Case report: Effective treatment of rituximab-resistant minimal change disease with obinutuzumab in an adult.

Background: Minimal change disease (MCD) is a common cause of adult nephrotic syndrome. Most adults with MCD achieve complete remission (CR) after initial steroid therapy. However, approximately 30% of adults who respond to steroids experience frequent relapses, becoming steroid-dependent and potentially developing refractory MCD. Treating refractory MCD in adults poses a significant challenge. Main body: A 37-year-old woman presented to the nephrology department with a 6-year history of MCD. The diagnosis of MCD was confirmed via renal biopsy. She initially achieved CR with steroid treatment but experienced relapse during steroid tapering. Subsequent CR was achieved with a regimen of steroids and tacrolimus although multiple relapses occurred. Rituximab led to another CR, but its maintenance lasted only 6 months. The response to subsequent rituximab treatments was unsatisfactory. Ultimately, obinutuzumab was selected, resulting in the induction and maintenance of CR for 12 months. Conclusions: This case demonstrates the successful treatment of frequently relapsed, steroid-dependent, and rituximab-resistant MCD with obinutuzumab. Obinutuzumab is a promising therapeutic option for rituximab-resistant MCD.

Anterior cervical corpectomy and fusion-derived adjacent segment disease managed via channel-repairing anterior endoscopic transcorporeal cervical discectomy: a case report.

BACKGROUND: Management of anterior cervical corpectomy and fusion (ACCF)-derived adjacent segment disease (ASD) represented a challenge facing the surgeons. METHODS: A 41-year man diagnosed as C3-4 level ASD derived from C5-level ACCF surgery 13 years ago was admitted to the hospital for numbness and pain in the right shoulder and upper limb. Percutaneous full-endoscopic anterior transcorporeal cervical discectomy (PEATCD) was performed, and pre- and postoperative clinical and imaging data were collected. RESULTS: The operation was completed within 70 min, and no clinical or radiological complication was reported. The visual analog scale (VAS) score decreased from preoperative 5 points to postoperative 1 point. Numbness was relieved postoperatively and disappeared completely at postoperative 3 months. Imaging data indicated sufficient spinal cord decompression, good channel repairing and cervical alignment. CONCLUSIONS: Channel-repairing PEATCD was successfully performed to treat ACCF-derived ASD, nevertheless, the long-term efficacy remained tracing and further clinical trials were needed to validate its efficacy.

Vascular reconstruction provides short-term and long-term survival benefits for patients with hilar cholangiocarcinoma: A retrospective, multicenter study.

BACKGROUND: In patients with hilar cholangiocarcinoma (HCCA), radical resection can be achieved by resection and reconstruction of the vasculature. However, whether vascular reconstruction (VR) improves long-term and short-term prognosis has not been demonstrated comprehensively. METHODS: This was a retrospective multicenter study of patients who received surgery for HCCA with or without VR. Variables associated with overall survival (OS) and recurrence-free survival (RFS) were identified based on Cox regression. Kaplan-Meier curves were used to explore the impact of VR. Restricted mean survival time (RMST) was used for comparisons of short-term survival between the groups. Patients' intraoperative and postoperative characteristics were compared. RESULTS: Totally 447 patients were enrolled. We divided these patients into 3 groups: VR with radical resections (n = 84); non-VR radical resections (n = 309) and non-radical resection (we pooled VR-nonradical and non-VR nonradical together, n = 54). Cox regression revealed that carbohydrate antigen 242 (CA242), vascular invasion, lymph node metastasis and poor differentiation were independent risk factors for OS and RFS. There was no significant difference of RMST between the VR and non-VR radical groups within 12 months after surgery (10.18 vs. 10.76 mon, P = 0.179), although the 5-year OS (P < 0.001) and RFS (P < 0.001) were worse in the VR radical group. The incidences of most complications were not significantly different, but those of bile leakage (P < 0.001) and postoperative infection (P = 0.009) were higher in the VR radical group than in the non-VR radical group. Additionally, the levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) up to 7 days after surgery tended to decrease in all groups. There was no significant difference in the incidence of postoperative liver failure between the VR and non-VR radical groups. CONCLUSIONS: Radical resection can be achieved with VR to improve the survival rate without worsening short-term survival compared with resection with non-VR. After adequate assessment of the patient's general condition, VR can be considered in the resection.

TRIP13 Activates Glycolysis to Promote Cell Stemness and Strengthen Doxorubicin Resistance of Colorectal Cancer Cells.

BACKGROUND: Chemotherapy resistance is one of the main causes of clinical chemotherapy failure. Current cancer research explores the drug resistance mechanism and new therapeutic targets. This work aims to elucidate the mechanism of thyroid hormone receptor interactor 13 (TRIP13) affecting doxorubicin (DOX) resistance in colorectal cancer (CRC). METHODS: Bioinformatics analyses were employed to clarify TRIP13 expression in CRC tissues and predict the correlation of the TRIP13 enrichment pathway with glycolysis-related genes and stemness index mRNAsi. Quantitative real-time polymerase chain reaction and western blot were adopted to analyze the expression of TRIP13 and glycolysis- related genes. Cell Counting Kit-8 was utilized to determine the cell viability and IC50 value. Western blot was employed to measure the expression of stemness-related factors. Cell function assays were performed to detect cells' sphere-forming ability and glycolysis level. Animal models were constructed to determine the effects of TRIP13 expression on CRC tumor growth. RESULTS: TRIP13 was significantly overexpressed in CRC, concentrated in the glycolysis signaling pathway, and positively correlated with stemness index mRNAsi. High expression of TRIP13 facilitated DOX resistance in CRC. Further mechanistic studies revealed that overexpression of TRIP13 could promote cell stemness through glycolysis, which was also confirmed in animal experiments. CONCLUSION: TRIP13 was highly expressed in CRC, which enhanced the DOX resistance of CRC cells by activating glycolysis to promote cell stemness. These findings offer new insights into the pathogenesis of DOX resistance in CRC and suggest that TRIP13 may be a new target for reversing DOX resistance in CRC.

Cleavage fragments of the C-terminal tail of polycystin-1 are regulated by oxidative stress and induce mitochondrial dysfunction.

Mutations in the gene encoding polycystin-1 (PC1) are the most common cause of autosomal dominant polycystic kidney disease (ADPKD). Cysts in ADPKD exhibit a Warburg-like metabolism characterized by dysfunctional mitochondria and aerobic glycolysis. PC1 is an integral membrane protein with a large extracellular domain, a short C-terminal cytoplasmic tail and shares structural and functional similarities with G protein-coupled receptors. Its exact function remains unclear. The C-terminal cytoplasmic tail of PC1 undergoes proteolytic cleavage, generating soluble fragments that are overexpressed in ADPKD kidneys. The regulation, localization, and function of these fragments is poorly understood. Here, we show that a ∼30 kDa cleavage fragment (PC1-p30), comprising the entire C-terminal tail, undergoes rapid proteasomal degradation by a mechanism involving the von Hippel-Lindau tumor suppressor protein. PC1-p30 is stabilized by reactive oxygen species, and the subcellular localization is regulated by reactive oxygen species in a dose-dependent manner. We found that a second, ∼15 kDa fragment (PC1-p15), is generated by caspase cleavage at a conserved site (Asp-4195) on the PC1 C-terminal tail. PC1-p15 is not subject to degradation and constitutively localizes to the mitochondrial matrix. Both cleavage fragments induce mitochondrial fragmentation, and PC1-p15 expression causes impaired fatty acid oxidation and increased lactate production, indicative of a Warburg-like phenotype. Endogenous PC1 tail fragments accumulate in renal cyst-lining cells in a mouse model of PKD. Collectively, these results identify novel mechanisms regarding the regulation and function of PC1 and suggest that C-terminal PC1 fragments may be involved in the mitochondrial and metabolic abnormalities observed in ADPKD.

Dimethyladenosine Transferase 1 Homolog Promotes Human Gastric Carcinoma Cell Proliferation and Inhibits Apoptosis via the AKT Pathway.

BACKGROUND/AIMS: Our previous work identified the dimethyladenosine transferase 1 homolog as a novel prognostic factor for detecting human gastric carcinoma with high sensitivity and specificity. The high expression of dimethyladenosine transferase 1 is closely associated with the occurrence and progression of gastric carcinoma. However, the underlying mechanism of dimethyladenosine transferase 1 for the occurrence and development of gastric carcinoma is not well elucidated yet. MATERIALS AND METHODS: In our present study, the biological role of dimethyladenosine transferase 1 on cell proliferation, apoptosis, and cell cycle progression in human gastric carcinoma cells was investigated through in vitro and in vivo assays by the overexpression and knockdown of dimethyladenosine transferase 1 2-way authentication method. RESULTS: We found that the overexpression of dimethyladenosine transferase 1 significantly promotes cell proliferation (P < .001) and inhibition of cell apoptosis (P < .01) in SGC-7901 cells. However, the in vivo experiment results of the knockdown dimethyladenosine transferase 1 using small interfering RNAs in the MKN-45 are just the opposite. Reverse-transcriptase polymerase chain reaction and western blotting analysis revealed that overexpressed dimethyladenosine transferase 1 in SGC-7901 cells significantly activated the AKT pathway compared to control cells. In contrast, we found that apoptosis genes such as Caspase-3 and Caspase-9 were downregulated in those cells. The xenograft nude mice model exhibited increased tumor growth (P < .01) and weight loss (P < .01), with the overexpression of dimethyladenosine transferase 1 homolog in the SGC-7901 cells. These results have been further confirmed through backward verification in dimethyladenosine transferase 1 knockdown cells. CONCLUSIONS: Taken together, our results indicated that the dimethyladenosine transferase 1 plays a crucial role in stimulating cancer cell proliferation and contributes to apoptosis resistance in human gastric carcinoma. Meanwhile, it provides a potential therapeutic target for gastric carcinoma treatment and is worthy of further studies.

The GLI2/CDH6 axis enhances migration, invasion and mitochondrial fission of stomach adenocarcinoma cells.

It has been reported that cadherin 6 (CDH6) upregulation is associated with enhanced epithelial-to-mesenchymal transition (EMT) in several types of solid tumor cells. The current study aimed to explore the effect of CDH6 on the migration and invasion of stomach adenocarcinoma (STAD) cells, the transcription factors involved in CDH6 dysregulation and their effect on mitochondrial fission. Bioinformatics analysis was performed using data extracted from the Genotype-Tissue Expression Project, the Cancer Genome Atlas and Kaplan-Meier plotter. AGS and HGC27 cells were used to establish an in vitro STAD cell model. The results showed that higher CDH6 expression was associated with significantly shorter overall survival in patients with STAD. In addition, CDH6 overexpression promoted wound healing, enhanced the invasion ability of tumor cells and increased mitochondrial fission. Glioma-associated oncogene family zinc finger 2 (GLI2) could bind to the CDH6 promoter and activate its transcription. Fluorescent labeling also showed that GLI2 overexpression promoted mitochondrial fission. However, CDH6 silencing significantly reduced mitochondrial fragmentation. Besides, GLI2 overexpression notably upregulated phosphorylated-focal adhesion kinase and dynamin-related protein 1. However, the above effects were largely abrogated by CDH6 knockdown. In conclusion, the present study suggested that the novel GLI2/CDH6 axis could enhance the migration, invasion and mitochondrial fission of STAD cells.

FOSL1 transcriptionally regulates PHLDA2 to promote 5-FU resistance in colon cancer cells.

BACKGROUND: Tumor drug resistance is a leading cause of tumor treatment failure. To date, the association between FOS-Like antigen-1 (FOSL1) and chemotherapy sensitivity in colon cancer is unclear. The present study investigated the molecular mechanism of FOSL1 regulating 5-Fluorouracil (5-FU) resistance in colon cancer. METHODS: FOSL1 expression in colon cancer was analyzed by bioinformatics methods, and its downstream regulatory factors were predicted. Pearson correlation analyzed the expression of FOSL1 and downstream regulatory gene. Meanwhile, the expression of FOSL1 and its downstream factor Pleckstrin Homology-Like Domain Family A Member 2 (PHLDA2) in colon cancer cell lines was measured by qRT-PCR and western blot. The regulatory relationship between FOSL1 and PHLDA2 was verified by chromatin immunoprecipitation (ChIP) assay and dual-luciferase reporter assay. The effects of the FOSL1/PHLDA2 axis on the resistance in colon cancer cells to 5-FU were analyzed by cell experiments. RESULTS: FOSL1 expression was evidently up-regulated in colon cancer and 5-FU resistant cells. FOSL1 was positively correlated with PHLDA2 in colon cancer. In vitro cell assays showed that low expression of FOSL1 significantly enhanced 5-FU sensitivity in colon cancer cells, significantly suppressed the proliferation of cancer cells, and induced apoptosis. Overexpression of FOSL1 presented the opposite regulatory trend. Mechanistically, FOSL1 activated PHLDA2 and up-regulated its expression. Moreover, by activating glycolysis, PHLDA2 promoted 5-Fu resistance and cell proliferation, and reduced cell apoptosis in colon cancer. CONCLUSION: Down-regulated FOSL1 expression could enhance the 5-FU sensitivity of colon cancer cells, and FOSL1/PHLDA2 axis may be an effective target for overcoming chemotherapy resistance in colon cancer.

Depletion of CUL4B in macrophages ameliorates diabetic kidney disease via miR-194-5p/ITGA9 axis.

Diabetic kidney disease (DKD) is the most prevalent chronic kidney disease. Macrophage infiltration in the kidney is critical for the progression of DKD. However, the underlying mechanism is far from clear. Cullin 4B (CUL4B) is the scaffold protein in CUL4B-RING E3 ligase complexes. Previous studies have shown that depletion of CUL4B in macrophages aggravates lipopolysaccharide-induced peritonitis and septic shock. In this study, using two mouse models for DKD, we demonstrate that myeloid deficiency of CUL4B alleviates diabetes-induced renal injury and fibrosis. In vivo and in vitro analyses reveal that loss of CUL4B suppresses migration, adhesion, and renal infiltration of macrophages. Mechanistically, we show that high glucose upregulates CUL4B in macrophages. CUL4B represses expression of miR-194-5p, which leads to elevated integrin α9 (ITGA9), promoting migration and adhesion. Our study suggests the CUL4B/miR-194-5p/ITGA9 axis as an important regulator for macrophage infiltration in diabetic kidneys.

Severe secondary hyperparathyroidism in a chronic kidney disease patient treated with Radiofrequency ablation: One case report.

End-stage renal disease (ESRD) is a global health problem with a high incidence (1) and a steadily increasing prevalence (2). Secondary hyperparathyroidism (SHPT) is a common and serious complication of chronic renal failure (CRF) in dialysis patients (3). It is mainly manifested as parathyroid hyperplasia caused by abnormal calcium and phosphorus metabolism and active vitamin D resistance, resulting in excessive secretion of parathyroid hormone (PTH), which leads to complications such as bone deformity, osteoarthralgia, pruritus, ectopic calcification, and cardiovascular calcification in CKD patients, significantly reducing the quality of life in CKD patients (4, 5). In patients with chronic kidney disease, secondary parathyroid gland hyperplasia needs to be treated as early as possible (6). Currently, there are a variety of treatment options, including vitamin D receptor agonists, xenacax hydrochloride, parathyroidectomy and ablation techniques, etc. (7, 8). Medical treatment is the main choice among these treatments, but it is invalid in patients with severe hyperparathyroidism. So, parathyroidectomy is suggested to do in those patients (9). However, many dialysis patients who have severe cardiopulmonary dysfunction cannot tolerate the trauma caused by surgery as the concept of minimally invasive surgery has been gradually introduced into all fields of surgery and medical treatment. Traditional surgery is no longer the only option. Radiofrequency ablation has been widely applied due to its advantages of less trauma, simple operation, and good repeatability. It has been reported to achieve good effects in treating secondary hyperparathyroidism patients (8). This case reports that one severe secondary hyperparathyroidism patient gets good therapeutic results from parathyroid radiofrequency ablation.

Cell-cell communication inference and analysis in the tumour microenvironments from single-cell transcriptomics: data resources and computational strategies.

Carcinomas are complex ecosystems composed of cancer, stromal and immune cells. Communication between these cells and their microenvironments induces cancer progression and causes therapy resistance. In order to improve the treatment of cancers, it is essential to quantify crosstalk between and within various cell types in a tumour microenvironment. Focusing on the coordinated expression patterns of ligands and cognate receptors, cell-cell communication can be inferred through ligand-receptor interactions (LRIs). In this manuscript, we carry out the following work: (i) introduce pipeline for ligand-receptor-mediated intercellular communication estimation from single-cell transcriptomics and list a few available LRI-related databases and visualization tools; (ii) demonstrate seven classical intercellular communication scoring strategies, highlight four types of representative intercellular communication inference methods, including network-based approaches, machine learning-based approaches, spatial information-based approaches and other approaches; (iii) summarize the evaluation and validation avenues for intercellular communication inference and analyze the advantages and limitations for the above four types of cell-cell communication methods; (iv) comment several major challenges while provide further research directions for intercellular communication analysis in the tumour microenvironments. We anticipate that this work helps to better understand intercellular crosstalk and to further develop powerful cell-cell communication estimation tools for tumor-targeted therapy.

Corrigendum to "SOX4 contributions to TGF-ß-induced endothelial-mesenchymal transition and stem cell characteristics of gastric cancer cells" [Genes & Diseases 5 (2018) 49-61].

[This corrects the article DOI: 10.1016/j.gendis.2017.12.005.].

Wogonin Induces Apoptosis and Reverses Sunitinib Resistance of Renal Cell Carcinoma Cells via Inhibiting CDK4-RB Pathway.

Wogonin, an active component derived from Scutellaria baicalensis, has shown anti-tumor activities in several malignancies. However, the roles of wogonin in RCC cells remain elusive. Here, we explored the effects of wogonin on RCC cells and the underlying mechanisms. We found that wogonin showed significant cytotoxic effects against RCC cell lines 786-O and OS-RC-2, with much lower cytotoxic effects on human normal embryonic kidney cell line HEK-293 cells. Wogonin treatment dramatically inhibited the proliferation, migration, and invasion of RCC cells. We further showed that by inhibiting CDK4-RB pathway, wogonin transcriptionally down-regulated CDC6, disturbed DNA replication, induced DNA damage and apoptosis in RCC cells. Moreover, we found that the levels of p-RB, CDK4, and Cyclin D1 were up-regulated in sunitinib resistant 786-O, OS-RC-2, and TK-10 cells, and inhibition of CDK4 by palbociclib or wogonin effectively reversed the sunitinib resistance, indicating that the hyperactivation of CDK4-RB pathway may at least partially contribute to the resistance of RCC to sunitinib. Together, our findings demonstrate that wogonin could induce apoptosis and reverse sunitinib resistance of RCC cells via inhibiting CDK4-RB pathway, thus suggesting a potential therapeutic implication in the future management of RCC patients.

Probing antiviral drugs against SARS-CoV-2 through virus-drug association prediction based on the KATZ method.

It is urgent to find an effective antiviral drug against SARS-CoV-2. In this study, 96 virus-drug associations (VDAs) from 12 viruses including SARS-CoV-2 and similar viruses and 78 small molecules are selected. Complete genomic sequence similarity of viruses and chemical structure similarity of drugs are then computed. A KATZ-based VDA prediction method (VDA-KATZ) is developed to infer possible drugs associated with SARS-CoV-2. VDA-KATZ obtained the best AUCs of 0.8803 when the walking length is 2. The predicted top 3 antiviral drugs against SARS-CoV-2 are remdesivir, oseltamivir, and zanamivir. Molecular docking is conducted between the predicted top 10 drugs and the virus spike protein/human ACE2. The results showed that the above 3 chemical agents have higher molecular binding energies with ACE2. For the first time, we found that zidovudine may be effective clues of treatment of COVID-19. We hope that our predicted drugs could help to prevent the spreading of COVID.

The CUL4B-miR-372/373-PIK3CA-AKT axis regulates metastasis in bladder cancer.

CUL4B, which acts as a scaffold protein in CUL4B-RING ubiquitin ligase (CRL4B) complexes, participates in a variety of biological processes. Previous studies have shown that CUL4B is often overexpressed and exhibits oncogenic activities in a variety of solid tumors. However, the roles and the underlying mechanisms of CUL4B in bladder cancer (BC) were poorly understood. Here, we showed that CUL4B levels were overexpressed and positively correlated with the malignancy of BC, and CUL4B could confer BC cells increased motility, invasiveness, stemness, and chemoresistance. The PIK3CA/AKT pathway was identified as a critical downstream mediator of CUL4B-driven oncogenicity in BC cells. Furthermore, we demonstrated that CRL4B epigenetically repressed the transcription of miR-372/373, via catalyzing monoubiquitination of H2AK119 at the gene cluster encoding miR-372/373, leading to upregulation of PIK3CA and activation of AKT. Our findings thus establish a critical role for the CUL4B-miR-372/373-PIK3CA/AKT axis in the pathogenesis of BC and have important prognostic and therapeutic implications in BC.

Compound Mutations of the COL4A3 including a Novel Allele Identified in a Patient with Alport Syndrome.

Alport syndrome (AS) is a hereditary nephropathy which is characterized by molecular abnormalities in collagen IV. Here, we report compound mutations of the COL4A3 gene including a novel allele identified in a patient with Alport syndrome. The patient was a 25-year-old Chinese woman. She has a history of proteinuria and hematuria with cleft lip and palate. The pathologic results were consistent with Alport syndrome. The patient received ACEI treatment but did not respond well to the treatment. Sequencing results revealed that the patient carried two heterozygous mutations in the COL4A3 gene, including a known mutation (c.4243G>C, p.G1415R), which was inherited from her father, and a previously undescribed allele (c.4216G>A, p.G1406R) inherited from her mother. To date, at least 294 different variants of COL4A3 have been reported according to the Human Gene Mutation Database (HGMD). Identification of c.4216G>A as a new AS-related mutation may contribute to both genetic diagnosis of AS and further functional study of COL4A3.

Generative Adversarial Networks-Based Semi-Supervised Automatic Modulation Recognition for Cognitive Radio Networks.

With the recently explosive growth of deep learning, automatic modulation recognition has undergone rapid development. Most of the newly proposed methods are dependent on large numbers of labeled samples. We are committed to using fewer labeled samples to perform automatic modulation recognition in the cognitive radio domain. Here, a semi-supervised learning method based on adversarial training is proposed which is called signal classifier generative adversarial network. Most of the prior methods based on this technology involve computer vision applications. However, we improve the existing network structure of a generative adversarial network by adding the encoder network and a signal spatial transform module, allowing our framework to address radio signal processing tasks more efficiently. These two technical improvements effectively avoid nonconvergence and mode collapse problems caused by the complexity of the radio signals. The results of simulations show that compared with well-known deep learning methods, our method improves the classification accuracy on a synthetic radio frequency dataset by 0.1% to 12%. In addition, we verify the advantages of our method in a semi-supervised scenario and obtain a significant increase in accuracy compared with traditional semi-supervised learning methods.

Emphysematous pyelonephritis and cystitis in a patient with uremia and anuria: A case report and literature review.

INTRODUCTION: Emphysematous pyelonephritis (EPN) or cystitis (EC) is a severe infection of the urinary tract with high mortality. EPN is uncommon among the patients of end stage of renal failure (ESRD) CASE PRESENTATION:: A 38-year-old male with uremia and anuria who was on hemodialysis was found to have gas formation in the bilateral pelvis, ureters, and urinary bladder by CT scan. The diagnosis was emphysematous pyelonephritis and cystitis. And Foley catheter was placed and bladder irrigation was performed. Escherichia coli infection was identified in urine culture and antibiotic was prescribed accordingly. Gas disappeared completely and the patient recovered uneventfully. CONCLUSION: This is the first case report of asymptomatic EPN and EC in uremic patient, and conservative management was optimistic in this condition. More attention should be paid to EPN and EC happening to ESRD patients.

SOX4 contributes to TGF-ß-induced epithelial-mesenchymal transition and stem cell characteristics of gastric cancer cells.

SOX4 is highly expressed in gastric cancer (GC) and is associated with tumor grade, metastasis and prognosis, however the mechanism is not clear. We report herein that SOX4 was upregulated and overexpression of SOX4 was associated with increased expression of the markers of Epithelial-mesenchymal transition (EMT) and stemness in clinic patient samples. In vitro, overexpression of SOX4 promoted the invasion as showed by Transwell assay and stemness of GC cells as assessed by sphere formation assay, which was suppressed by silencing SOX4 with shRNA. Further studies showed that SOX4 up-regulated the expression of EMT transcription factors Twist1, snail1 and zeb1 and stemness transcription factors SOX2 and OCT4, and promoted the nuclear translocation of ß-catenin. Moreover, we revealed that TGF-ß treatment significantly up-regulated the expression of SOX4 and silencing SOX4 reversed TGF-ß induced invasion and sphere formation ability of GC cells. Finally, we showed that SOX4 promoted the lung metastasis and tumor formation ability of gastric cancer cells in nude mice. Our results suggest that SOX4 is a target TGF-ß signaling and mediates TGF-ß-induced EMT and stem cell characteristics of GC cells, revealing a novel role of TGF-ß/SOX4 axis in the regulation of malignant behavior of GC.

Left ventricular lipoma resected using thoracoscope-assisted limited sternotomy: A case report and literature review.

RATIONALE: A cardiac lipoma is an uncommon primary tumor, with a reported incidence ranging from 2.9% to 8% among all benign cardiac tumors. Although the prognosis in most asymptomatic cases is good during longterm follow-up, some reports have shown that untreated cardiac lipomas may be fatal when they cause arrhythmic or obstructive symptoms. PATIENT CONCERNS: We present a rare case of left ventricular (LV) lipoma. The mass measured 25 mm 10 mm, with a pedicle on the LV posterior wall near the apex. DIAGNOSES: The patient was diagnosed as left ventricular lipoma using echocardiography. INTERVENTIONS: The LV lipoma was resected using thoracoscopy-assisted limited sternotomy. OUTCOMES: Histopathologic examination was consistent with lipoma. No signs of recurrence were detected on an echocardiogram during a 3-month follow-up period. LESSONS: We performed a comprehensive review of relevant literature and summarized the known 21 cases from 1980 to 2017. LV lipoma may present with or without symptoms, and endoscopic resection may be a good alternative to open surgery.