The disappearance of gastric metastasis and liver metastasis in non-small cell lung adenocarcinoma is due to osimertinib.

PURPOSE: Gastric metastasis of lung cancer is rare, and the cases of disappearance of gastric metastasis and liver metastasis caused by oxitinib treatment have not been reported. METHODS: A 47-year-old male patient with no history of diabetes, hypertension or smoking presented with chest discomfort after eating. At the time of consultation, the diagnosis of adenocarcinoma of the right lower lobe of the lung with liver and gastric metastasis was considered by pathological examination of biopsy of the fundus of the stomach near the cardia, pathological examination of CT-guided lung aspiration and pathological examination of liver occupancy aspiration, combined with immunohistochemical results. He was found to have exon 19 deletion in next generation sequencing. We performed osimertinib on him (EGFR-TKI) systemic therapy, followed by local radiation therapy to the right lower lung primary lesion. RESULTS: After systemic treatment with osimertinib and local radiotherapy of the primary site, the metastases disappeared and the primary site showed post-radiotherapy changes, and the evaluated efficacy was complete remission. CONCLUSIONS: This is the first report to our knowledge of a patient who presented with gastric and hepatic metastases from lung cancer and achieved complete remission with osimertinib and local radiotherapy, with good quality of life, which also provides a basis for future clinical work and is of great significance.

Efficacy of anti-programmed cell death protein 1 monoclonal antibody combined with bevacizumab and/or Pseudomonas aeruginosa injection in transplanted tumor of mouse forestomach carcinoma cell gastric cancer in mice and its mechanism in regulating tumor immune microenvironment.

Tumor immunotherapy represented by programmed cell death protein 1 (PD-1) inhibitors is considered as the most promising cancer treatment method and has been widely used in the treatment of advanced gastric cancer (GC). However, the effective rate of PD-1 inhibitor monotherapy is low. In this study, we constructed a transplanted tumor model in GC mice by inoculating mouse forestomach carcinoma cell (MFC) GC cells into 615 mice. Interventions were conducted with normal saline, anti-PD-1 monoclonal antibody (mAb), bevacizumab, Pseudomonas aeruginosa-mannose-sensitive hemagglutinin (PA-MSHA), anti-PD-1 mAb combined with bevacizumab, anti-PD-1 mAb combined with PA-MSHA, bevacizumab combined with PA-MSHA, anti-PD-1 mAb combined with bevacizumab and PA-MSHA, respectively. The tumor growth curves were drawn. TUNEL assay, western blotting, and immunohistochemistry were used to detect tumor proliferation and apoptosis. Flow cytometry and ELISA were used to detect the expression of tumor infiltrating lymphocytes and cytokines. This study found that anti-PD-1 mAb alone could not significantly inhibit the growth of transplanted tumors in mice. Anti-PD-1 mAb combined with bevacizumab, anti-PD-1 mAb combined with PA-MSHA, anti-PD-1 mAb combined with bevacizumab and PA-MSHA could all significantly inhibit tumor growth in mice, and the combination of three drugs presented the highest tumor inhibition rate. Anti-PD-1 mAb combined with bevacizumab and PA-MSHA could significantly upregulate the number of Th1-type cells, CD8 + T cells, and Type I tumor-associated macrophages (TAMs), while downregulate the number of Th2-type cells, myeloid-derived suppressor cells, regulatory T cells, and Type II TAMs. Therefore, we conclude that anti-PD-1 mAb combined with bevacizumab and/or PA-MSHA has a synergistic effect. Bevacizumab and PA-MSHA can transform the tumor immunosuppressive microenvironment into a supportive immune microenvironment, thus maximizing the antitumor effect of anti-PD-1 mAb.

circPDSS1 Stimulates the Development of Colorectal Cancer via Activating the Wnt/ß-Catenin Signaling.

OBJECTIVE: This study aims to illustrate the role of circPDSS1 and the Wnt/ß-catenin signaling in the development of colorectal cancer (CRC). PATIENTS AND METHODS: Cancerous mucosa and normal paracancerous mucosa tissues more than 5 cm away from the tumor were surgically collected from 56 CRC patients. circPDSS1 levels in collected tissues and CRC cell lines were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The influence of circPDSS1 on clinical features of CRC patients was analyzed. After knockdown of circPDSS1 in HCT-8 and HCT-116 cells, phenotype changes were examined by Transwell, tube formation and wound healing assay. Western blot and rescue experiments were finally performed to uncover the role of circPDSS1 and the Wnt/ß-catenin signaling in the development of CRC. RESULTS: circPDSS1 was upregulated in CRC mucosa tissues than controls. High level of circPDSS1 predicted high rates of lymphatic metastasis and distant metastasis, and poor prognosis in CRC patients. Knockdown of circPDSS1 attenuated migratory ability and angiogenesis in CRC cells. Protein levels of key genes in the Wnt/ß-catenin signaling, including ß-catenin, GSK-3ß, c-Myc, MMP-9 and cyclin D1 were downregulated in CRC cells transfected with sh-circPDSS1. Overexpression of ß-catenin reversed the role of circPDSS1 in attenuating migratory ability and angiogenesis in CRC cells. CONCLUSION: Upregulated circPDSS1 in CRC is closely linked to lymphatic metastasis, distant metastasis and overall survival. It stimulates the migratory ability and angiogenesis in CRC cells via activating the Wnt/ß-catenin signaling.

Up-regulation of SALL4 associated with poor prognosis in gastric cancer. .

BACKGROUND/AIMS: SALL4 [encoding the Sal-Like 4 (Drosophila) protein, also known as spalt-like transcription factor 4] plays crucial roles in the development of different cancers, as well as vital embryogenic roles. However, knowledge of its relationship to gastric cancer is limited, and its association with prognosis in gastric cancer has not yet been reported. METHODOLOGY: comprehensive bioinformatics analyses including mRNA expression, gene occurrence, protein/gene interaction, pathway enrichment and biological processes annotation were performed. RESULTS: we indicated that the expression of SALL4 was up-regulated at least 2.2-fold in 103 cases of gastric cancers, compared with its expression in 65 normal controls. Further analysis indicated that SALL4 was co-occurred and interacted with 23 proteins/genes which all were associated with a poor gastric cancer prognosis. It also associated with 14 biological processes and Wnt signaling pathway, which have been proven to be closely related to gastric cancer and its prognosis. CONCLUSIONS: for the first time, we have shown that the up-regulation of SALL4 in gastric cancers should serve as a worthwhile biological marker of poor prognosis in gastric cancer therapies, via the strong interactions with a number of proteins, genes, biological processes and pathways which all were associated with poor prognosis in gastric and other cancer.