Junki Fukuda

Robot‐assisted radical prostatectomy (RARP) is the standard treatment for prostate cancer; however, inguinal hernias (IH) development is a common complication. Current guidelines generally recommend an anterior approach following RARP for the initial IH. However, the optimal surgical strategy for patients with recurrent IH after RARP who have a history of anterior mesh repair remains unclear. This report describes the first successful transabdominal preperitoneal (TAPP) repair of a recurrent IH in a patient with a history of RARP and Kugel plug repair. Intraoperative findings revealed displacement of the mesh plug and recurrence of the IH (Japan Hernia Society classification R1, L2). The prevesical space was severely scarred because of the effects of RARP, making dissection of the inner side of the hernia orifice difficult; however, mesh placement was successfully completed. This case demonstrated the feasibility and efficacy of the TAPP approach as a radical treatment for complex recurrences in a specialized patient population.

Supplementary methods, tables, and figures

Significant progress has been made in understanding the pathogenesis of pancreatic ductal adenocarcinoma (PDAC) by generating and using murine models. To accelerate drug discovery by identifying novel therapeutic targets on a systemic level, here we generated a Drosophila model mimicking the genetic signature in PDAC (KRAS, TP53, CDKN2A, and SMAD4 alterations), which is associated with the worst prognosis in patients. The ‘4-hit’ flies displayed epithelial transformation and decreased survival. Comprehensive genetic screening of their entire kinome revealed kinases including MEK and AURKB as therapeutic targets. Consistently, a combination of the MEK inhibitor trametinib and the AURKB inhibitor BI-831266 suppressed the growth of human PDAC xenografts in mice. In patients with PDAC, the activity of AURKB was associated with poor prognosis. This fly-based platform provides an efficient whole-body approach that complements current methods for identifying therapeutic targets in PDAC.Significance:Development of a Drosophila model mimicking genetic alterations in human pancreatic ductal adenocarcinoma provides a tool for genetic screening that identifies MEK and AURKB inhibition as a potential treatment strategy.

This case report describes a rare, late complication of radiofrequency ablation for hepatocellular carcinoma. A 77-year-old woman with a history of hepatocellular carcinoma presented with an incarcerated diaphragmatic hernia (DH), which was successfully repaired using emergency laparoscopic surgery. However, 2 months later, she developed hepatic encephalopathy due to severe fecal impaction. Imaging and endoscopy revealed significant colonic stenosis at the hernia repair site. The stenosis was successfully resolved with two sequential balloon dilations, leading to a complete recovery from the encephalopathy. This is the first reported case of secondary hepatic encephalopathy caused by colonic stenosis following laparoscopic repair of DH after radiofrequency ablation. This report demonstrates the feasibility of laparoscopic surgery for DH and emphasizes the necessity for meticulous long-term monitoring to avoid such rare but serious delayed complications.

INTRODUCTION: Heterotopic pancreas refers to pancreatic tissue located outside its normal position and lacking anatomical or vascular continuity with the pancreas. Gastric heterotopic pancreas (GHP) is generally asymptomatic, but in rare cases large GHP lesions can cause gastric outlet syndrome or gastroduodenal invagination. GHP may also occasionally cause acute pancreatitis and abscess formation in the gastric wall. This report describes a rare case of GHP with concurrent gastroduodenal invagination and gastric wall abscess treated via laparoscopic distal gastrectomy.CASE PRESENTATION: A 46-year-old man was admitted to the hospital with abdominal pain and vomiting. Computed tomography revealed a 40-mm low-density mass in the gastric pylorus, and gastroduodenal invagination. Gastroscopy confirmed a submucosal lesion at the gastric pylorus causing pyloric stenosis. The patient underwent laparoscopic distal gastrectomy with Roux-en-Y reconstruction. Histopathological examination revealed a gastric submucosal lesion containing pancreatic tissue with acinar cells and ducts, without islets of Langerhans, leading to a diagnosis of Heinrich type II GHP. The submucosal lesion also contained inflammatory components such as neutrophils and foamy histiocytes, forming a gastric wall abscess. Finally, the patient was discharged on postoperative day 11 and is progressing well 7 months after surgery.CONCLUSIONS: Herein we report the first case of laparoscopic distal gastrectomy for GHP with concurrent gastroduodenal invagination and gastric wall abscess resulting in a favorable outcome.

Significant progress has been made in understanding the pathogenesis of pancreatic ductal adenocarcinoma (PDAC) by generating and using murine models. To accelerate drug discovery by identifying novel therapeutic targets on a systemic level, here we generated a Drosophila model mimicking the genetic signature in PDAC (KRAS, TP53, CDKN2A, and SMAD4 alterations), which is associated with the worst prognosis in patients. The ‘4-hit’ flies displayed epithelial transformation and decreased survival. Comprehensive genetic screening of their entire kinome revealed kinases including MEK and AURKB as therapeutic targets. Consistently, a combination of the MEK inhibitor trametinib and the AURKB inhibitor BI-831266 suppressed the growth of human PDAC xenografts in mice. In patients with PDAC, the activity of AURKB was associated with poor prognosis. This fly-based platform provides an efficient whole-body approach that complements current methods for identifying therapeutic targets in PDAC.Significance:Development of a Drosophila model mimicking genetic alterations in human pancreatic ductal adenocarcinoma provides a tool for genetic screening that identifies MEK and AURKB inhibition as a potential treatment strategy.

Supplementary methods, tables, and figures

Supplementary methods, tables, and figures

Supplementary methods, tables, and figures

Significant progress has been made in understanding the pathogenesis of pancreatic ductal adenocarcinoma (PDAC) by generating and using murine models. To accelerate drug discovery by identifying novel therapeutic targets on a systemic level, here we generated a Drosophila model mimicking the genetic signature in PDAC (KRAS, TP53, CDKN2A, and SMAD4 alterations), which is associated with the worst prognosis in patients. The ‘4-hit’ flies displayed epithelial transformation and decreased survival. Comprehensive genetic screening of their entire kinome revealed kinases including MEK and AURKB as therapeutic targets. Consistently, a combination of the MEK inhibitor trametinib and the AURKB inhibitor BI-831266 suppressed the growth of human PDAC xenografts in mice. In patients with PDAC, the activity of AURKB was associated with poor prognosis. This fly-based platform provides an efficient whole-body approach that complements current methods for identifying therapeutic targets in PDAC.Significance:Development of a Drosophila model mimicking genetic alterations in human pancreatic ductal adenocarcinoma provides a tool for genetic screening that identifies MEK and AURKB inhibition as a potential treatment strategy.