Predictive Value of Newly Diagnosed IgG Level in Patients with IgG-type Multiple Myeloma after Initial Treatment / 中国实验血液学杂志

OBJECTIVE@#To explore the predictive value of newly diagnosed IgG levels in the recurrence of IgG-type multiple myeloma (MM) patients after initial treatment.@*METHODS@#The clinical and pathological data of 91 patients newly diagnosed IgG-type MM who were hospitalized in the Department of Hematology of the Second People's Hospital of Yichang and Department of Oncology of The Affiliated Hospital of Jianghan University from April 2010 to March 2019 were collected. According to the median IgG level at the time of initial diagnosis, patients were divided into high IgG group and low IgG group. The recurrence time after initial treatment was followed up, and the correlation between newly diagnosed IgG level and recurrence was analyzed by univariate and multivariate analysis, as well as the influencing factors of IgG levels in order to predict furtherly the potential mechanism of recurrence.@*RESULTS@#Univariate survival analysis showed that high revised international staging system (R-ISS) staging, high level of bone marrow plasma cell (BMPC), lactate dehydrogenase (LDH), creatinine, β@*CONCLUSION@#The higher the serum IgG concentration of IgG-type MM patients at first diagnosis, the earlier the recurrence, which is related to the low level of serum albumin, and can be used as a potential recurrence predictor after complete remission of IgG-type MM patients.

Selective killing of K-ras-transformed pancreatic cancer cells by targeting NAD(P)H oxidase / 癌症

<p><b>INTRODUCTION</b>Oncogenic activation of the K-ras gene occurs in >90% of pancreatic ductal carcinoma and plays a critical role in the pathogenesis of this malignancy. Increase of reactive oxygen species (ROS) has also been observed in a wide spectrum of cancers. This study aimed to investigate the mechanistic association between K-ras-induced transformation and increased ROS stress and its therapeutic implications in pancreatic cancer.</p><p><b>METHODS</b>ROS level, NADPH oxidase (NOX) activity and expression, and cell invasion were examined in human pancreatic duct epithelial E6E7 cells transfected with K-ras (G12V) compared with parental E6E7 cells. The cytotoxic effect and antitumor effect of capsaicin, a NOX inhibitor, were also tested in vitro and in vivo.</p><p><b>RESULTS</b>K-ras transfection caused activation of the membrane-associated redox enzyme NOX and elevated ROS generation through the phosphatidylinositol 3'-kinase (PI3K) pathway. Importantly, capsaicin preferentially inhibited the enzyme activity of NOX and induced severe ROS accumulation in K-ras-transformed cells compared with parental E6E7 cells. Furthermore, capsaicin effectively inhibited cell proliferation, prevented invasiveness of K-ras-transformed pancreatic cancer cells, and caused minimum toxicity to parental E6E7 cells. In vivo, capsaicin exhibited antitumor activity against pancreatic cancer and showed oxidative damage to the xenograft tumor cells.</p><p><b>CONCLUSIONS</b>K-ras oncogenic signaling causes increased ROS stress through NOX, and abnormal ROS stress can selectively kill tumor cells by using NOX inhibitors. Our study provides a basis for developing a novel therapeutic strategy to effectively kill K-ras-transformed cells through a redox-mediated mechanism.</p>