LINC01305 recruits basonuclin 1 to act on G-protein pathway suppressor 1 to promote esophageal squamous cell carcinoma.

EsophageaL squamous cell carcinoma (ESCC) is one of the most common and lethal tumors, however, its underlying molecular mechanisms are not completely understood and new therapeutic targets are needed. Here, we found that the transcription factor basonuclin 1 (BNC1) was significantly upregulated and closely related to the differentiation and metastasis of ESCC. Furthermore, BNC1, LINC01305, and G-protein pathway suppressor 1 (GPS1) had significant oncogenic roles in ESCC. In addition, in vivo experiments showed that knockdown of BNC1 indeed significantly inhibited the proliferation and metastasis of ESCC. We also revealed the molecular mechanism by which LINC01305 recruits BNC1 to the promoter of GPS1, and then GPS1 could mediate the JNK signaling pathway to promote the proliferation and metastases of ESCC. Taken together, we discovered the novel molecular mechanism by which LINC01305/BNC1 upregulates GPS1 expression to promote the development of ESCC, providing a new therapeutic target for ESCC.

Coincidently oral lesions in Crohn's disease.

A 21-year-old patient with Crohn's disease, who was undergoing Infliximab treatment, presented at the hospital due to a painful oral mass. After confirming the absence of malignant cells through frozen sections, a complete excision of the infiltrated bone surrounding the lesion was performed. The postoperative pathology confirmed the presence of Central type giant cell granuloma in the mandible, which is distinct from non-caseating granulomas in oral CD and Infliximab-induced Sarcoidosis. As far as we are aware, this is the first to report an association between CGCG and both CD and anti-tumor necrosis factor therapy treatment.

Differential diagnostic value of periampullary mass: A nomogram established by random forest based on clinical characteristics and contrast-enhanced ultrasound.

PURPOSES: To develop a nomogram model for distinguishing benign from malignant ampullary lesions more intuitive and accurate. MATERIALS AND METHODS: A total of 124 patients with periampullary lesions from January 2016 to June 2020 were enrolled in this retrospective study. Their clinical information, ultrasound (US), dual contrast-enhanced ultrasound (DCEUS) and MRI image features were used for research. Twenty features were collected in our study. Random forest was used to select the first five most important indicators to construct the prediction model. RESULTS: Patients' age, common bile duct (CBD) diameter, the shape, vascularity, and boundary of lesion, lesion size with or without enlarged after CEUS, the enhancement patterns of arterial phase, the washout patterns of venous phase, CEUS diagnosis, and MRI diagnosis were statistically significant (p < 0.05). After screening for statistically significant indicators by random forest, the first five most important indicators were age, CBD diameter, the enhancement patterns of arterial phase, the washout patterns of venous phase, lesion size with or without enlarged after CEUS, which were used to construct nomogram. The area under curves (AUC) and 95% confidence intervals (CI) for nomogram, MRI + MRCP + DCEUS, DCEUS, MRI + MRCP were 0.98(0.94-1.00), 0.91(0.84-0.97), 0.89(0.80-0.98), 0.68(0.60-0.77), respectively. The sensitivity and specificity were 100.00% and 84.62% for nomogram, 88.29% and 92.31% for MRI + MRCP+DCEUS, 86.49% and 92.31% for DCEUS, 51.35%, and 100.00% for MRI + MRCP. CONCLUSIONS: We combined clinical indicators, gray-scale ultrasound characteristics, and CEUS characteristics to build the nomogram, which can be intuitively and accurately used for preoperative malignant prediction of ampullary lesion patients, worthy of clinical generalizability and application.

[Causes of death in STZ-induced rat models of diabetes mellitus].

OBJECTIVE: To identify conditions that may improve the successful rate of STZ-induced rat models of diabetes mellitus (DM). METHODS: 100 male SD rats were randomly divided into control group (n = 10) and experimental group (n = 90). Rats in the experimental group were treated with intraperitoneal injection of STZ 65 mg/kg once, and were then categorized into succeeded DM model group and failed group. Their body masses and levels of fasting blood glucose (FBG), urine glucose (UG), urine protein (UP), urine routine, renal function, liver function, blood lipids and kidney hypertrophy index (KHI) were monitored and compared. Dead rats were dissected to observe diseased organs. Pathological changes of those diseased organs were examined by HE staining. RESULTS: DM rat models were established through a single intraperitoneal injection of STZ, with a success rate of 58.89%. During the experiment, 43.33% of rats died. Compared with the rats in the failed group, the DM rat models had significantly higher levels of body mass, food intake, water intake, urine output, FBG, creatinine, blood urea nitrogen, KHI, urinary tract infections, and mortality; but lower levels of total protein, albumin and cholesterol and triglyceride (P < 0.05). Nine rats died of pulmonary edema; 19 died of renal abscess. The causes of 11 dead rats were not clear. CONCLUSION: DM rat models can be established through a single intraperitoneal injection of STZ 65 mg/kg, but with high mortality rate. The deaths may be associated with infection, malnutrition, suffocation of lymphatic circulation, toxicity of STZ, and changes in environmental and climate conditions.

Chromothripsis is a novel biomarker for prognosis and differentiation diagnosis of pancreatic neuroendocrine neoplasms.

This study aimed to identify the role of chromothripsis as a novel biomarker in the prognosis and differentiation diagnosis of pancreatic neuroendocrine neoplasms (pNENs). We conducted next-generation gene sequencing in a cohort of 30 patients with high-grade (G3) pNENs. As a reference, a similar analysis was also performed on 25 patients with low-grade (G1/G2) pancreatic neuroendocrine tumors (pNETs). Chromothripsis and its relationship with clinicopathological features and prognosis were investigated. The results showed that DNA damage response and repair gene alteration and TP53 mutation were found in 29 and 11 patients, respectively. A total of 14 out of 55 patients had chromothripsis involving different chromosomes. Chromothripsis had a close relationship with TP53 alteration and higher grade. In the entire cohort, chromothripsis was associated with a higher risk of distant metastasis; both chromothripsis and metastasis (ENETS Stage IV) suggested a significantly shorter overall survival (OS). Importantly, in the high-grade pNENs group, chromothripsis was the only independent prognostic indicator significantly associated with a shorter OS, other than TP53 alteration or pathological pancreatic neuroendocrine carcinomas (pNECs) diagnosis. Chromothripsis can guide worse prognosis in pNENs, and help differentiate pNECs from high-grade (G3) pNETs.

HOXD11 upregulates JAM-A and exerts oncogenic properties via NF-κB signaling pathway in esophageal squamous cell carcinoma.

Esophageal squamous cell carcinoma (ESCC) is a tumor with high incidence and poor prognosis in developing countries. Junctional adhesion molecule A (JAM-A, also known as F11R) affects numerous biological processes, which is a vital regulator of the development of malignant tumors. However, its exact role and underlying mechanism in ESCC remain obscure. Our present study demonstrated that JAM-A was upregulated in ESCC tissues and cell lines by RNA sequencing and immunohistochemistry (IHC). JAM-A knockdown significantly suppressed the proliferation of the ESCC cells, induced cell cycle arrest at the G1 and promoted apoptosis, and suppressed the ability of invasion and migration in vivo and in vitro. Mechanistically, JAM-A may activate the NF-κB signaling pathway to regulate malignant behavior of ESCC. Further research showed that Homeobox D11 (HOXD11) could directly regulate JAM-A transcription by binding to specific sequences of JAM-A promoter region, thereby activating NF-κB signaling pathway to regulate malignant behavior of ESCC. Functional experiments indicated that HOXD11 could exert an oncogenic role in ESCC. Collectively, our findings support the hypothesis that the HOXD11/JAM-A/NF-κB signal axis plays a role in regulating malignant behavior in ESCC patients, highlighting its potential therapeutic value for ESCC.

Diagnostic pitfalls: a case of prostate cancer and rectal cancer accompanied by prostate cancer invasion of the rectum.

INTRODUCTION: Case of double primary cancer of the prostate and rectum is rare, prostate cancer involving the postoperative intestinal anastomotic mucosal tissue is even rarer. CASE PRESENTATION: We report a case of rectal cancer discovered 1 year after a diagnosis of prostate cancer and a tumour in the postoperative anastomotic intestinal mucosal tissue involving prostatic adenocarcinoma at 1 year after the diagnosis of rectal cancer. Due to the poor differentiation of both prostate and rectal cancers, there are some pitfalls in the diagnosis of intestinal mucosal lesions at an anastomosis. The lack of an accurate diagnosis of a tumour in anastomosis intestinal mucosal tissue will affect treatment and patient survival. CONCLUSIONS: The pathologists should have a detailed understanding of the patient's medical history and carefully observe the histopathological morphology and, if necessary, immunohistochemistry or other techniques should be used to assist in the pathological diagnosis and avoid both misdiagnosis and missed diagnosis.

Role of endometrial cancer abnormal MMR protein in screening Lynch-syndrome families.

OBJECTIVE: To identify patients with endometrial cancer with potential Lynch-related DNA mismatch repair (MMR) protein expression defects and to explore the role of these defects in screening for LS. METHODS: Endometrial cancers from 173 patients recruited to the Nanchong Central Hospital were tested for MMR (MLH1, MSH2, PMS2, and MSH6) protein expression using immunohistochemistry (IHC). RESULTS: In the 173 tumor tissue samples, the expression loss rates of MSH6, MSH2, PMS2 and MLH1 protein were 16.18% (28/173), 12.14% (21/173), 7.51% (13/173) and 5.78% (10/173), respectively. The total loss rate of MMR protein was 29.89% (27/87). There were 19 patients with a family history of cancer, of which 18 patients demonstrated loss of expression of MMR protein. In the 22 abnormal MMR patients without family history, five families were found to have Lynch-associated cancer (colorectal cancer, endometrial cancer, ovarian cancer, stomach cancer) after follow-up for two years. CONCLUSION: MMR proteins play an important role in the progress of endometrial cancer. The routine testing of MMR proteins in endometrial cancer can contribute to the screening of LS families, especially small families.