Background: Upfront resection (UR) followed by adjuvant chemotherapy remains the standard treatment for resectable pancreatic cancer. There is increasing evidence suggesting favourable outcomes toward neoadjuvant chemotherapy (NAC) followed by surgery. Methods: All clinical staging with resectable pancreatic cancer patients treated at a tertiary medical centre from 2013 to 2020 were identified. The baseline characteristics, treatment course, surgery outcome and survival results of UR or NAC were compared. Results: Finally, in 159 resectable patients, 46 patients (29%) underwent NAC and 113 patients (71%) received UR. In NAC, 11 patients (24%) did not receive resection, 4 (36.4%) for comorbidity, 2 (18.2%) for patient refusal and 2 (18.2%) for disease progression. In UR, 13 patients (12%) were unresectable intraoperatively; 6 (46.2%) for locally advanced and 5 (38.5%) for distant metastasis. Overall, 97% of patients in NAC and 58% of patients in UR completed adjuvant chemotherapy. As of data cut-off, 24 patients (69%) in NAC and 42 patients (29%) in UR were still tumour free. The median recurrence-free survival in NAC, UR with adjuvant chemotherapy and without adjuvant chemotherapy were 31.3 months (95% CI, 14.4–not estimable), 10.6 months (95% CI, 9.0–14.3) and 8.5 months (95% CI, 5.8–11.8), P=0.036; and the median overall survival in each group were not reached (95% CI, 29.7–not estimable), 25.9 months (95% CI, 21.1–40.5) and 21.7 months (12.0–32.8), P=0.0053. Based on initial clinical staging, the median overall survival of NAC was not significantly different from UR with a tumour less than or equal to 2 cm, P=0.29. NAC patients had a higher R0 resection rate (83% versus 53%), lower recurrence rate (31% versus 71%) and harvested median number lymph node (23 versus 15). Conclusion: This study demonstrates that NAC is superior to UR in resectable pancreatic cancer with better survival.

Recurrent miscarriage is used to refer to more than three pregnancy failures before 20 weeks of gestation. Defective trophoblast cell growth and invasion are frequently observed in recurrent miscarriage. Several microRNAs (miRs), including miR‑155‑5p, are aberrantly upregulated in recurrent miscarriage; however, the underlying molecular mechanisms remain unclear. The centrosome orchestrates microtubule networks and coordinates cell cycle progression. In addition, it is a base for primary cilia, which are antenna‑like organelles that coordinate signaling during development and growth. Thus, deficiencies in centrosomal functions can lead to several disease, such as breast cancer and microcephaly. In the present study, the signaling cascades were analyzed by western blotting, and the centrosome and primary cilia were observed and analyzed by immunofluorescence staining. The results showed that overexpression of miR‑155‑5p induced centrosome amplification and blocked primary cilia formation in trophoblast cells. Notably, centrosome amplification inhibited trophoblast cell growth by upregulating apoptotic cleaved‑caspase 3 and cleaved‑poly (ADP‑ribose) polymerase in miR‑155‑5p‑overexpressing trophoblast cells. In addition, overexpression of miR‑155‑5p inhibited primary cilia formation, thereby inhibiting epithelial‑mesenchymal transition and trophoblast cell invasion. All phenotypes could be rescued when cells were co‑transfected with the miR‑155‑5p inhibitor, thus supporting the role of miR‑155‑5p in centrosomal functions. It was also found that miR‑155‑5p activated autophagy, whereas disruption of autophagy via the depletion of autophagy‑related 16‑like 1 alleviated miR‑155‑5p‑induced apoptosis and restored trophoblast cell invasion. In conclusion, the present study indicated a novel role of miR‑55‑5p in mediating centrosomal function in recurrent miscarriage.

Background: As survival following PD improved, long-term complications have emerged as an issue in current era. Pancreaticojejunostomy stenosis is the common long-term sequel after PD but rarely addressed. This study aimed to investigate the benefit of pancreatic duct stent in reducing PJ stenosis after PD. Methods: Between July 2006 and July 2019, patients undergoing PD with follow-up more than 1 year were recruited. Patients were divided into internal stent, external stent, and no stent groups. We reviewed the Computed tomography (CT) to measure the diameter of pancreatic duct and stent migration at 3 months and 1 year after PD. PJ stenosis was defined as pancreatic duct diameter > 3 mm. Perioperative variables were collected for analysis. Results: Totally, 506 patients were included 349 patients in internal stent group, 84 patients in the external stent, and 73 patients in no stent group. There was no difference in preoperative P-duct size between the IS and ES group (3.39 ± 1.78 mm vs 3.26 ± 1.89 mm, p = 0.481), while the P-duct size was larger in ES group compared to the IS group (3.22 ± 2.44 mm vs. 1.94 ± 2.08 mm, p < 0.001) one year after PD. In the internal stent group, the rate of stent migration was 22.1% at 3 months and 67.9% at 1 year post-operatively. CR-POPF (OR 2.24, p = 0.015) and P-duct stent retention at PJ > 3 months (OR 0.45, p < 0.001) were the independent factors for 1-year PJ stenosis in multivariate analysis. Conclusion: Retention of internal pancreatic duct stents at the anastomosis for more than 3 months can reduce post-PD PJ stenosis. Extended retention of internal pancreatic duct stents reduces PJ stenosis, highlighting its critical role in preventing long-term complications.

The centrosome is essential for maintaining cell shape and facilitating cell division. Thus, precise control of centrosome copy numbers is crucial for proper chromosome segregation. Pericentriolar material 1 (PCM1) is a scaffold component of centriolar satellites-electron-dense granules dispersed around the centrosome-that regulate the centrosome or primary cilia. It has been shown that disrupting PCM1 aggregation by treating cells with sodium orthovanadate inhibits centrosome amplification. However, sodium orthovanadate is a protein tyrosine phosphatase and may have off-target effects on the centrosome. To further confirm the role of PCM1 aggregation in promoting centrosome amplification, we disrupted PCM1 aggregation by interfering with microtubule networks, inhibiting the dynactin motor complex, or depleting PCM1. Centrosome copy numbers were then examined under conditions of prolonged replication stress. Our data suggest that PCM1 aggregation does not promote centrosome amplification in osteosarcoma U2-OS or pancreatic ductal adenocarcinoma PANC-1 cell lines. Instead, we found that centrosome amplification promoted PCM1 aggregation in a PLK4-dependent manner. Furthermore, we observed that PCM1 depletion inhibited U2-OS cell survival under prolonged replication stress. Prolonged replication stress induced DNA damage signaling via the ATM-CHK1 axis and autophagy to maintain cell survival, while PCM1 depletion alleviated ATM, CHK1, and autophagy activity, thereby reducing cell survival. Our findings propose that PCM1 does not facilitate centrosome amplification but instead induces activation of the ATM-CHK1 axis and autophagy to sustain osteosarcoma cell viability during prolonged replication stress.

New-onset diabetes mellitus (NODM) following distal pancreatectomy (DP) significantly impacts long-term quality of life. This study developed a prediction model for post-DP NODM. Retrospective analysis of 159 patients undergoing DP for benign/low-grade malignant lesions (2014-2023). Cox regression identified risk factors incorporated into a scoring system. Among 130 non-diabetic patients, 26.9 ​% developed NODM (median 10 months). Five independent predictors: prediabetes (HR 11.02), concomitant splenectomy (HR 2.45), age ≥65 (HR 2.03), BMI ≥25 (HR 1.96), neck/proximal tumor (HR 1.50). The risk scoring system (0-10 points) stratified patients into low-risk (0-2 points), intermediate-risk (3-5 points), and high-risk (6-10 points) categories with significantly different cumulative incidence of NODM at 5 years (4.4 ​%, 27.9 ​%, and 87.5 ​%, respectively). AUC exceeded 0.85 across timepoints. This simple model enables accurate risk stratification for post-DP NODM, facilitating personalized counseling and tailored surveillance.

Pancreatic heterotopia mimicking a common bile duct tumor