plasma for malignant digestive system tumors (0.71 vs 0.54; P = .04). This meta-analysis suggests that the circulating miR-29 family has good diagnostic performance for digestive system malignant tumors, with moderate sensitivity and good specificity.