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Objective: To investigate the role of RPRD1B in the progression of diffuse large B-cell lymphoma (DLBCL) and its potential as a therapeutic target. Methods: This study analyzed RPRD1B expression in DLBCL and normal tissues using public databases and assessed its prognostic impact through survival analysis. In vitro and in vivo experiments were conducted to explore the mechanisms by which RPRD1B influences tumor growth and apoptosis. Results: RPRD1B expression was significantly elevated in DLBCL compared to normal tissues and was associated with poor prognosis. In vitro and in vivo experiments demonstrated that RPRD1B promoted lymphoma cell proliferation and inhibited apoptosis through the NF-κB signaling pathway. Conclusions: RPRD1B plays a critical role in the progression of DLBCL by modulating apoptosis and cellular proliferation. Targeting RPRD1B may offer a novel therapeutic strategy for DLBCL, suggesting its potential as a prognostic marker and therapeutic target in hematological malignancies. [ABSTRACT FROM AUTHOR]

Purpose: Anti-angiogenic agents have shown promise for treating advanced hepatocellular carcinoma (HCC), and the primary mechanism of low-dose metronomic chemotherapy using traditional cytotoxic drugs is anti-angiogenic. This study evaluated the efficacy of metronomic capecitabine and thalidomide after cool-tip radiofrequency ablation (RFA), relative to RFA alone, for treating patients with HCC.Methods and materials: Patients with HCC were randomly apportioned to a test group (n = 22) receiving metronomic chemotherapy with capecitabine and thalidomide after RFA, or a control group (n = 28) receiving RFA only. Serum circulating endothelial cells (CECs) and vascular endothelial growth factor (VEGF) were measured in all patients before and 1 month after RFA treatment. Enhanced computed tomography or ultrasound imaging was performed to evaluate efficacy during 12 months of follow-up. The treatment groups were further stratified as HCC within or outside the Milan criteria for transplantation.Results: One month post-treatment, the tumour response rate (TRR), including complete response and partial response rate, of the test and control groups was statistically similar. At 12 months, the TRR of the test group (68.2%) was significantly higher than that of the control group (35.7%). In the test group, the TRR of patients whose tumour burdens were outside the Milan criteria was significantly higher than that of the control group. One month post-treatment, CECs and VEGF levels of the test group were significantly lower than baseline, while those of the control group were significantly higher. At the end of the 12-month follow-up, there was a progression-free survival (PFS) benefit of 2 months in the test group.Conclusion: Metronomic capecitabine and thalidomide after RFA significantly reduced recurrence of HCC and extended PFS, especially for HCC outside the Milan criteria, perhaps via reduction of serum CECs and VEGF levels and inhibition of tumour angiogenesis. [ABSTRACT FROM PUBLISHER]

Background: Adding radiotherapy (RT) to systemic therapy improves progression-free survival (PFS) and overall survival (OS) in oligometastatic non-small cell lung cancer (NSCLC). Whether these findings translate to epidermal growth factor receptor (EGFR)-mutated NSCLC remains unknown. The SINDAS trial (NCT02893332) evaluated first-line tyrosine kinase inhibitor (TKI) therapy for EGFR-mutated synchronous oligometastatic NSCLC and randomized to upfront RT vs no RT; we now report the prespecified interim analysis at 68% accrual., Methods: Inclusion criteria were biopsy-proven EGFR-mutated adenocarcinoma (per amplification refractory mutation system or next generation sequencing), with synchronous (newly diagnosed, treatment naïve) oligometastatic (≤5 metastases; ≤2 lesions in any one organ) NSCLC without brain metastases. All patients received a first-generation TKI (gefitinib, erlotinib, or icotinib), and randomization was between no RT vs RT (25-40 Gy in 5 fractions depending on tumor size and location) to all metastases and the primary tumor/involved regional lymphatics. The primary endpoint (intention to treat) was PFS. Secondary endpoints included OS and toxicities. All statistical tests were 2-sided., Results: A total of 133 patients (n = 65 TKI only, n = 68 TKI with RT) were enrolled (2016-2019). The median follow-up was 23.6 months. The respective median PFS was 12.5 months vs 20.2 months (P < .001), and the median OS was 17.4 months vs 25.5 months (P < .001) for TKI only vs TKI with RT. Treatment yielded no grade 5 events and a 6% rate of symptomatic grade 3-4 pneumonitis in the TKI with RT arm. Based on the efficacy results of this prespecified interim analysis, the ethics committee recommended premature cessation of this trial., Conclusions: As compared with a first-line TKI alone, addition of upfront local therapy using RT statistically significantly improved PFS and OS for EGFR-mutated NSCLC., (© The Author(s) 2022. Published by Oxford University Press.)

Aim: To investigate the inhibitory role of toxicarioside A on the gastric cancer cell line human gastric cancer cell line (SGC-7901) and determine the underlying molecular mechanism., Methods: After SGC-7901 cells were treated with toxicarioside A at various concentrations (0.5, 1.5, 4.5, 9.0 μg/mL) for 24 h or 48 h, cell viability was determined by 3-(4,5-dimethyl-thiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide assay, and the motility and invasion of tumor cells were assessed by the Transwell chamber assay. Immunofluorescence staining, reverse transcription polymerase chain reaction and Western blotting were performed to detect the expression of basic fibroblast growth factor (bFGF) and fibroblast growth factor receptor-1 (FGFR1), and nuclear factor-kappa B (NF-κB) activation was examined by electrophoretic mobility shift assay., Results: The results showed that toxicarioside A was capable of reducing cell viability, inhibiting cell growth, and suppressing cell migration and invasion activities in a time- and dose-dependent manner in SGC-7901 cells. Further analysis revealed that not only the expression of bFGF and its high-affinity receptor FGFR1 but also the NF-κB-DNA binding activity were effectively blocked by toxicarioside A in a dose-dependent manner compared with the control group (P < 0.05 or P < 0.01). Interestingly, application of the NF-κB specific inhibitor, pyrrolidinedithiocarbamate (PDTC), to SGC-7901 cells significantly potentized the toxicarioside A-induced down-regulation of bFGF compared with the control group (P < 0.05)., Conclusion: These findings suggest that toxicarioside A has an anti-gastric cancer activity and this effect may be achieved partly through down-regulation of NF-κB and bFGF/FGFR1 signaling.

Background & Objective: Dendritic cells (DCs) are the strongest antigen presenting cells (APCs). But immune therapy based on DCs for osteosarcoma has seldom been reported. This study was designed to investigate the immunologic potency and antitumor effects of fused vaccine of rat DCs on osteosarcoma., Methods: Mononuclear cells in rat bone marrow were propagated in vitro under the condition of recombinant granulocytemacrophage colony-stimulating factor (rGM-CSF), recombinant interleukin-4 (rIL-4), and recombinant tumor necrosing factor-alpha (rTNF-alpha) to obtain DCs. DCs were purified by monoclonal antibody OX62 and magnetic beads, and confirmed by morphologic observation, phenotype determine, and functional experiments. Osteosarcoma cell line UMR-106 was fused with allogeneic or syngeneic DCs by electrofusion to produce the tumor vaccine. Each kind of tumor vaccine was injected subcutaneously into 10 rats to observe its specific antitumor effects., Results: Survival rate of rats after injection of 1x10(7) UMR-106 cells was 70% in allogeneic tumor vaccine group, and 50% in syngeneic tumor vaccine group. The survival rats stood up to the second challenge of 1x10(7) UMR-106 cells 7 weeks after injection. After immunization of 2x10(6) UMR106-DCs, tumors in 60% of the rats bearing pre-established tumor cells diminished or vanished., Conclusion: Fused tumor vaccine of UMR-106 cells and allogeneic DCs might induce specific anti-tumor effects on osteosarcoma.

Background & Objective: Recently, it has been reported that reverse transcription polymerase chain reaction(RT-PCR) for the detection of related tumor marker genes expression in lymph nodes can be used to evaluate tumor metastasis and results in higher sensitivity. The objective of this study was to investigate the clinical significance of RT-PCR for detecting axillary lymph node metastases of breast cancer., Methods: RT-PCR was used to examine the mRNA of MUC1 and keratin19 in axillary lymph nodes. The lymph node metastases was assessed referring to the results of both RT-PCR and hematoxylin-eosin(HE) staining. All 37 patients with negative HE staining had been followed up for at least three years., Results: Both MUC1 and keratin19 expression were detected in all 86 breast cancer specimens, while it was undetectable in all lymph nodes from patients with benign diseases. Among 37 patients with negative HE staining in lymph nodes, 11 were positive for keratin19 expression (29.7%), whose 3-year recurrence rate was 45.5% (5/11), while the patients with negative keratin19 expression was just 12.5% (2/26, P< 0.01)., Conclusion: The expression of MUC1 and keratin19 in lymph nodes detected by RT-PCR can be regarded as a sign of breast cancer micrometastasis, which can be used to evaluate prognosis in patients as well as to choose the postoperative treatment protocols.

Background & Objective: Osteosarcoma is the most common malignant bone tumor in adolescents and yound adults. It is characterized by a high propensity for pulmonary metastasis. In spite of successful control of the primary tumor, death from pulmonary metastases occurs in > 30% of patients within 5 years. A better understanding of the molecular mechanisms that regulate the process of metastasis can provide a biological foundation for the design of more effective therapy. We established a metastatic model in nude mice with the method of orthotopically transplanting human osteosarcoma cell line SOSP-9607 and selected and isolated SOSP-M with highly metastatic potential. This study is to clone genes associated with osteosarcoma metastasis and to investigate the molecular mechanism of osteosarcoma metastasis by comparing the levels of gene expression between the two cells lines., Methods: Using suppression subtractive hybridization, the substracted cDNA library of highly metastatic human osteosarcoma cell line SOSP-M was constructed. Positive clones were screened by differential screen technique. Partial positive clones were sequenced. The interested upexpressed clones in SOSP-M cells were analyzed through Northern blot and RT-PCR for the low metastatic cell lines SOSP-9607 and OS-9901, highly metastatic cell line SOSP-M and three pulmonic metastatic nodules., Results: Two positive cDNA clones from highly metastatic cell line SOSP-M subtracted cDNA library were identical(99% homology) to apoptosis antagonizing transcription factor. Northern blot and RT-PCR analysis demonstrated that apoptosis antagonizing transcription factor expressed highly in high metastatic cell line SOSP-M and three pulmonic metastatic nodules, but not in low metastatic cell line SOSP-9607 and OS-9901., Conclusion: Apoptosis antagonizing transcription factor may play an important role in promoting metastasis of osteosarcoma.