患者 男性，49岁，主因“右上腹间断隐痛2个月余”于2020年2月28日收入我院。2个月前患者无明显诱因出现右上腹间断隐痛，无放射痛。自行口服“消炎利胆片”，其间症状加重，至当地医院行上腹增强CT检查，结果提示肝实性占位，考虑肝癌；实验室检查诊断乙肝，予口服恩替卡韦片（0.5 mg/d）抗病毒治疗。为进一步治疗就诊于我院。既往史无特殊。母亲曾患肝硬化，因“肝病”去世。入院后体检未见明显阳性体征。实验室检查：甲胎蛋白>1 210.00 μg/L，癌胚抗原及CA19-9均在正常范围，乙肝表面抗原、表面e抗体、核心抗体阳性，乙肝病毒DNA定量检测549 IU/ml。肝功能Child-Pugh分级为A级。入院行腹部增强MRI检查结果提示肝右叶占位，大小约10.3 cm×10.7 cm×14.3 cm，动脉期不均匀强化，静脉期及延迟期强化减退，腔静脉、肝右静脉、肝门静脉右支及主干多发栓子形成；肝硬化、脾大（图1）。根据《原发性肝癌诊疗指南（2019年版）》，初步诊断为：（1）原发性肝癌，中国肝癌分期Ⅲa期；巴塞罗那肝癌临床分期为C期；（2）慢性乙肝；（3）肝硬化；（4）脾大、脾功能亢进。

The present study aimed to explore the role of histone chaperone anti-silencing function 1B (ASF1B) in pancreatic cancer and the underlying mechanism. The biological function of ASF1B was investigated in pancreatic cancer cell lines (PANC-1 and SW1990) and a mouse xenograft model. Chromatin immunoprecipitation was used to detect the effect of ASF1B on the transcriptional activity of c-Myc. ASF1B was highly expressed in pancreatic adenocarcinoma (PAAD) samples from The Cancer Genome Atlas. ASF1B expression was positively associated with poor survival rates in patients with PAAD. Silencing of ASF1B in PANC-1 and SW1990 cells inhibited cell proliferation, migration and invasion, and induced apoptosis. Mechanistically, ASF1B increased H3K56 acetylation (H3K56ac) in a CREB-binding protein (CBP)-dependent manner. ASF1B promoted H3K56ac at the c-Myc promoter and increased c-Myc expression. In PANC-1 and SW1990 cells, the CBP inhibitor curcumin and the c-Myc inhibitor 10058-F4 reversed the promoting effects of ASF1B on cell proliferation, migration and invasion. In the mouse xenograft model, ASF1B silencing inhibited tumor growth, and was associated with low H3K56ac and c-Myc expression. ASF1B promoted pancreatic cancer progression by activating c-Myc via CBP-mediated H3K56ac.

Nanoparticles possess the ability to adsorb and load other compounds. This study aimed to synthesize a gene carrier with polyethyleneimine (PEI), hyaluronic acid (HA) and mesoporous silica nanoparticles (MSNs) for circ_0086375 delivery to investigate the role and mechanism of circ_0086375 in pancreatic cancer (PC) progression. The expression of genes and proteins was detected by quantitative real-time polymerase chain reaction and Western blot. In vitro experiments were performed by cell counting Kit-8 (CCK-8), 5-Ethynyl-2′-deoxyuridine (EdU) assay, flow cytometry, transwell assay, and wound healing assay, respectively. Dual-luciferase activity assay was used to investigate the target relationship between miR-646 and circ_0086375 or SLC4A4 (solute carrier family 4 member 4). Circ_0086375 loaded PEI/HA-based mesoporous silica nanoparticles (MSNs) were prepared, and in vivo assay was performed by using xenograft tumor model. Circ_0086375 expression was decreased in PC tissues and cells. Restoration of circ_0086375 suppressed PC cell proliferation, migration and invasion in vitro and in vivo. Mechanistically, circ_0086375 acted as a sponge for miR-646 to elevate SLC4A4 expression, which was confirmed to be a target of miR-646. The prepared circ_0086375/MSN/PEI/HA nanocomplexes showed excellent fluorescent properties and a higher cellular uptake of circ_0086375 in PC cells. Moreover, circ_0086375/MSN/PEI/HA showed relatively more anticancer effects in PC than that of circ_0086375 alone in vitro and in vivo. Delivery of circ_0086375 by nanoparticles suppresses the tumorigenicity of pancreatic cancer by miR-646/SLC4A4 axis, suggesting a new potential target for future pancreatic cancer treatment.

骨尤文肉瘤是一种多见于儿童及青少年的原发性骨肿瘤.骨外尤文肉瘤/外周原始神经外胚层肿瘤较为少见,多位于深部软组织,其中位于十二指肠更为罕见,治疗方式多以手术为主,现报道1例患者的治疗经过,供临床参考.