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Assessment of minimally invasive pancreatoduodenectomy (MIPD) in patients with pancreatic ductal adenocarcinoma (PDAC) is scarce and limited to non-randomized studies. This study aimed to compare oncological and surgical outcomes after MIPD compared to open pancreatoduodenectomy (OPD) for patients after resectable PDAC from published randomized controlled trials (RCTs). A systematic review was performed to identify RCTs comparing MIPD and OPD including PDAC (Jan 2015–July 2021). Individual data of patients with PDAC were requested. Primary outcomes were R0 rate and lymph node yield. Secondary outcomes were blood-loss, operation time, major complications, hospital stay and 90-day mortality. Overall, 4 RCTs (all addressed laparoscopic MIPD) with 275 patients with PDAC were included. In total, 128 patients underwent laparoscopic MIPD and 147 patients underwent OPD. The R0 rate (risk difference(RD) −1%, P = 0.740) and lymph node yield (mean difference(MD) +1.55, P = 0.305) were comparable between laparoscopic MIPD and OPD. Laparoscopic MIPD was associated with less perioperative blood-loss (MD -91ml, P = 0.026), shorter length of hospital stay (MD -3.8 days, P = 0.044), while operation time was longer (MD +98.5 min, P = 0.003). Major complications (RD -11%, P = 0.302) and 90-day mortality (RD -2%, P = 0.328) were comparable between laparoscopic MIPD and OPD. This individual patient data meta-analysis of MIPD versus OPD in patients with resectable PDAC suggests that laparoscopic MIPD is non-inferior regarding radicality, lymph node yield, major complications and 90-day mortality and is associated with less blood loss, shorter hospital stay, and longer operation time. The impact on long-term survival and recurrence should be studied in RCTs including robotic MIPD. [ABSTRACT FROM AUTHOR]

We sought to combine skeletal muscle index and inflammatory immune markers to stratify long-term survival in patients with pancreatic cancer after pancreatoduodenectomy (PD). A total of 581 patients with pancreatic cancer underwent PD were included, and divided into the training and validation cohort. Image analysis of computed tomography scans was used to calculate the ratio of skeletal muscle (SM) area to body mass index (BMI). Naples prognostic score (NPS) was calculated from blood-test inflammatory immune markers. Propensity score matching (PSM) analysis was performed to minimize biases of clinicopathological characteristics. To estimate the overall survival (OS), a nomogram was developed using the training cohort. The predictive accuracy of nomogram was estimated by concordance index (C-index), calibration curve, and receiver operating characteristics (ROC) curve. After PSM analysis, SM/BMI ratio, NPS, lymph node metastasis, TNM stage, surgical margin, tumor grade and adjuvant therapy were independent predictors of OS, which were all assembled into nomogram. The SM/BMI ratio was the best single-predictor for 3- and 5-year OS, with an AUC of 0.805 (95% CI: 0.755–0.855) and 0.812 (95% CI: 0.736–0.888), respectively. Harrell's c-index of the nomogram in the training cohort was 0.786 (95% CI: 0.770–0.802), and the area under ROC curve of 1-year, 3- and 5-year OS prediction were 0.869 (95%CI: 0.837–0.901), 0.846 (95%CI: 0.810–0.882) and 0.849 (95%CI: 0.801–0.896). The nomogram based on SM/BMI ratio and NPS had excellent predictive performance, which should be incorporated to conventional risk scores to stratify survival of patients with PDAC after PD. [ABSTRACT FROM AUTHOR]

Background: Delayed gastric emptying (DGE) is a common complication following laparoscopic pancreaticoduodenectomy (LPD), although it remains incompletely understood, and only few studies have investigated the clinical benefits of hepatic branch of the vagus nerve (HBVN) preservation on DGE after LPD until now. We intended to evaluate the effect of preservation of the HBVN during LPD on the incidence of DGE. Methods: A total of 274 consecutive LPDs performed at a single center between July 2014 and December 2019 with available videos were retrospectively reviewed. DGE was defined according to the International Study Group of Pancreatic Surgery (ISGPS) criteria, and HBVN condition during the LPD procedure was evaluated through a video review. Risk factors associated with DGE were assessed by performing univariate and multivariate logistic regression analyses. Postoperative outcomes between the HBVN-preserved and HBVN-injury groups were compared before and after propensity score matching (PSM). Results: One hundred fifty-six (56.93%) patients underwent LPD with HBVN-preserved and 118 (43.07%) with HBVN injury. DGE occurred in 33.2% of patients (n = 91) with grades B and C occurring at 13.9% (n = 38) and 7.7% (n = 21), respectively. Longer operative time, more EIBL, HBVN injury, POPF (grades B and C), postoperative hemorrhage, intra-abdominal infection, and Clavien-Dindo ≥III were identified as risk factors for DGE in the univariate analysis. Then, in the multivariate analysis, HBVN injury and intra-abdominal infection were found to be independent risk factors affecting the incidence of DGE (any grade) or clinically relevant DGE (grades B and C). Furthermore, the prevalence of DGE was significantly higher in the HBVN-injury group than in the HBVN-preserved group before and after PSM analysis (46.61% vs. 23.08%, P<0.001; 42.59% vs. 23.15%, P=0.013). Conclusions: HBVN preservation during LPD might be associated with a reduced incidence of DGE as a framework for prospective quality improvement. [ABSTRACT FROM AUTHOR]

Background Aspartate aminotransferase to platelet ratio index (APRI) and the fibrosis index based on four factors (FIB-4) are the two most focused non-invasive models to assess liver fibrosis. Aims We aimed to examine the validity of these two models for predicting hepatitis B virus (HBV)-related liver fibrosis accompanied with hepatocellular carcinoma (HCC). Methods We enrolled HBV-infected patients with liver cancer who had received hepatectomy. The accuracy of APRI and FIB-4 for diagnosing liver fibrosis was assessed based on their sensitivity, specificity, diagnostic efficiency, positive predictive value (PPV), negative predictive value (NPV), kappa ( κ ) value and area under the receiver-operating characteristic curve (AUC). Results Finally 2176 patients were included, with 1682 retrospective subjects and 494 prospective subjects. APRI ( r s = 0.310) and FIB-4 ( r s = 0.278) were positively correlated with liver fibrosis. And χ 2 analysis demonstrated that APRI and FIB-4 values correlated with different levels of liver fibrosis with all P values less than 0.01. The AUC values for APRI and FIB-4 were 0.685 and 0.626 ( P = 0.73) for predicting significant fibrosis, 0.681 and 0.648 ( P = 0.81) for differentiation of advanced fibrosis and 0.676 and 0.652 ( P = 0.77) for diagnosing cirrhosis. Conclusion APRI and FIB-4 correlate with liver fibrosis. However these two models have low accuracy for predicting HBV-related liver fibrosis in HCC patients. [ABSTRACT FROM AUTHOR]

Postoperative pancreatic fistula (POPF) remains a persistent problem after pancreaticoduodenectomy (PD), especially in the presence of a soft, nonfibrotic pancreas. To reduce the risk of POPF, pancreaticogastrostomy (PG) is an optional reconstruction technique for surgeons after PD. This study presents a new technique of PG for a soft, nonfibrotic pancreas with double-binding continuous hemstitch sutures and evaluates its safety and reliability. From January 2011 to June 2012, 92 cases of patients with periampullary malignancy with a soft pancreas underwent this technique. A modified technique of PG was performed with two continuous hemstitch sutures placed in the mucosal and seromuscular layers of the posterior gastric wall, respectively. Then the morbidity and mortality was calculated. This technique was applied in 92 patients after PD all with soft pancreas. The median time for the anastomosis was 12 min (range, 8-24). Operative mortality was zero, and morbidity was 16.3 % ( n = 15), including hemorrhage ( n = 2), biliary fistula ( n = 2), pulmonary infection ( n = 1), delayed gastric emptying (DGE; n = 5, 5.4 %), abdominal abscess ( n = 3, one caused by PF), and POPF ( n = 2, 2.2 %). Two patients developed a pancreatic fistula (one type A and one type B) classified according to the International Study Group on Pancreatic Fistula. The described technique is a simple and safe reconstruction procedure after PD, especially for patients with a soft and fragile pancreas. [ABSTRACT FROM AUTHOR]

Examines the effect of ischemic reperfusion injury and particle infusion embolism on the apoptosis of rats with pancreatic cancer in China. Development of methods in treating pancreatic cancer; Implantation of dimethylbeneanthracine into rats; Cell apoptosis indicators of pancreatic cancer.

Hepatocellular carcinoma (HCC) is a cancer with multiple aetiologies and widespread prevalence. Largely refractory to current treatments, HCC is the fourth leading cause of cancer-related deaths worldwide. MicroRNAs (miRNAs) are important regulators in HCCs. We aimed to identify tumour suppressor miRNAs during tumour regression in a conditional c-MYC -driven mouse model (LT2/MYC) of HCC, and to evaluate their therapeutic potential for HCC treatment. We performed miRNA expression profiling of developed and regressing LT2/MYC tumours and in-depth in vitro gain- and loss-of-function analyses. The effect of adeno-associated virus (AAV) vector-mediated miR-342-3p treatment was evaluated in 3 HCC mouse models. We identified miR-342-3p as a tumour suppressor miRNA in HCC, with increased expression in regressing tumours. Forced miR-342-3p expression in hepatoma cells showed significantly decreased cell proliferation, migration, and colony formation. In vivo administration of AAV-miR-342-3p led to significant attenuation of tumour development and increased overall survival. We identified monocarboxylic acid transporter 1 (MCT1) as a bona fide target of miR-342-3p in HCC. We show that the tumour suppressor role of miR-342-3p is executed partly by modulating the lactate transport function of MCT1. Importantly, we find miR-342-3p downregulated in tumours from patients with HCC compared with matched non-tumour tissues, inversely correlating with MCT1 expression. We observed similar findings in TCGA-LIHC data. In our study, we identified and validated miR-342-3p as a tumour suppressor miRNA in HCC. We demonstrated its therapeutic efficacy in significantly attenuating tumour development, and prolonging survival, in different HCC mouse models. Identification of miR-342-3p as an effective tumour suppressor opens a therapeutic avenue for miRNA-mediated attenuation of HCC development. Hepatocellular carcinoma (HCC), the most common type of liver cancer, affects diverse populations and has a global impact, being the fourth leading cause of cancer deaths worldwide. There are currently no systemic therapies for HCC that can significantly prolong long-term survival. Thus, novel effective treatment options are urgently required. To understand the molecular basis of tumour regression, we compared tumours and regressing liver tumours in mice. We show that a small non-coding miRNA, miR-342-3p, is a tumour suppressor in HCC. Expression of miR-342-3p is low in tumours and high in regressing tumours. When miR-342-3p is delivered to mouse livers with HCC, it can significantly slow down liver tumour development and improve survival. Our study highlights the promising therapeutic potential of miR-342-3p intervention in HCC. • Distinct global microRNA landscape in regressing liver tumours compared with tumours. • Identification and validation of miR-342-3p as a tumour suppressor in HCCs. • MiR-342-3p significantly attenuates tumour development in 3 mouse models of HCC. • MiR-342-3p prolongs survival of LT2/MYC and LT2/RAS mice with liver tumours. • MiR-342-3p plays a role in metabolic reprogramming in HCC, by targeting MCT1. [ABSTRACT FROM AUTHOR]

Abstract In contrast to the steady increase in survival observed for most cancer types, advances have been slow for pancreatic cancers. Current chemotherapy has limited benefits for patients with pancreatic cancer. Therefore, there is an urgent need for effective pancreatic cancer treatment strategies. At present, targeting the autophagic pathway is regarded as a promising new strategy for cancer treatment. Danthron (1,8-dihydroxyanthrquinone), a component from Rheum palmatum L. (polygonaceae), has several biological activities. However, the inhibition of autophagy by danthron has never been recognized, previously.Here we find that danthron may prevent autophagy, inhibit proliferation and induce apoptosis in pancreatic cancer cells in vitro. Autophagy induced by doxorubicin plays a protective role in pancreatic cancer cells and inhibition of autophagy by chloroquine or silencing autophagy protein 5 (Atg5) may chemosensitize pancreatic cancer cell lines to doxorubicin. Similarly, inhibition of autophagy by danthron also enhances toxicity of doxorubicin to pancreatic cancer cells. These results indicate that danthron has an anticancer effect and can sensitize the chemotherapeutic effect of doxorubicin on pancreatic cancer cells. These findings also suggest that inhibition of autophagy may be an effective way to promote the chemotherapy of pancreatic cancer. Highlights • We first found that danthron can inhibit autophagy. • Autophagy induced by doxorubicin plays a protective role in pancreatic cancer cells. • Inhibition of autophagy by danthron enhances toxicity of doxorubicin to pancreatic cancer cells. [ABSTRACT FROM AUTHOR]

There is currently limited knowledge regarding the involvement of long non-coding RNAs (lncRNAs) in cancer development. We aimed to identify lncRNAs with important roles in pancreatic cancer progression. We screened for lncRNAs that were differentially expressed in pancreatic cancer tissues. Among 349 differentially expressed lncRNAs, Linc01060 showed the lowest expression in pancreatic cancer tissues compared with normal pancreatic tissues. Lower Linc01060 expression in pancreatic cancer tissues was significantly associated with a poor prognosis. Linc01060 inhibited pancreatic cancer proliferation and invasion in vitro and in vivo. Vinculin overexpression inhibited Linc01060KD-mediated increases in FAK and paxillin phosphorylation, whereas vinculin knockdown reversed the Linc01060-mediated repression of FAK and inactivation of focal adhesion turnover. Vinculin knockdown also accelerated pancreatic cancer cell proliferation by upregulating ERK activity. In biological function analyses, vinculin overexpression abrogated Linc01060-mediated repression of pancreatic cancer cell proliferation and invasion, whereas vinculin counteracted the Linc01060-mediated repression of PC cell proliferation and invasion. These data demonstrate that Linc01060 plays a key role in suppressing pancreatic cancer progression by regulating vinculin expression. These findings suggest that the Linc01060-vinculin-focal adhesion axis is a therapeutic target for pancreatic cancer treatment. [ABSTRACT FROM AUTHOR]