Ping-Jui Su

Pancreatic heterotopia mimicking a common bile duct tumor

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.

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: 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.