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Objective. The aim of the study is to explore the relationship between lymphatic metastasis genes, prognosis, and immune cell infiltration in patients with colon cancer. Methods. Based on the Cancer Genome Atlas Program (TCGA) database, differentially expressed genes and prognostic genes related to colon adenocarcinoma (COAD) lymphatic metastasis were screened and intersected. We used lasso and univariate Cox regression analysis to screen core genes and establish a preliminary prediction model. GO and KEGG enrichment analysis was used for lymphatic metastasis-related genes, and single GSEA was used for the final screening results. Finally, we evaluated the relationship between identified genes and immune cell infiltration. Results. A total of 1727 genes were differentially expressed between COAD patients with TNM stages of N0 and N1. After further screening, six core genes (RNU4-2, ZNF556, RNVU1-15, NSA2P6, RN7SL767P, and RN7SL473P) were obtained, and a preliminary prediction model was established, in which ZNF556 was a risk factor, and the rest were protective factors. Single GSEA showed that pathways such as systemic lupus erythematosus might play an important role in the initial lymphatic metastasis of COAD. GO and KEGG enrichment analysis of 1727 genes supported this result. Immune infiltration analysis showed that six genes were significantly correlated with T cell and NK cell families. Conclusion. Six core genes may affect COAD initial lymphatic metastasis through the systemic lupus erythematosus pathway and immune cell infiltration.

Clear cell renal cell carcinoma (ccRCC) is the most common histologic subtype of renal cell carcinoma and long non-coding RNAs (lncRNAs) play important roles in the progression of ccRCC. In this study, we aim to explore the potential function of ITGB2-AS1 in ccRCC progression and its underlying molecular mechanism. We first explored the association between ITGB2-AS1 expression level and ccRCC prognosis. We found that the expression level of ITGB2-AS1 was significantly higher in ccRCC tumor and cell lines, and highly expressed ITGB2-AS1 was also associated with a poorer prognosis. Consistently, silencing ITGB2-AS1 inhibited proliferation, promoted apoptosis in ccRCC cell lines, and curbed the tumorigenesis in the Xenograft model, reduced tumorigenesis in a xenograft tumor growth model. We further identified and confirmed the miRNA miR-328-5p as a target of ITGB2-AS1, and miR-328-5p negatively regulated the expression of HMGA1 protein. The anti-tumor effect of silencing ITGB2-AS1 could be partially rescued by inhibiting miR-328-5p activity or overexpressing HMGA1, indicating that ITGB2-AS1 promotes the survival and progression of ccRCC by modulating miR-328-5p/HMGA1 axis. Collectively, our data demonstrated that ITGB2-AS1 expression level is positively correlated with the survival and tumorigenesis of ccRCC. As a target of ITGB2-AS1, miR-328-5p seems to function as a tumor-suppressor, and the oncogenic effect of ITGB2-AS1 is partially mediated via the miR-328-5p/HMGA1 axis.

BACKGROUND: Gastric cancer is one of the most common gastrointestinal tumors. Evidence has pointed to the fact that miRNAs play critical roles in the occurrence, development, and metastasis of gastric cancer by regulating cell proliferation, differentiation, apoptosis, and invasion. METHODS: In this study, first the relationship of miR-873-5p level and tissues types/LN(+/-)/metastasis(+/-)/tumor size was analysis, respectively. Second, the CCK8 and Transwell assay was used to determine the proliferation, invasion and migration of GC cells transfected with overexpression-/low expression-miR-873-5p. Third, the cell viability were analysis in the GC cells transfected with overexpression-/low expression-miR-873-5p treatment with different chemotherapy drugs. Fourth, the target gene of miR-873-5p was predicted using bioinformation methods. Fifth, the relationship of miR-873-5p with target gene-THUMPD1 were explored by using Wb and luciferase activity assay, et al. RESULTS: We confirmed that miR-873-5p was negatively correlated with GC including tumor size, LN metastasis, distant metastasis. The miR-873-5p enhanced the sensitivity of Doxorubicin/Fluorouracil and cisplatin. The THUMPD1 was the target gene of miR-873-5p. Moreover, miR-873-5p could target the THUMPD1 axis so as to inhibit gastric cancer cell behavior as well as chemoresistance. CONCLUSIONS: MiR-873-5p plays a role in regulating cell behavior as well as regulating chemoresistance in gastric cancer. In addition, THUMPD1, as a downstream molecule of miR-873-5p, plays an important role in the cell behavior and chemoresistance of gastric cancer. The research first confirmed that miR-873-5p could inhibit gastric cancer cell behavior and chemoresistance by targeting the THUMPD1.

Background. Aglaia (Meliaceae) species are used for treating autoimmune disorders and allergic diseases in Asian countries. Rocaglamide, an extract obtained from Aglaia species, exhibits suppressive effect by regulating the T cell subset balance and cytokine network in cancer. However, whether it can be used in organ transplantation is unknown. In this study, we investigated the antirejection effect and mechanism of action of rocaglamide in a mouse cardiac allograft model. Methods. Survival studies were performed by administering mice with phosphate-buffered saline (PBS) ( n = 6 ) and rocaglamide ( n = 8 ). Heart grafts were monitored until they stopped beating. After grafting, the mice were sacrificed on day 7 for histological, mixed lymphocyte reaction (MLR), enzyme-linked immunosorbent assay (ELISA), and flow cytometric analyses. Results. Rocaglamide administration significantly prolonged the median survival of the grafts from 7 to 25 days compared with PBS treatment ( P < 0.001 ). On posttransplantation day 7, the rocaglamide-treated group showed a significant decrease in the percentage of Th1 cells ( 7.9 ± 0.9 % vs. 1.58 ± 0.5 % , P < 0.001 ) in the lymph nodes and spleen ( 8.0 ± 2.5 % vs. 2.4 ± 1.3 % , P < 0.05 ). Rocaglamide treatment also significantly inhibited the production of Th17 cells ( 6.4 ± 1.0 % vs. 1.8 ± 0.4 % , P < 0.01 ) in the lymph nodes and spleen ( 5.9 ± 0.3 % vs. 2.9 ± 0.8 % , P < 0.01 ). Furthermore, the prolonged survival of the grafts was associated with a significant decrease in IFN-γ and IL-17 levels. Our results also showed that NF-AT activation was inhibited by rocaglamide, which also induced p38 and Jun N-terminal kinase (JNK) phosphorylation in Jurkat T cells. Furthermore, by using inhibitors that suppressed p38 and JNK phosphorylation, rocaglamide-mediated reduction in NF-AT protein levels was prevented. Conclusion. We identified a new immunoregulatory property of rocaglamide, wherein it was found to regulate oxidative stress response and reduce inflammatory cell infiltration and organ injury, which have been associated with the inhibition of NF-AT activation in T cells.

Organ donation has been suspended for almost 3 months in Wuhan due to COVID‐19 outbreak. Donation and transplantation were performed on 8th April, the very day Wuhan lifted its lockdown. Two weeks after donation, COVID‐19 screenings of the liver recipient and medical staffs present negative.

Coronavirus disease 2019 (COVID-19) pandemic spreads rapidly and may be an increasing challenge for transplant community. Clinical data on COVID-19 infection in transplant population is very limited. Herein we presented the clinical course and outcome of a 50-year-old male post liver transplantation who contracted COVID-19, with subsequent infection of his wife. The process of illness was representative. A therapeutic regime with temporary immunosuppression withdrawal and systemic low-dose corticosteroid as principle was involved in the management of the patient which made him recover from severe COVID-19 pneumonia.

In December 2019, an outbreak of COVID-19 occurred in Wuhan, China, and spread to the whole of China and to multiple countries worldwide. Unlike SARS and MERS, where secondary transmission mostly occurred in hospital settings, COVID-19 transmission occurs in large numbers within families. Herein we report three cases of a familial cluster with one family member being a kidney transplant recipient. The initial clinical symptoms of COVID-19 in these three patients were the same, but their progression was different. Based on the severity of clinical symptoms, chest computer tomography findings and SARS-Cov-2 RNA test results, we admitted the husband to the respiratory intensive care unit (RICU) and used a treatment consisting of immunosuppressant reduction/cessation and low dose methylprednisolone-based therapy, and his wife to the respiratory isolation ward. In contrast, the son received in-home isolation and home-based care. All three family members made a full recovery.

HER2 mutations have emerged as oncogenic driver gene mutations in non-small cell lung cancer (NSCLC), which have not been described in detail like other driver gene mutations. Here, 295 patients with advanced lung adenocarcinoma were retrospectively screened for HER2 mutations using next-generation sequencing (NGS), and the positive cases were validated by Sanger sequencing. We identified five cases with HER2 exon 20 insertions, representing 1.7% of 295 lung adenocarcinomas. Among them, four different subtypes of HER2 exon 20 insertions were identified, including a rare subtype G778_S779insCPG never reported before with a partial response (PR) to pyrotinib and progression-free survival (PFS) of 12.8 months. Our findings reveal that HER2 exon 20 insertion mutations were detected in a small subset of lung adenocarcinomas. Given the different drug sensitivities, determining the mutation subtype by next-generation sequencing at the time of diagnosis might make sense.

Due to the severe shortage of the donor pool in China, a large number of patients are waiting for a suitable liver, or even worse lose the opportunity of transplantation. Reasonable use of hepatitis B surface antigen-positive (HBsAg-positive) donors is one possible strategy to increase the donor pool but the long-term outcome in a Chinese population is unknown. To evaluate the safety of using of HBsAg-positive donor for liver transplantation, we set up a multicentric retrospective study from 1 January 2007 to 31 December 2012. A total of 8632 patients underwent liver transplantation during the period and 282 (2.97%) received a liver from a HBsAg-positive donor. A total of 259 cases in both the case and control groups were matched. The incidence of postoperative liver dysfunction, early-stage and long-term complications and the 1-, 3- and 5-year patient survival (78.92% vs 85.65%, 60.41% vs 69.14%, 58.08% vs 69.14%, respectively) showed no difference between the two groups (P value > 0.05). However, the 1-, 3- and 5-year HBV recurrence for patients received the HBsAg-positive donor was higher compared with controls (5.85% vs 1.97%, 11.63% vs 4.46%, 17.94% vs 4.46%, respectively, P value = 0.016). Our results showed the use of HBsAg-positive donors is feasible and postoperative antiviral therapy should be managed.

Kidney tubular damage caused by ischemia-reperfusion injury is considered the major cause of delayed graft function (DGF) after renal transplantation. It is not clear whether early generated de novo donor specific antibodies (DSA) play a role in DGF. Here, we report 2 cases of renal transplant with DGF, which seems to be associated with de novo DSA. When the early produced de novo DSA are not potent enough to mediate acute rejection, they may cause mild intra-graft injury, which has a significant impact on the degree of DGF and its recovery. Antibody-targeted therapy seems to be beneficial to the recovery of patients with DGF.