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Anastomotic leakage (AL) is a major cause of postoperative morbidity and mortality in the treatment of colorectal cancer. The aim of this study was to investigate an innovative and convenient technique of laparoscopic demucositized suture the overlapping point of the "dog ear" area after the double stapling anastomosis (lds-DSA), as an improved alternative for conventional DSA, and whether it could reduce the AL rate in laparoscopic anterior resection (Lapa-AR). Between January 2018 and December 2020, a total of 245 patients who underwent Lapa-AR for the treatment of adenocarcinoma of the sigmoid colon or rectal cancer were divided into the lsd-DSA group (n = 99) and the DSA group (n = 146). Data were analyzed retrospectively. Morbidity, AL rate and other perioperative outcomes were compared between the two groups. Patient demographics, preoperative comorbidity, preoperative chemoradiotherapy, tumor size, stage, and other operative details were comparable between the two groups. There was no difference in surgical time between the two groups (196.41 ± 76.71 vs. 182.39 ± 49.10 min, p = 0.088). The overall complication rate was also without a difference (11/99, 11.11% vs. 21/146, 14.38%, p = 0.456), but AL rate significantly lower in the lsd-DSA group than in the DSA group (2/99, 2.02% vs. 12/146, 8.22%, p = 0.040). For other perioperative outcomes, the lsd-DSA group shortened the total and postoperative hospital stay, and the time to pull out drainage tube than in the DSA group. Our comparative study demonstrates lds-DSA to have a better short-term outcome in reducing AL compared with DSA. This technique could be an alternative approach to maximize the patients' benefit in Lapa-AR.

Background The purpose of this study was to compare the “caudal to cranial” (CC) versus “medial to lateral” (ML) approach for laparoscopic right hemicolectomy. Methods Pertinent data from all patients with stage II and III between January 2015 and August 2017 were entered into a retrospective database. Results A total of 175 patients underwent the ML (n = 109) or CC approach (n = 66). Patient characteristics were equivalent between groups. The CC group showed a shorter surgical time 170.00 (145.00, 210.00) vs. (206.50 (178.75, 226.25) min) than the ML group (p＜0.001). The time to oral intake was shorter in the CC group than in the ML group ((3.00 (1.00, 4.00) vs. 3.00 (2.00, 5.00) days; p=0.007). For the total harvested lymph nodes, there was no statistical significance between the CC group 16.50 (14.00, 21.25) and the ML group 18.00 (15.00, 22.00) (p = 0.327), and no difference was found in the positive harvested lymph nodes (0 (0, 2.00) vs. 0 (0, 1.50); p=0.753). Meanwhile, no differences were found in other perioperative or pathological outcomes, including blood loss and complications. For 5-year prognosis, overall survival rates were 75.76% in the CC group and 82.57% in the ML group (HR 0.654, 95% CI 0.336–1.273, p = 0.207); progress-free survival rates were 80.30% in the CC group and 85.32% in the ML group (HR 0.683, 95% CI 0.328–1.422, p = 0.305). Conclusions Both approaches were safe and feasible and resulted in excellent survival. The CC approach was beneficial in terms of the surgical time and rapid recovery after operation.

Colorectal cancer (CRC) is a malignant tumor and morbidity rates are among the highest in the world. The variation in CRC patients' prognosis prompts an urgent need for new molecular biomarkers to improve the accuracy for predicting the CRC patients' prognosis or as a complement to the traditional TNM staging for clinical practice. CRC patients' gene expression data of HTSeq‐FPKM and matching clinical information were downloaded from The Cancer Genome Atlas (TCGA) datasets. Patients were randomly divided into a training dataset and a test dataset. By univariate and multivariate Cox regression survival analyses and Lasso regression analysis, a prediction model which divided each patient into high‐or low‐risk group was constructed. The differences in survival time between the two groups were compared by the Kaplan–Meier method and the log‐rank test. The weighted gene co‐expression network analysis (WGCNA) was used to explore the relationship between all the survival‐related genes. The survival outcomes of patients whose overall survival (OS) time were significantly lower in the high‐risk group than that in the low‐risk group both in the training and test datasets. Areas under the ROC curves which termed AUC values of our 9‐gene signature achieved 0.823 in the training dataset and 0.806 in the test dataset. A nomogram was constructed for clinical practice when we combined the 9‐gene signature with TNM stage and age to evaluate the survival time of patients with CRC, and the C‐index increased from 0.739 to 0.794. In conclusion, we identified nine novel biomarkers that not only are independent prognostic indexes for CRC patients but also can serve as a good supplement to traditional clinicopathological factors to more accurately evaluate the survival of CRC patients., We identified a 9‐gene signature screened out based on batch survival analysis that can be used not only as an independent prognostic index for CRC patients but also as a favorable supplement to traditional clinicopathological factors for clinicians to more accurately and effectively evaluate the survival of CRC patients.

Background SLC2A5 is a high-affinity fructose transporter, which is frequently upregulated in multiple human malignant tumours. However, the function and molecular mechanism of SLC2A5 in colorectal cancer (CRC) remain unknown. Methods We detected the expression levels of SLC2A5 in CRC tissues and CRC cell lines by western blotting, qRT-PCR and immunohistochemistry. CRC cell lines with stable overexpression or knockdown of SLC2A5 were constructed to evaluate the functional roles of SLC2A5 in vitro through conventional assays. An intrasplenic inoculation model was established in mice to investigate the effect of SLC2A5 in promoting metastasis in vivo. Methylation mass spectrometry sequencing, methylation specific PCR, bisulphite sequencing PCR, ChIP-qPCR and luciferase reporter assay were performed to investigate the molecular mechanism underlying transcriptional activation of SLC2A5. Results We found that SLC2A5 was upregulated in colorectal tumour tissues. Functionally, a high level of SLC2A5 expression was associated with increased invasion and metastasis capacities of CRC cells both in vitro and in vivo. Mechanistically, we unveiled that S100P could integrate to a specific region of SLC2A5 promoter, thereby reducing its methylation levels and activating SLC2A5 transcription. Conclusions Our results reveal a novel mechanism that S100P mediates the promoter demethylation and transcription activation of SLC2A5, thereby promoting the metastasis of CRC.

Colorectal cancer (CRC) is a leading cause of cancer-related deaths worldwide. Abundant metabolic fuels have been implicated as potential drivers of CRC. However, it remains unclear whether fructose, an ample sugar in daily diets, is essential for CRC growth. In the present study, we found that glucose levels were always insufficient in human CRC tissues. Compensating for this, fructose was flexibly utilized by tumor cells as an alternative energy source to maintain proliferation and exert chemotherapy resistance in vitro by upregulating GLUT5, a major fructose transporter encoded by SLC2A5. Mechanistically, in glucose-deprived but fructose-rich environments, GLUT5 could interact with ketohexokinase and inhibit its autophagy-dependent degradation, thus trapping fructose into glycolysis and tricarboxylic acid cycle for the malignant growth of CRC cells. In addition, reducing dietary fructose or pharmacological blockade of fructose utilization significantly reduced CRC growth and sensitized CRC cells to chemotherapy in vivo. Taken together, our findings highlight the role of elevated fructose utilization mediated by the GLUT5-KHK axis in governing CRC growth and imply that efforts to refine fructose intake or inhibit fructose-mediated actions may serve as potential therapeutic strategies.

Sorting nexin 16 (SNX16), a member of the sorting nexin family, has been implicated in tumor development. However, the function of SNX16 has not yet been investigated in colorectal cancer (CRC). Here, we showed that SNX16 expression was significantly upregulated in CRC tissues compared with normal counterparts. Upregulated mRNA levels of SNX16 predicted poor survival of CRC patients. Functional experiments showed that SNX16 could promote CRC cells growth both in vitro and in vivo. Knockdown of SNX16 induced cell cycle arrest and apoptosis, whereas ectopic overexpression of SNX16 had the opposite effects. Mechanistically, SNX16‐eukaryotic translation elongation factor 1A2 (eEF1A2) interaction could inhibit the degradation and ubiquitination of eEF1A2, followed by activation of downstream c‐Myc signaling. Our study unveiled that the SNX16/eEF1A2/c‐Myc signaling axis could promote colorectal tumorigenesis and SNX16 might potentially serve as a novel biomarker for the diagnosis and an intervention of CRC., Sorting nexin 16 (SNX16), which is significantly upregulated in colorectal cancer, could interact with and inhibit proteasome‐dependent ubiquitination of eukaryotic translation elongation factor 1 A2 (eEF1A2), thereby activating c‐myc signaling, Our study unveiled that SNX16/eEF1A2/c‐Myc signaling axis could promote colorectal tumorigenesis and SNX16 might potentially serve as a novel biomarker for the diagnosis and intervention of colorectal cancer.

BackgroundDistribution of regional lymph nodes (LNs) is decisive for the lymphadenectomy boundary in radical resection of a right-sided colon cancer (RCC). Currently, the data of LNs in central area remains ambiguous and scarce. Herein we aim to provide a more detailed anatomical research on LNs surrounding the superior mesenteric vessels for RCC and investigated the metastasis rate.MethodsCarbon Nanoparticles (CNs) or Indocyanine Green (ICG) were used as dye and we laparoscopically observed the stained LNs distribution pattern and analyzed the harvested LNs combined with pathology report. Lastly, 137 RCC patients who received a “superior mesenteric artery (SMA)-oriented” hemicolectomy from September 2016 to September 2020 were included to calculate the probability of LNs metastasis in our target area.Results20 patients diagnosed as RCC (mean age 55.55 years, 13 male) were included. 13 patients underwent CNs injection and 7 patients consented to the ICG, while 4 cases suffered from imaging failure. The unequal number of the regional LNs located between SMV and SMA was detected in 17 cases (85%), posterior to SMV area in 6 cases (30%), and anterior to SMA in 11 cases (55%), respectively. The presence of LNs posterior to SMV was associated with the crossing pattern of ileocolic artery (²= 5.38, p= 0.020). The probability of LNs metastasis in the above areas (target areas) was 2.19% (3/137). No dyed LNs occurred when the SMA sheath was exposed. What’s more, the number of total harvested LNs in patients with dye injection was significant more than dye-free RCC patients (22.44±13.78 vs 43.20±22.70, p

The diverse expression pattern of CD36 reflects its multiple cellular functions. However, the roles of CD36 in colorectal cancer (CRC) remain unknown. Here, we discover that CD36 expression is progressively decreased from adenomas to carcinomas. CD36 loss predicts poor survival of CRC patients. In CRC cells, CD36 acts as a tumor suppressor and inhibits aerobic glycolysis in vitro and in vivo. Mechanically, CD36-Glypcian 4 (GPC4) interaction could promote the proteasome-dependent ubiquitination of GPC4, followed by inhibition of β-catenin/c-myc signaling and suppression of downstream glycolytic target genes GLUT1, HK2, PKM2 and LDHA. Moreover, disruption of CD36 in inflammation-induced CRC model as well as ApcMin/+ mice model significantly increased colorectal tumorigenesis. Our results reveal a CD36-GPC4-β-catenin-c-myc signaling axis that regulates glycolysis in CRC development and may provide an intervention strategy for CRC prevention., CD36 is a membrane glycoprotein that has been shown to have tumour promoting or suppressor function depending on tumour type. Here, the authors address CD36 function in colorectal cancer and show it acts as a tumour suppressor by inhibiting B-catenin/myc signalling, resulting in downregulation of glycolysis.

Aberrant gene expression plays critical roles in the development of colorectal cancer (CRC). Here we show that POTEE, which was identified as a member E of POTE ankyrin domain family, was significantly upregulated in colorectal tumors and predicted poor overall survival of CRC patients. In CRC cells, POTEE could act as an oncogene and could promote cell growth, cell-cycle progression, inhibit apoptosis, and elevates xenograft tumor growth. Mechanically, we used microarray analysis and identified a POTEE/SPHK1/p65 signaling axis, which affected the biological functions of CRC cells. Further evaluation showed that overexpression of POTEE could increase the protein expression of SPHK1, followed by promoting the phosphorylation and activation of p65 protein. Altogether, our findings suggested a POTEE/SPHK1/p65 signaling axis could promote colorectal tumorigenesis and POTEE might potentially serve as a novel biomarker for the diagnosis and an intervention of colorectal cancer.

This study aimed to verify whether the open-ended coaxial line tumor sensor with radio frequency was effective or not in detecting the differences in permittivity and conductivity between the breast malignant tissues and adjacent tissues.Sixteen breast infiltrating ductal carcinoma samples were freshly obtained from the department of general surgery in Zhujiang Hospital.The permittivity and conductivity of cancerous nidus points of breast samples,3cm adjacent tissue points and 5cm adjacent tissue points were detected respectively by the open-ended coaxial line tumor sensor with radio frequency noninvasively in conjunction with vector network analyzer at the frequency ranging from 42.85~500 MHz.All the detected points were marked.After finishing the detection,we conducted postoperative pathological examinations on all the marked points.According to the statistics,there were statistically significant differences between the breast cancerous tissues and the 3cm adjacent tissues for the dielectric properties(P0.01).There were statistically significant differences between the breast cancerous tissues and the 5cm adjacent tissues for the dielectric properties(P0.01).There was no statistically significant difference in the dielectric properties between the 3cm adjacent tissues and 5cm adjacent tissues(P0.05).Both the 3cm adjacent tissues and5 cm adjacent tissues were found no breast cancer cell infiltration.The results indicated that the open-ended coaxial line tumor sensor at radio frequency could be effective in detecting the differences in permittivity and conductivity between breast cancerous tissues and adjacent tissues and,therefore,it may have a potential prospect in making a final diagnosis to confirm whether the detected breast tissue is malignant or not.