Journal of Oncology最新文献

[This retracts the article DOI: 10.1155/2021/6103092.].

Helicobacter pylori (H. pylori) infection affects cell survival pathways, including apoptosis and proliferation in host cells, and disruption of this balance is the key event in the development of H. pylori-induced gastric cancer (HPGC). H. pylori infection induces alterations in microRNAs expression that may be involved in GC development. Bioinformatic analysis showed that microRNA-21 (miR-21) is significantly upregulated in HPGC. Furthermore, quantitative proteomics and in silico prediction were employed to identify potential targets of miR-21. Following functional enrichment and clustered interaction network analyses, five candidates of miR-21 targets, PDCD4, ASPP2, DAXX, PIK3R1, and MAP3K1, were found across three functional clusters in association with cell death and survival, cellular movement, and cellular growth and proliferation. ASPP2 is inhibited by H. pylori-induced miR-21 overexpression. Moreover, ASPP2 levels are inversely correlated with miR-21 levels in HPGC tumor tissues. Thus, ASPP2 was identified as a miR-21 target in HPGC. Here, we observed that H. pylori-induced ASPP2 suppression enhances resistance to apoptosis in GC cells using apoptosis assays. Using protein interaction network and coimmunoprecipitation assay, we identified CHOP as a direct mediator of the ASPP2 proapoptotic activity in H. pylori-infected GC cells. Mechanistically, ASPP2 suppression promotes p300-mediated CHOP degradation, in turn inhibiting CHOP-mediated transcription of Noxa, Bak, and suppression of Bcl-2 to enact antiapoptosis in the GC cells after H. pylori infection. Clinicopathological analysis revealed correlations between decreased ASPP2 expression and higher HPGC risk and poor prognosis. In summary, the discovery of H. pylori-induced antiapoptosis via miR-21-mediated suppression of ASPP2/CHOP-mediated signaling provides a novel perspective for developing HPGC management and treatment.

[This retracts the article DOI: 10.1155/2022/3290479.].

[This retracts the article DOI: 10.1155/2022/3434430.].

[This retracts the article DOI: 10.1155/2022/7517821.].

[This retracts the article DOI: 10.1155/2022/9119245.].

[This retracts the article DOI: 10.1155/2022/4948943.].

Aim: The aim of this study is to evaluate the efficacy and safety of afatinib in the treatment of non-small cell lung cancer (NSCLC) patients with brain metastasis based on meta-analysis.

Methods: Related literatures were searched in the following databases: EMbase, PubMed, China Knowledge Network (CNKI), Wanfang, Weipu, Google Scholar, the China Biomedical Literature Service System, and other databases. Clinical trials and observational studies that met the requirements were selected for meta-analysis using Revman 5.3. The hazard ratio (HR) was used as an indicator of the impact of afatinib.

Results: A total of 142 related literatures were acquired, but after screening, five literatures were selected for data extraction. The following indices were compared: the progression-free survival (PFS), overall survival (OS), and common adverse reactions (ARs) of grade 3 and above. A total of 448 patients with brain metastases were included and were divided into two groups: the control group (no afatinib treatment, with chemotherapy alone and the first-generation EGFR-TKIs) and the afatinib group. The results showed that afatinib could improve PFS (HR: 0.58, 95% CI: 0.39-0.85, P < 0.05) and ORR (OR = 2.86, 95% CI: 1.45-2.57, P < 0.05), but had no benefit on OS (HR: 1.13, 95% CI: 0.15-8.75, P > 0.05) and DCR (OR = 2.87, 95% CI: 0.97-8.48, P > 0.05). For the safety of afatinib, the incidence of grade-3-and-above ARs was low (HR: 0.01, 95% CI: 0.00-0.02, P < 0.05).

Conclusion: Afatinib improves the survival of NSCLC patients with brain metastases and shows satisfactory safety.

Background: Acute myeloid leukemia (AML) is a malignant clonal disease of the myeloid hematopoietic system. Clinically, standard treatment options include conventional chemotherapy as well as hematopoietic stem cell transplantation. Among them, chemotherapy has a remission rate of 60% to 80% and nearly 50% relapse in consolidation therapy. Some patients have a poor prognosis due to the presence of unfavorable factors such as advanced age, hematologic history, poor prognosis karyotype, severe infection, and organ insufficiency, which cannot tolerate or are not suitable for standard chemotherapy regimens, and scholars have tried to find new treatment strategies to improve this situation. In the pathogenesis and treatment of leukemia, epigenetics has received attention from experts and scholars.

Objective: To investigate the relationship between OLFML2A overexpression and AML patients.

Methods: From The Cancer Genome Atlas, researchers used the data of OLFML2A gene to analyze and study the pan-cancer using R language and then divided the high and low levels of this protein into two groups to study its relationship with the clinical characteristics of the disease. The relationship between the high levels of OLFML2A and various clinical features of the disease was studied with emphasis on the relationship between the high levels of OLFML2A and various clinical features of the disease. A multidimensional Cox regression analysis was also performed to study the factors affecting patient survival. The correlation between OLFML2A expression and immune infiltration through the immune microenvironment was analyzed. The researchers then conducted a series of studies to analyze the data collected in the study. The focus was on the relationship between the high levels of OLFML2A and immune infiltration. Gene ontology analysis was also performed to study the interactions between the different genes associated with this protein.

Results: According to the pan-cancer analysis, OLFML2A was differentially expressed in different tumors. More importantly, the analysis of OLFML2A in the TCGA-AML database revealed that OLFML2A was highly expressed in AML. The researchers found that the high levels of OLFML2A were associated with different clinical features of the disease, and that the expression of the protein was different in different groups. Those patients with the high levels of OLFML2A were found to have substantially longer survival times compared to those with low-protein levels.

Conclusions: The OLFML2A gene is able to act as a molecular indicator involved in the diagnosis, prognosis, and immune process of AML. It improves the molecular biology prognostic system of AML, provides help for the selection of AML treatment options, and provides new ideas for future biologically targeted therapy of AML.