Objective: To analyze the clinical characteristics and prognosis of primary and secondary pancreatic diffuse large B-cell lymphoma (DLBCL) . Methods: Clinical data of patients with pancreatic DLBCL admitted at Shanghai Rui Jin Hospital affiliated with Shanghai Jiao Tong University School of Medicine from April 2003 to June 2020 were analyzed. Gene mutation profiles were evaluated by targeted sequencing (55 lymphoma-related genes). Univariate and multivariate Cox regression models were used to evaluate the prognostic factors of overall survival (OS) and progression-free survival (PFS) . Results: Overall, 80 patients were included; 12 patients had primary pancreatic DLBCL (PPDLBCL), and 68 patients had secondary pancreatic DLBCL (SPDLBCL). Compared with those with PPDLBCL, patients with SPDLBCL had a higher number of affected extranodal sites (P<0.001) and had higher IPI scores (P=0.013). There was no significant difference in the OS (P=0.120) and PFS (P=0.067) between the two groups. Multivariate analysis indicated that IPI intermediate-high/high risk (P=0.025) and double expressor (DE) (P=0.017) were independent adverse prognostic factors of OS in patients with pancreatic DLBCL. IPI intermediate-high/high risk (P=0.021) was an independent adverse prognostic factor of PFS in patients with pancreatic DLBCL. Targeted sequencing of 29 patients showed that the mutation frequency of PIM1, SGK1, BTG2, FAS, MYC, and MYD88 in patients with pancreatic DLBCL were all >20%. PIM1 (P=0.006 for OS, P=0.032 for PFS) and MYD88 (P=0.001 for OS, P=0.017 for PFS) mutations were associated with poor OS and PFS in patients with SPDLBCL. Conclusion: There was no significant difference in the OS and PFS between patients with PPDLBCL and those with SPDLBCL. IPI intermediate-high/high risk and DE were adverse prognostic factors of pancreatic DLBCL. PIM1, SGK1, BTG2, FAS, MYC, and MYD88 were common mutations in pancreatic DLBCL. PIM1 and MYD88 mutations indicated worse prognosis.
Humans ; Myeloid Differentiation Factor 88 ; Disease-Free Survival ; Retrospective Studies ; China/epidemiology* ; Prognosis ; Lymphoma, Large B-Cell, Diffuse/drug therapy* ; Antineoplastic Combined Chemotherapy Protocols ; Pancreas/pathology* ; Immediate-Early Proteins/therapeutic use* ; Tumor Suppressor Proteins

Humans ; Sarcoma, Ewing/pathology* ; Pancreas/pathology*

Pancreatic cancer is a malignant tumor of digestive system with poor prognosis,and surgical resection is still the only hope for a radical cure. Although the current consensus and guidelines describe in detail the standard and extended range of lymph node dissection,the selection of specific range of lymph node dissection and its impact on prognosis are still controversial. Current studies have not only proposed some improved extent of lymph node dissection, such as total mesopancreas excision and Heidelberg triangle dissection, but also suggested different extent of lymph node dissection for ventral and dorsal pancreatic head cancer. In addition, the prognosis of pancreatic head cancer in uncinate process and non-uncinate process is different after para-aortic lymph node dissection, which is worthy of further study. Neoadjuvant therapy or conversion therapy provides more surgical opportunities for patients with pancreatic cancer. For these patients, Heidelberg triangle dissection has potential value in improving prognosis. This paper summarizes the exploration and latest progress of standard and extended lymph node dissection, lymph node dissection of specific site of pancreatic head cancer and the extent of lymph node dissection after neoadjuvant/transformation therapy in recent years.
Humans ; Lymph Node Excision ; Pancreatic Neoplasms/pathology* ; Lymph Nodes/pathology* ; Pancreas/pathology* ; Prognosis

Pancreatic cancer, notorious for its late diagnosis and aggressive progression, poses a substantial challenge owing to scarce treatment alternatives. This review endeavors to furnish a holistic insight into pancreatic cancer, encompassing its epidemiology, genomic characterization, risk factors, diagnosis, therapeutic strategies, and treatment resistance mechanisms. We delve into identifying risk factors, including genetic predisposition and environmental exposures, and explore recent research advancements in precursor lesions and molecular subtypes of pancreatic cancer. Additionally, we highlight the development and application of multi-omics approaches in pancreatic cancer research and discuss the latest combinations of pancreatic cancer biomarkers and their efficacy. We also dissect the primary mechanisms underlying treatment resistance in this malignancy, illustrating the latest therapeutic options and advancements in the field. Conclusively, we accentuate the urgent demand for more extensive research to enhance the prognosis for pancreatic cancer patients.
Humans ; Pancreatic Neoplasms/therapy* ; Prognosis ; Pancreas/pathology* ; Genetic Predisposition to Disease ; Genomics

Acute pancreatitis (AP) is a common and potentially life-threatening pancreatic inflammatory disease. Although it is usually self-limiting, up to 20% of patients will develop into severe AP. It may lead to systemic inflammatory response syndrome and multiple organ dysfunction, affecting the lungs, kidneys, liver, heart, etc. Surviving patients usually have sequelae of varying degrees, such as chronic hyperglycemia after AP (CHAP), pancreatic exocrine insufficiency, and chronic pancreatitis. Lacking specific target treatments is the main reason for high mortality and morbidity, which means that more research on the pathogenesis of AP is needed. Ferroptosis is a newly discovered regulated cell death (RCD), originally described in cancer cells, involving the accumulation of iron and the depletion of plasma membrane polyunsaturated fatty acids, and a caspase-independent RCD. It is closely related to neurological diseases, myocardial infarction, ischemia/reperfusion injury, cancer, etc. Research in the past years has also found the effects of ferroptosis in AP, pancreatic cancer, and AP complications, such as acute lung injury and acute kidney injury. This article reviews the research progress of ferroptosis and its association with the pathophysiological mechanisms of AP, trying to provide new insight into the pathogenesis and treatment of AP, facilitating the development of better-targeted drugs.
Humans ; Pancreatitis/pathology* ; Acute Disease ; Ferroptosis ; Pancreas/pathology* ; Acute Lung Injury/metabolism*

Humans ; Consensus ; Pancreatic Neoplasms/pathology* ; Pancreas/pathology* ; Specimen Handling ; Neoplasms, Glandular and Epithelial

Carcinoma/pathology* ; Giant Cells/pathology* ; Humans ; Osteoclasts/pathology* ; Pancreas/pathology* ; Pancreatic Neoplasms/surgery*

Objective: To compare the short-term and long-term prognosis of irreversible electroporation(IRE) and conversional resection for locally advanced pancreatic cancer(LAPC). Methods: The clinical and pathological data of 98 LAPC patients who underwent IRE or conversional resection at the Department of Pancreatobiliary Surgery,Sun Yat-sen University Cancer Center from August 2015 to December 2020 were retrospectively collected and analyzed.The study comprised of 53 males and 45 females, with age(M(IQR)) of 57.5(13.5)years old(range:20 to 87 years old). Fifty-three patients received IRE treatment(IRE group) and 45 patients received surgical resection(resection group). The differences of clinical and pathological data between both groups were not significant(all P<0.05). The Mann-Whitney U test was used for quantitative data and the χ² test was used for categorical data.Survival was analyzed using Kaplan-Meier method and compared using Log-rank test. Results: The operation time and intraoperative blood loss were 5.0(2.4)hours and 50(100) ml in the IRE group,respectively,which were significantly less than those of resection group(7.0(3.3)hours and 400(200)ml,both P<0.05).The hospital stay and hospitalization cost were 9.0(3.0)days and 79 154 (83 738) yuan in the IRE group,respectively,which were also significantly less than those in the resection group(16.0(8.5)days and 109 557(37 795)yuan,both P<0.05).The complication rate of IRE group was significantly lower than that of the resection group(18.8% vs. 55.6%,χ²=14.270,P<0.01).The median overall survival(OS) time of IRE group was 28.9 months(95%CI:23.2 to 34.6 months),with the 1-,2-,and 3-year OS rates of 91.6%,61.7%,and 24.6%,respectively.The median survival of OS of resection group was 27.1 months(95%CI:20.9 to 33.3 months),with the 1-,2-,and 3-year OS rates of 81.8%,53.9%,and 30.3%,respectively.There was no significant difference in OS between the two groups(χ²=0.900,P=0.760).The median progression free survival(PFS) time of IRE group was 18.0 months(95%CI:14.7 to 21.3 months),with the 1-,2-,and 3-year PFS rates of 68.3%,29.7%,and 9.9%,respectively.The median survival of PFS of resection group was 11.1 months(95%CI:6.1 to 16.2 months),with the 1-,2-,and 3-year PFS rates of 45.2%,21.9%,and 14.6%,respectively.There was no significant difference in PFS between the two groups(χ²=1.850,P=0.170). Conclusion: IRE can achieve similar survival for LAPC and may has less complications compared to those with conversion resection.
Adolescent ; Adult ; Aged ; Aged, 80 and over ; Electroporation/methods* ; Female ; Humans ; Male ; Middle Aged ; Neoplasms, Second Primary ; Pancreas/pathology* ; Pancreatic Neoplasms/pathology* ; Prognosis ; Retrospective Studies ; Treatment Outcome ; Young Adult

OBJECTIVE: To investigate the expression of Ca²⁺/calmodulin-dependent protein kinase II (CaMK Ⅱ) in pancreatic tissues of mice with severe acute pancreatitis (SAP) and explore the protective effect of KN93, a CaMK Ⅱ inhibitor, against pancreatic injury in SAP and the possible mechanism. METHODS: Thirty-six healthy male C57 mice were randomly divided into sham operation group, SAP group, KN93 group and SAP + KN93 group (n=9). Serum and pancreatic tissue samples were collected 24 h after modeling. The pathological changes in the pancreatic tissues were observed using HE staining. Serum lipase and amylase activities and the levels of inflammatory factors were detected using ELISA. Western blotting was used to detect the expressions of CaMK Ⅱ, p-CaMK Ⅱ, p-NF-κB, MAPK and p-MAPK in mouse pancreas. RESULTS: Compared with those in sham operation group, the expressions of p-CaMK Ⅱ, p-NF-κB and p-MAPK were significantly increased in SAP group (P < 0.05). KN93 treatment obviously alleviated pathological injuries of the pancreas in SAP mice, and significantly lowered serum levels of lipase, amylase and inflammatory factors (TNF-α and IL-6) and phosphorylation levels of NF-κB, ERK and MAPK proteins (P < 0.05). CONCLUSION The activity of CaMK Ⅱ is significantly increased in the pancreatic tissue of SAP mice. KN93 can alleviate pancreatic injury and inflammation in SAP mice possibly through the ERK/MAPK signaling pathway.
Acute Disease ; Animals ; Inflammation/metabolism* ; Male ; Mice ; NF-kappa B/metabolism* ; Pancreas/pathology* ; Pancreatitis/pathology*

OBJECTIVE: To assess the effect of early abdominal puncture drainage (APD) on autophagy and Nrf-2/HO-1 pathway in rats with severe acute pancreatitis (SAP) and explore the possibile mechanism. METHODS: Thirty-two male SD rats were randomly divided into sham-operated (SO) group, SAP group with retrograde injection of 4% sodium taurocholate, APD group with insertion of a drainage tube into the lower right abdomen after SAP induction, and APD + ZnPP group with intraperitoneal injection of 30 mg/kg ZnPP 12 h before APD modeling. Blood samples were collected from the rats 12 h after modeling for analysis of amylase and lipase levels and serum inflammatory factors. The pathological changes of the pancreatic tissue were observed with HE staining. Oxidative stress in the pancreatic tissue was detected with colorimetry, and sub-organelle structure and autophagy in pancreatic acinar cells were observed by transmission electron microscopy. The expressions of autophagy-related proteins and Nrf-2/HO-1 pathway were detected using RT-PCR and Western blotting. RESULTS: Compared with those in SAP group, the rats with APD treatment showed significantly alleviated pathologies in the pancreas, reduced serum levels of lipase, amylase and inflammatory factors, lowered levels of oxidative stress, and activated expressions of Nrf-2/HO-1 pathway in the pancreas. The ameliorating effect of ADP was significantly inhibited by ZnPP treatment before modeling. APD obviously reversed mitochondrial and endoplasmic reticulum damages and p62 accumulation induced by SAP. CONCLUSION APD treatment can suppress oxidative stress and repair impaired autophagy in rats with SAP by activating the Nrf-2/HO-1 pathway, thereby reducing the severity of SAP.
Acute Disease ; Amylases/blood* ; Animals ; Autophagy ; Drainage ; Heme Oxygenase (Decyclizing) ; Lipase/blood* ; Male ; NF-E2-Related Factor 2 ; Oxidative Stress ; Pancreas/pathology* ; Pancreatitis/surgery* ; Punctures ; Rats ; Rats, Sprague-Dawley