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Numerous papers have been published on the microbiota in lung cancer in recent years. However, there is still a lack of bibliometric analysis of the microbiota in lung cancer in this field. Our paper did bibliometric analyses and elucidated the knowledge structure and study hotspots related to the microbiota in lung cancer patients. We screened publications reporting on the microbiota in lung cancer from 2008 to 2023 from the Web of Science Core Collection (WoSCC) database, and carried out bibliometric analyses by the application of the VOSviewers, CiteSpace and R package “bibliometrix.” The 684 documents enrolled in the analysis were obtained from 331 institutions in 67 regions by 4,661 authors and were recorded in 340 journals. Annual papers are growing rapidly, and the countries of China, the United States and Italy are contributing the most to this area of research. Zhejiang University is the main research organization. Science and Cancer had significant impacts on this area. Zhang Yan had the most articles, and the Bertrand Routy had the most co-cited times. Exploring the mechanism of action of the lung and/or gut microbiota in lung cancer and therapeutic strategies involving immune checkpoint inhibitors in lung cancer are the main topics. Moreover, “gut microbiota,” “immunotherapy,” and “short-chain fatty acids” are important keywords for upcoming study hotspots. In conclusion, microbiota research offers promising opportunities in lung cancer, with pivotal studies exploring the mechanisms that link lung and gut microbiota to therapeutic strategies, particularly through immune checkpoint inhibitors. Moreover, the gut-lung axis emerges as a novel target for innovative treatments. Further research is essential to unravel the detailed mechanisms of this connection.

Organoids, characterized by their high physiological attributes, effectively preserve the genetic characteristics, physiological structure, and function of the simulated organs. Since the inception of small intestine organoids, other organoids for organs including the liver, lungs, stomach, and pancreas have subsequently been developed. However, a comprehensive summary and discussion of research findings on gastrointestinal tract (GIT) organoids as disease models and drug screening platforms is currently lacking. Herein, in this review, we address diseases related to GIT organoid simulation and highlight the notable advancements that have been made in drug screening and pharmacokinetics, as well as in disease research and treatment using GIT organoids. Organoids of GIT diseases, including inflammatory bowel disease, irritable bowel syndrome, necrotizing enterocolitis, and Helicobacter pylori infection, have been successfully constructed. These models have facilitated the study of the mechanisms and effects of various drugs, such as metformin, Schisandrin C, and prednisolone, in these diseases. Furthermore, GIT organoids have been used to investigate viruses that elicit GIT reactions, including Norovirus, SARS-CoV-2, and rotavirus. Previous studies by using GIT organoids have shown that dasabuvir, gemcitabine, and imatinib possess the capability to inhibit viral replication. Notably, GIT organoids can mimic GIT responses to therapeutic drugs at the onset of disease. The GIT toxicities of compounds like gefitinib, doxorubicin, and sunset yellow have also been evaluated. Additionally, these organoids are instrumental for the study of immune regulation, post-radiation intestinal epithelial repair, treatment for cystic fibrosis and diabetes, the development of novel drug delivery systems, and research into the GIT microbiome. The recent use of conditioned media as a culture method for replacing recombinant hepatocyte growth factor has significantly reduced the cost associated with human GIT organoid culture. This advancement paves the way for large-scale culture and compound screening of GIT organoids. Despite the ongoing challenges in GIT organoid development (e.g., their inability to exist in pairs, limited cell types, and singular drug exposure mode), these organoids hold considerable potential for drug screening. The use of GIT organoids in this context holds great promises to enhance the precision of medical treatments for patients living with GIT diseases.

Abstract The SARS-CoV-2 virus, belonging to the Coronavirus genus, which poses a threat to human health worldwide. Current therapies focus on inhibiting viral replication or using anti-inflammatory/immunomodulatory compounds to enhance host immunity. This makes the active ingredients of traditional Chinese medicine compounds ideal therapies due to their proven safety and minimal toxicity. Previous research suggests that andrographolide and baicalin inhibit coronaviruses; however, their synergistic effects remain unclear. Here, we studied the antiviral mechanisms of their synergistic use in vitro and in vivo. We selected the SARS-CoV-2 pseudovirus for viral studies and found that synergistic andrographolide and baicalein significantly reduced angiotensin-converting enzyme 2 protein level and viral entry of SARS-CoV-2 into cells compared to singal compound individually and inhibited the major protease activity of SARS-CoV-2. This mechanism is essential to reduce the pathogenesis of SARS-CoV-2. In addition, their synergistic use in vivo also inhibited the elevation of pro-inflammatory cytokines, including IL-6 and TNF-α—the primary cytokines in the development of acute respiratory distress syndrome (the main cause of COVID-19 deaths). In conclusion, this study shows that synergistic andrographolide and baicalein treatment acts as potent inhibitors of coronavirus mechanisms in vitro and in vivo—and is more effective together than in isolation.

Abstract Background The incidence and mortality of gastric cancer (GC) are high worldwide. Tumor stemness is a major contributor to tumorigenesis and development of GC, in which long non-coding RNAs (lncRNAs) are deeply involved. The purpose of this study was to investigate the influences and mechanisms of LINC00853 in the progression and stemness of GC. Methods The level of LINC00853 was assessed based on The Cancer Genome Atlas (TCGA) database and GC cell lines by RT-PCR and in situ hybridization. An evaluation of biological functions of LINC00853 including cell proliferation, migration, and tumor stemness was conducted via gain-and loss-of-function experiments. Furthermore, RNA pull-down and RNA immunoprecipitation (RIP) assay were utilized to validate the connection between LINC00853 and the transcription factor Forkhead Box P3 (FOXP3). Nude mouse xenograft model was used to identify the impacts of LINC00853 on tumor development. Results We identified the up-regulated levels of lncRNA-LINC00853 in GC, and its overexpression correlates with poor prognosis in GC patients. Further study indicated that LINC00853 promoted cell proliferation, migration and cancer stemness while suppressed cell apoptosis. Mechanistically, LINC00853 directly bind to FOXP3 and promoted FOXP3-mediated transcription of PDZK1 interacting protein 1(PDZK1IP1). Alterations of FOXP3 or PDZK1IP1 reversed the LINC00853-induced biological effects on cell proliferation, migration and stemness. Moreover, xenograft tumor assay was used to investigate the function of LINC00853 in vivo. Conclusions Taken together, these findings revealed the tumor-promoting activity of LINC00853 in GC, expanding our understanding of lncRNAs regulation on GC pathogenesis.

Colorectal cancer (CRC) is a globally prevalent malignancy with a high potential for metastasis. Existing cancer treatments have limitations, including drug resistance and adverse effects. Researchers are striving to develop effective therapies to address these challenges. Impressively, contemporary research has discovered that many natural products derived from foods, plants, insects, and marine invertebrates can suppress the progression, metastasis, and invasion of CRC. In this review, we conducted a comprehensive search of the CNKI, PubMed, Embase, and Web of Science databases from inception to April 2023 to evaluate the efficacy of natural products targeting mitochondria to fight against CRC. Mitochondria are intracellular energy factories involved in cell differentiation, signal transduction, cell cycle regulation, apoptosis, and tumorigenesis. The identified natural products have been classified and summarized based on their mechanisms of action. These findings indicate that natural products can induce apoptosis in colorectal cancer cells by inhibiting the mitochondrial respiratory chain, ROS elevation, disruption of mitochondrial membrane potential, the release of pro-apoptotic factors, modulation of the Bcl-2 protein family to facilitate cytochrome c release, induction of apoptotic vesicle activity by activating the caspase protein family, and selective targeting of mitochondrial division. Furthermore, diverse apoptotic signaling pathways targeting mitochondria, such as the MAPK, p53, STAT3, JNK and AKT pathway, have been triggered by natural products. Natural products such as diosgenin, allopurinol, and clausenidin have demonstrated low toxicity, high efficacy, and multi-targeted properties. Mitochondria-targeting natural products have great potential for overcoming the challenges of CRC therapy.

Abstract Background Combining antiangiogenic therapy with radioimmunotherapy is believed to further improve antitumor efficacy, but there is still a lack of evidence to support this. This study aimed to investigate the role of the tumor vascular‐targeted agent famitinib with a combination of radiotherapy and an immune checkpoint inhibitor in murine lung cancer. Methods The effect of VEGFA and HIF1A on clinical prognosis and the tumor immune microenvironment was analyzed using public databases. Enrichment analyses of post‐irradiation gene expression and mRNAs related to immunotherapy efficacy were carried out based on GEO datasets. A C57BL/6 mouse subcutaneous tumor model was used to evaluate the antitumor effects of different treatment schemes. The tumor immunophenotyping was identified by flow cytometry. Results We demonstrated that high level of VEGFA and HIF1A expression in lung cancer was related to poor prognosis and immunosuppressive tumor microenvironment. In a mouse model, the triple therapy of famitinib, radiotherapy and immunotherapy had the most dramatic antitumor activity. It significantly increased tumor infiltrating lymphocytes and reversed the immunosuppressive state of the tumor microenvironment in mice. Compared with radioimmunotherapy, the addition of famitinib further promoted the infiltration of CD8+ T cells and M1 type tumor associated macrophages, and reduced the number of myeloid suppressor cells. Therefore, triple therapy converted the immunosuppressive tumor microenvironment into an immunostimulatory one. Conclusion Famitinib can synergize with radioimmunotherapy by regulating the tumor immune microenvironment in murine lung cancer.

BackgroundThe severe acute abdomen associated with Henoch-Schonlein purpura (HSP) is an acute intussusception (AI). There is no reliable specific marker for AI with abdominal-type HSP. The serum total bile acid (TBA) level is a new prognostic marker associated with the severity of intestinal inflammation. The purpose of this study was to identify the prognostic value of serum TBA levels for the diagnosis of AI in children with abdominal-type HSP.MethodsA retrospective study of 708 patients with abdominal-type HSP was conducted, with demographic data, clinical symptoms, hepatic function index, immune function markers, and clinical outcomes assessed. Patients were divided into two groups: HSP (613 patients) and HSP with AI (95 patients). The data were analysed using SPSS 22.0.ResultsOf the 708 patients, the serum TBA levels were higher in the HSP with AI group than in the HSP group (P 3 μmol/L for predicting AI in children with abdominal-type HSP. In this group of HSP patients with AI, a serum TBA level ≥6.98 μmol/L was significantly associated with an increased incidence of operative treatment (51.85% vs. 75.61%, P = 0.0181), intestinal necrosis (9.26% vs. 29.27%, P = 0.0117), and length of hospital stay [15.76 ± 5.31 vs. 10.98 ± 2.83 (days), P

Abstract Background For patients with ypN2 non‐small cell lung cancer (NSCLC) after neoadjuvant chemotherapy followed by surgery (NCS), the role of postoperative radiotherapy (PORT) is unclear. The aim of our study was to evaluate the effect of PORT on survival of ypN2 NSCLC patients after NCS. Methods Between 2004 and 2015, patients with ypN2 NSCLC after NCS were filtrated from the Surveillance, Epidemiology, and End Results (SEER) database. Propensity score matching (PSM) was used to balance the baseline characteristics of the PORT and non‐PORT groups. Kaplan–Meier method and Cox proportional hazards models were adopted to estimate overall survival (OS) and cancer‐specific survival (CSS). Results A total of 257 patients who met the criteria were included in the study. After PSM, 115 patients remained in each group. The survival of patients in the PORT group was significantly better than those in the non‐PORT group. Median OS was 36 months vs. 26 months, and 5‐year OS rate was 40.5% vs. 21.0% (p = 0.002). The median CSS was 38 months vs. 27 months, and the 5‐year CSS rate was 43.7% vs. 22.1% (p 3. Conclusions For patients with ypN2 NSCLC after NCS, PORT significantly improves OS and CSS. These results need to be confirmed by further randomized studies.

Cancer stem cells (CSCs) are the core factors leading to recurrence, insensitivity to radiotherapy and chemotherapy, and immunotherapy resistance in patients with colorectal cancer. AT7867, a potent oral AKT inhibitor, was found to have antitumor activity in colorectal cancer; however, the effect on colorectal cancer stem cells is still unclear. This study was conducted to clarify the molecular mechanism underlying the CSC growth inhibitory effects of AT7867. We cultured colorectal cancer cells (CRCs) in a serum-free medium and enriched colorectal cancer stem cells. Subsequently, the effects of AT7867 on CSCs were analyzed by CCK-8, colony formation, flow cytometry, and immunofluorescence assays. The results indicated that AT7867 induces G2/M phase arrest and cell apoptosis in cancer stem cells. Subsequently, we identified Ascl2 as the main gene affecting the stemness of colorectal cancer in AT7867 by RNA sequencing. The current study showed that Ascl2 is involved in the metastasis, invasion, and proliferation of CRCs. The next experiments demonstrated that overexpression of Ascl2 did affect the therapeutic effect of AT7867 on CRC stemness. Furthermore, compared with other Akt inhibitors, AT7867 could promote the differentiation of colorectal cancer stem cells. Thus, AT7867 might be a potential antitumor drug candidate to treat CRC by targeting CSCs.

Gastric cancer, a common malignant disease, seriously endangers human health and life. The high mortality rate due to gastric cancer can be attributed to a lack of effective therapeutic drugs. Cancer cells utilize the glycolytic pathway to produce energy even under aerobic conditions, commonly referred to as the Warburg effect, which is a characteristic of gastric cancer. The identification of new targets based on the glycolytic pathway for the treatment of gastric cancer is a viable option, and accumulating evidence has shown that phytochemicals have extensive anti-glycolytic properties. We reviewed the effects and mechanisms of action of phytochemicals on aerobic glycolysis in gastric cancer cells. Phytochemicals can effectively inhibit aerobic glycolysis in gastric cancer cells, suppress cell proliferation and migration, and promote apoptosis, via the PI3K/Akt, c-Myc, p53, and other signaling pathways. These pathways affect the expressions of HIF-1α, HK2, LDH, and other glycolysis-related proteins. This review further assesses the potential of using plant-derived compounds for the treatment of gastric cancer and sheds insight into the development of new drugs.

The etiology of radiation-induced pulmonary fibrosis is not clearly understood yet, and effective interventions are still lacking. This study aimed to identify genes responsive to irradiation and compare the genome expression between the normal lung tissues and irradiated ones, using a radiation-induced pulmonary fibrosis mouse model. We also aimed to map the mRNA alterations as a predictive model and a potential mode of intervention for radiation-induced pulmonary fibrosis. Thirty C57BL/6 mice were exposed to a single dose of 16 Gy or 20 Gy thoracic irradiation, to establish a mouse model of radiation-induced pulmonary fibrosis. Lung tissues were harvested at 3 and 6 months after irradiation, for histological identification. Global gene expression in lung tissues was assessed by RNA sequencing. Differentially expressed genes were identified and subjected to functional and pathway enrichment analysis. Immune cell infiltration was evaluated using the CIBERSORT software. Three months after irradiation, 317 mRNAs were upregulated and 254 mRNAs were downregulated significantly in the low-dose irradiation (16 Gy) group. In total, 203 mRNAs were upregulated and 149 were downregulated significantly in the high-dose irradiation (20 Gy) group. Six months after radiation, 651 mRNAs were upregulated and 131 were downregulated significantly in the low-dose irradiation group. A total of 106 mRNAs were upregulated and 4 downregulated significantly in the high-dose irradiation group. Several functions and pathways, including angiogenesis, epithelial cell proliferation, extracellular matrix, complement and coagulation cascades, cellular senescence, myeloid leukocyte activation, regulation of lymphocyte activation, mononuclear cell proliferation, immunoglobulin binding, and the TNF, NOD-like receptor, and HIF-1 signaling pathways were significantly enriched in the irradiation groups, based on the differentially expressed genes. Irradiation-responsive genes were identified. The differentially expressed genes were mainly associated with cellular metabolism, epithelial cell proliferation, cell injury, and immune cell activation and regulation.

Background: Blocking and even reversing gastric precancerous lesions (GPL) is a key measure to lower the incidence of gastric cancer. Atractylenolide III (AT-III) is a mainly active component of the Atractylodes rhizome and has been widely used in tumor treatment. However, the effects of AT-III on GPL and its mechanisms have not been reported.Methods: H & E staining and AB-PAS staining were employed to evaluate the histopathology in the gastric mucosa. In parallel, CD34 immunostaining was performed for angiogenesis assessment, and transmission electron microscope for microvessel ultrastructural observation. Investigation for the possible mechanism in vivo and in vitro was conducted using immunohistochemistry, RT-qPCR and western blotting.Results: In most GPL specimens, AT-III treatment reduced microvascular abnormalities and attenuated early angiogenesis, with the regression of most intestinal metaplasia and partial dysplasia. Meanwhile, the expression of VEGF-A and HIF-1α was enhanced in GPL samples of model rats, and their expressions were decreased in AT-III-treated GPL rats. Moreover, DLL4 mRNA and protein expression were higher in GPL rats than in control rats. DLL4 protein expression was significantly enhanced in human GPL tissues. In addition, AT-III treatment could diminish DLL4 mRNA level and protein expression in the MNNG-induced GPL rats. In vitro study showed that in AGS and HGC-27 cells, DLL4 mRNA level and protein expression were significantly decreased after AT-III treatment. However, AT-III had no significant regulatory effect on Notch1 and Notch4.Conclusion: AT-III treatment is beneficial in lessening gastric precancerous lesions and attenuating angiogenesis in rats, and that may be contributed by the decrease of angiogenesis-associated HIF-1α and VEGF-A, and downregulation of DLL4.

Abstract Background In this study, we aimed to investigate the association between postoperative radiotherapy (PORT) and cardiac‐related mortality in patients with stage IIIA‐N2 non‐small cell lung cancer (NSCLC) using the Surveillance, Epidemiology, and End Results (SEER) database. Methods The United States (US) population based on the SEER database was searched for cardiac‐related mortality among patients with stage IIIA‐N2 NSCLC. Cardiac‐related mortality was compared between the PORT and Non‐PORT groups. Accounting for mortality from other causes, Fine and Gray's test compared cumulative incidences of cardiac‐related mortality between both groups. Univariate and multivariate analysis were performed using the competing risk model. Results From 1988 to 2016, 7290 patients met the inclusion criteria: 3386 patients were treated with PORT and 3904 patients with Non‐PORT. The five‐year overall incidence of cardiac‐related mortality was 3.01% in the PORT group and 3.26% in the Non‐PORT group. Older age, male sex, squamous cell lung cancer, earlier year of diagnosis and earlier T stage were independent adverse factors for cardiac‐related mortality. However, PORT use was not associated with an increase in the hazard for cardiac‐related mortality (subdistribution hazard ratio [SHR] = 0.99, 95% confidence interval [CI]: 0.78–1.24, p = 0.91). When evaluating cardiac‐related mortality in each time period, the overall incidence of cardiac‐related mortality was decreased over time. There were no statistically significant differences based on PORT use in all time periods. Conclusions With a median follow‐up of 25 months, no significant differences were found in cardiac‐related mortality between the PORT and Non‐PORT groups in stage IIIA‐N2 NSCLC patients.

Background Lung cancer is the leading cause of cancer death and is commonly treated by cisplatin. Although cisplatin treatment may initially be successful, its effectiveness usually reduces significantly in disease‐recurrent patients. Aspirin, a nonselective COX inhibitor, has been shown to help reverse the status of cisplatin sensitivity in recurrent human ovarian cancer cells. This study aimed to explore the effect of aspirin on cisplatin resistance through the perspective of cancer cell stemness. Methods We used clustering analysis to predict the H460 cisplatin resistance from the GSE21656 dataset. The increased lung cancer cell stemness may contribute to enhanced tolerance. In this study, we used aspirin, a nonselective COX inhibitor, with cisplatin for several hours in cells and days in vivo, and studied the inhibition against human cisplatin‐resistant H460 cells. H460 cisplatin‐sensitive and H460 cisplatin‐resistant cells were treated with 16 μM aspirin or/and 0.3 μg/mL cisplatin for 72 hours. Results H460 cisplatin‐resistant cells showed stronger resistance, stemness, and invasiveness than H460 cisplatin‐sensitive, and cisplatin significantly reduced the survival of cisplatin‐sensitive cells, while cisplatin with aspirin dramatically reduced the surviving fractions of cisplatin‐resistant cells. Conclusions This study revealed that stemness is a latent inhibitor of the resistance of lung cancer cisplatin‐resistant cells and might be effectively inhibited by aspirin.

Background Despite the recent development of molecular‐targeted treatment and immunotherapy, survival of patients with esophageal adenocarcinoma (EAC) with poor prognosis is still poor due to lack of an effective biomarker. In this study, we aimed to explore the ceRNA and construct a multivariate gene expression predictor model using data from The Cancer Genome Atlas (TCGA) to predict the prognosis of EAC patients. Methods We conducted differential expression analysis using mRNA, miRNA and lncRNA transciptome data from EAC and normal patients as well as corresponding clinical information from TCGA database, and gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis of those unique differentially expressed mRNAs using the Integrate Discovery Database (DAVID) database. We then constructed the lncRNA‐miRNA‐mRNA competing endogenous RNA (ceRNA) network of EAC and used Cox proportional hazard analysis to generate a multivariate gene expression predictor model. We finally performed survival analysis to determine the effect of differentially expressed mRNA on patients' overall survival and discover the hub gene. Results We identified a total of 488 lncRNAs, 33 miRNAs, and 1207 mRNAs with differentially expressed profiles. Cox proportional hazard analysis and survival analysis using the ceRNA network revealed four genes (IL‐11, PDGFD, NPTX1, ITPR1) as potential biomarkers of EAC prognosis in our predictor model, and IL‐11 was identified as an independent prognostic factor. Conclusions In conclusion, we identified differences in the ceRNA regulatory networks and constructed a four–gene expression‐based survival predictor model, which could be referential for future clinical research.

Ginsenoside Rg3 (GRg3) is a ginsenoside extracted from Panax ginseng. GRg3 displays multiple pharmacological properties, such as antitumor, anti-inflammatory, antioxidative and antifibrotic properties. However, whether GRg3 inhibits angiogenesis in gastric precancerous lesions (GPLs) and the possible mechanisms remain unknown. GRg3 attenuated gastric intestinal metaplasia and gastric dysplasia, the hallmark of GPL pathology, in rats with MNNG-ammonia compound induced GPLs. Increased CD34+ microvessel density and VEGF expression, which indicate the presence of angiogenesis, were evident in the rats with GPLs. GRg3 administration reduced VEGF protein expression and CD34+ microvessel density. In addition, GRg3 was capable of attenuating microvascular abnormalities. Data analysis revealed that enhanced protein expression of GLUT1, GLUT3 and GLUT4 were present in both human and animal GPL specimens. The administration of GRg3 caused significant decreases in the mRNA and protein expression levels of GLUT1 and GLUT4 in the rats with GPLs. However, the GRg3-treated rats with GPLs did not demonstrate regulatory effects on GLUT3, GLUT6, GLUT10, and GLUT12. Consistent with in vitro results, GRg3 administration significantly reduced the protein expression levels of GLUT1 and GLUT4 in both AGS and HGC-27 human gastric cancer cells in vitro. In conclusion, GRg3 can attenuate angiogenesis and temper microvascular abnormalities in rats with GPLs, which may be associated with its inhibition on the aberrant activation of GLUT1 and GLUT4.

BackgroundCancer stem cells (CSCs) are able to survive after cancer therapies, resulting in tumor progression and recurrence, as is seen in colorectal cancer. Therapies targeting CSCs are regarded as novel and promising strategies for efficiently eradicating tumors. Berberine, an isoquinoline alkaloid extracted from the Chinese herbal medicine Coptis chinensis, was found to have antitumor activities against colorectal cancer, without knowing whether it exerts inhibitory effects on colorectal CSCs and the potential mechanisms.MethodsIn this study, we examined the inhibitory roles of Berberine on CSCs derived from HCT116 and HT29 by culturing in serum-free medium. We also examined the effects of Berberine on m6A methylation via regulating fat mass and obesity-associated protein (FTO), by downregulating β-catenin.ResultsWe examined the effects of Berberine on the tumorigenicity, growth, and stemness of colorectal cancer stem-like cells. The regulatory effect of Berberine on N6-methyladenosine (m6A), an abundant mRNA modification, was also examined. Berberine treatment decreased cell proliferation by decreasing cyclin D1 and increasing p27 and p21 and subsequently induced cell cycle arrest at the G1/G0 phase. Berberine treatment also decreased colony formation and induced apoptosis. Berberine treatment transcriptionally increased FTO and thus decreased m6A methylation, which was reversed by both FTO knockdown and the addition of the FTO inhibitor FB23-2. Berberine induced FTO-related decreases in stemness in HCT116 and HT29 CSCs. Berberine treatment also increased chemosensitivity in CSCs and promoted chemotherapy agent-induced apoptosis. Moreover, we also found that Berberine treatment increased FTO by decreasing β-catenin, which is a negative regulator of FTO.ConclusionsOur observation that Berberine effectively decreased m6A methylation by decreasing β-catenin and subsequently increased FTO suggests a role of Berberine in modulating stemness and malignant behaviors in colorectal CSCs.

Objective: To evaluate the safety and efficacy of additional radiotherapy after endoscopic resection (ER) for stage I esophageal carcinoma (EC) with high-risk factors. Materials and methods: Patients with stage cT1N0M0 EC who underwent ER and additional radiotherapy between January 2010 and August 2019 at our institution were retrospectively included. Overall survival (OS), disease-free survival (DFS), cancer-specific survival (CSS), local control rate, regional control rate, common acute toxicities, esophageal stricture, and dysphagia were analyzed. Results: Thirty-one consecutive patients were included in the study. The median age was 62 years (range, 49-78). Thirty patients (96.8%) had squamous cell carcinoma, and one patient (3.2%) had adenosquamous cell carcinoma. Twenty-six patients (83.9%) had submucosal invasion, 15 patients (48.4%) had lymphovascular invasion, and one patient (3.2%) had a venous invasion. The 1-, 3-, and 5-year OS rates were 100.0%, 86.9%, and 68.5%, respectively. The corresponding DFS rates were 100.0%, 85.2%, and 75.8%, respectively. The corresponding CSS rates were 100.0%, 89.8%, and 78.6%, respectively. The local and regional control rates were 100.0% and 93.5%, respectively. No grade 4-5 acute toxicities were observed. Fifteen patients (48.4%) were endoscopically diagnosed with esophageal strictures after ER. At the last follow-up, 28 patients (90.5%) were able to eat a regular diet, one patient (3.2%) could eat a soft diet, one needed a semifluid diet, and only one (3.2%) had to eat a fluid diet. Conclusions: For patients with stage I EC, additional radiotherapy following ER is safe and effective, with the swallowing function well-preserved. Nevertheless, prospective studies are needed to verify these results.

Background: Seeking novel and effective therapies for gastric precancerous lesions (GPL) is crucial to reducing the incidence of gastric cancer. Ginsenoside Rb1 (GRb1) is a major ginsenoside in ginseng and has been proved to possess multiple bioactivities. However, whether GRb1 could protect against GPL and the underlying mechanisms have not been explored.Methods: We evaluated the effects of GRb1 on gastric precancerous lesions in rats on macroscopic, microscopic and ultramicroscopic levels. Then, an antibody array was employed to screen differential expression proteins (DEPs). Validation for the targeting DEP and investigation for the possible mechanism was conducted using immunohistochemistry, qRT-PCR, TUNEL apoptosis assay, immunoprecipitation and immunoblotting.Results: GRb1 was found to reverse intestinal metaplasia and a portion of dysplasia in the MNNG-induced GPL rats. The antibody array assay revealed seven DEPs in GPL rats as compared to control rats (5 DEPs were up-regulated, while two DEPs were down-regulated). Among the DEPs, β-catenin, beta-NGF and FSTL1 were significantly down-regulated after GRb1 administration. Our validation results revealed that enhanced protein expression and nuclear translocation of β-catenin were present in animal GPL samples. In addition, analysis of human gastric specimens demonstrated that β-catenin up-regulation and nuclear translocation were significantly associated with advanced GPL pathology. GRb1 intervention not only decreased protein expression and nuclear translocation of β-catenin, but interfered with β-catenin/TCF4 interaction. Along with this, declined transcriptional and protein expression levels of downstream target genes including c-myc, cyclin D1 and Birc5 were observed in GRb1-treated GPL rats.Conclusion: GRb1 is capable of preventing the occurrence and progression of GPL, which might be contributed by diminishing protein expression and nuclear translocation of β-catenin and interfering with β-catenin/TCF4 interaction.

Male occult breast cancer has a lower incidence, later clinical stage at detection, poorer differentiation, worse prognosis, and metastasizes earlier than breast cancer in females due to its rarity and a lack of public awareness. We report a 64 year old male patient presenting with palpable masses in his left cervical region, in whom imaging was unremarkable, except for slightly enlarged axillary lymph nodes without increased metabolic activity and an area of high metabolic activity in the left supraclavicular fossa. The purpose of this case report is to present the imaging, pathological features, and our treatment for male OBC.