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Objective. To study the clinical efficacy of modified Yiwei Shengyang decoction combined with FOLFOX4 chemotherapy regimen in the treatment of advanced gastric cancer and its effect on tumor marker levels. Methods. A total of 106 patients with advanced gastric cancer who were treated in our hospital from September 2019 to September 2021 were recruited and assigned via random number allocation to receive either FOLFOX4 chemotherapy (control group) or modified Yiwei Shengyang decoction plus FOLFOX4 chemotherapy (observation group). Outcome measures included clinical efficacy and tumor marker levels. Results. Modified Yiwei Shengyang decoction plus FOLFOX4 chemotherapy was associated with a significantly higher efficacy (86.79%, including 22 (41.51%) cases of complete response (CR), 24 (45.28%) cases of partial response (PR), 6 (11.32%) cases of stable disease (SD), and 1 (1.89%) case of progressive disease (PD)) compared to FOLFOX4 chemotherapy alone (47.16%, including 10 (18.87%) cases of CR, 15 (28.30%) cases of PR, 21 (39.62%) cases of SD, and 7 (13.21%) cases of PD) (P < 0.05). There was no significant difference in the levels of CEA and CA19-9 between the two groups before treatment (P > 0.05). Modified Yiwei Shengyang decoction plus FOLFOX4 chemotherapy resulted in significantly lower levels of carcinoembryonic antigen (CEA) and carbohydrate antigen 19-9 (CA19-9) (2.08 ± 0.47, 15.12 ± 6.74) compared to FOLFOX4 chemotherapy alone (5.46 ± 1.84, 31.82 ± 7.48) (P < 0.05). Conclusion. Modified Yiwei Shengyang decoction plus FOLFOX4 chemotherapy regimen is effective in the treatment of advanced gastric cancer. It regulates the levels of various serum tumor markers in patients and controls the disease, so it is worthy of clinical application and promotion. [ABSTRACT FROM AUTHOR]

Nuclear factor erythroid 2-related factor 2 (Nrf2) is involved in tumor drug resistance, but its role in imatinib resistance of chronic myeloid leukemia (CML) remains elusive. We aimed to investigate the effects of Nrf2 on drug sensitivity, thioredoxin reductase (TrxR) expression, reactive oxygen species (ROS) production, and apoptosis induction in imatinib-resistant CML K562/G01 cells and explored their potential mechanisms. Stable K562/G01 cells with knockdown of Nrf2 were established by infection of siRNA-expressing lentivirus. The mRNA and protein expression levels of Nrf2 and TrxR were determined by real-time quantitative polymerase chain reaction and western blot, respectively. ROS generation and apoptosis were assayed by flow cytometry, while drug sensitivity was measured by the Cell Counting Kit-8 assay. Imatinib-resistant K562/G01 cells had higher levels of Nrf2 expression than the parental K562 cells at both mRNA and protein levels. Expression levels of Nrf2 and TrxR were positively correlated in K562/G01 cells. Knockdown of Nrf2 in K562/G01 cells enhanced the intracellular ROS level, suppressed cell proliferation, and increased apoptosis in response to imatinib treatments. Nrf2 expression contributes to the imatinib resistance of K562/G01 cells and is positively correlated with TrxR expression. Targeted inhibition of the Nrf2-TrxR axis represents a potential therapeutic approach for imatinib-resistant CML. [ABSTRACT FROM AUTHOR]

Brucea javanica is a traditional herbal medicine in China, and its antitumor activities are of research interest. Brucea javanica oil, extracted with ether and refined with 10% ethyl alcohol from Brucea javanica seed, was used to treat hepatoma H22-bearing mice in this study. The antitumor effect and probable mechanisms of the extracted Brucea javanica oil were studied in H22-bearing mice by WBC count, GOT, GPT levels, and western blotting. The H22 tumor inhibition ratio of 0.5, 1, and 1.5 g/kg bw Brucea javanica oil were 15.64%, 23.87%, and 38.27%. Brucea javanica oil could inhibit the involution of thymus induced by H22 tumor-bearing, but it could not inhibit the augmentation of spleen and liver. Brucea javanica oil could decrease the levels of WBC count and GOT and GPT in H22-bearing mice. The protein levels of GAPDH, Akt, TGF-β1, and α-SMA in tumor tissues decreased after being treated with Brucea javanica oil. Disturbing energy metabolism and neoplastic hyperplasia controlled by Akt and immunoregulation activity were its probable antitumor mechanisms in hepatoma H22-bearing mice. [ABSTRACT FROM AUTHOR]