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Background: The controlling nutritional status (CONUT) score effectively reflects a patient's nutritional status, which is closely related to cancer prognosis. This study investigated the relationship between the CONUT score and prognosis after radical surgery for colorectal cancer, and compared the predictive ability of the CONUT score with other indexes., Aim: To analyze the predictive performance of the CONUT score for the survival rate of colorectal cancer patients who underwent potentially curative resection., Methods: This retrospective analysis included 217 patients with newly diagnosed colorectal. The CONUT score was calculated based on the serum albumin level, total lymphocyte count, and total cholesterol level. The cutoff value of the CONUT score for predicting prognosis was 4 according to the Youden Index by the receiver operating characteristic curve. The associations between the CONUT score and the prognosis were performed using Kaplan-Meier curves and Cox regression analysis., Results: Using the cutoff value of the CONUT score, patients were stratified into CONUT low ( n = 189) and CONUT high groups ( n = 28). The CONUT high group had worse overall survival (OS) ( P = 0.013) and relapse-free survival (RFS) ( P = 0.015). The predictive performance of CONUT was superior to the modified Glasgow prognostic score, the prognostic nutritional index, and the neutrophil-to-lymphocyte ratio. Meanwhile, the predictive performances of CONUT + tumor node metastasis (TNM) stage for 3-year OS [area under the receiver operating characteristics curve (AUC) = 0.803] and 3-year RFS (AUC = 0.752) were no less than skeletal muscle mass index (SMI) + TNM stage. The CONUT score was negatively correlated with SMI ( P < 0.01)., Conclusion: As a nutritional indicator, the CONUT score could predict long-term outcomes after radical surgery for colorectal cancer, and its predictive ability was superior to other indexes. The correlation between the CONUT score and skeletal muscle may be one of the factors that play a predictive role., Competing Interests: Conflict-of-interest statement: All the Authors have no conflict of interest related to the manuscript., (©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.)

Family with sequence similarity 60A (FAM60A) has been reported as a new cancer-related protein that affects the malignant progression of some cancers. However, whether FAM60A plays a part in pancreatic carcinoma is undetermined. This work was designed to examine the impact of FAM60A in pancreatic carcinoma. Abundant expression of FAM60A was observed in the primary tumor tissue of pancreatic carcinoma. Moreover, a high FAM60A level was related to a poor overall survival in pancreatic carcinoma patients. Malignant behaviors of pancreatic carcinoma cells, such as proliferation and invasiveness, were markedly affected by FAM60A depletion. In addition, FAM60A depletion enhanced the drug sensitivity of pancreatic carcinoma cells to gemcitabine. Further study revealed that FAM60A depletion impaired the activities of Akt and β-catenin. Inhibiting the activity of Akt abolished FAM60A-mediated β-catenin activation. Re-expression of β-catenin partially diminished the FAM60A-depletion-mediated cancer suppressive effect in pancreatic carcinoma cells. In vivo experiments demonstrated that FAM60A depletion prohibited the xenograft formation of pancreatic carcinoma cells, with concurrent reductions of Akt and β-catenin activities. Collectively, our findings indicate that FAM60A exerts a cancer-promoting role in pancreatic carcinoma through affection of the Akt/β-catenin pathway. This work indicates that FAM60A acts as a tumor promoter in pancreatic carcinoma and can be utilized as a potential target for anti-pancreatic carcinoma therapy development., (© 2022 Wiley Periodicals LLC.)

LASP2 (LIM and SH3 protein 2), a member of the LIM-protein subfamily of the nebulin group, was first identified as a splice variant of the nebulin gene. In the past, investigators mainly focused on the impact of LASP2 on cardiac diseases because of its identification in the myocardium. Recently, several studies have reported that LASP2 is associated with the progression of various cancers. However, there have been no investigations on the expression and function of LASP2 in pancreatic cancer (PC). In this study, we performed the quantitative real-time polymerase chain reaction and Western blot analysis to detect the expression of LASP2 in PC tissues and cell lines. PC cells were transfected with LASP2 overexpression plasmid or the negative control in the presence or absence of tumor growth factor-β (TGF-β). The transwell assays were used to measure the effects of LASP2 on PC cell migration and invasion. The protein expression of epithelial-mesenchymal transition (EMT) markers was detected using Western blot assay. Our results demonstrated that LASP2 was downregulated in PC tissues and cell lines. In addition, upregulation of LASP2 inhibited the PC cell migration and invasion. We also found that LASP2 upregulation reversed TGF-β-induced EMT in PC cells. Taken together, we provided novel evidence supporting the tumor-suppressor role of LASP2 in PC and suggested it as a potential therapeutic target in PC treatment., (© 2019 Wiley Periodicals, Inc.)

Empty spiracles homeobox 2 (EMX2) is a homeodomain-containing transcription factor that plays an essential role in tumorigenesis. However, to the best of our knowledge, the role of EMX2 in human colorectal cancer (CRC) is still unclear. Thus, the aim of this study was to investigate the expression and role of EMX2 in CRC. Our results demonstrated that the expression of EMX2 was greatly decreased in CRC tissues and cell lines. Overexpression of EMX2 significantly inhibited the proliferation in vitro and CRC tumor growth in nude mice. In addition, EMX2 also inhibited the migration and invasion of CRC cells. Mechanically, overexpression of EMX2 downregulated the expression levels of β-catenin, cyclin D1, and c-Myc in CRC cells. Taken together, our study demonstrates that EMX2 inhibits proliferation and tumorigenesis through inactivation of the Wnt/β-catenin pathway in CRC cells. Therefore, EMX2 may be a potential therapeutic target for the treatment of CRC.

In this present paper, simultaneous determination of Ca(2+) and Mg(2+) cations in saliva, urine was achieved using an ion chromatography method, in which a piezoelectric quartz crystal (PQC) sensor was used as a detector, and a solution containing tartaric acid (4 mmol 1(-1)) and ethylenediamine (2 mmol 1(-1)) as a mobile phase. Good linearities were obtained over the ranges of 0.8-500 mg 1(-1) Ca(2+) and 1.0-500 mg 1(-1) Mg(2+). The detection limits were 0.4 mg 1(-1) for Ca and 0.2 mg 1(-1) for Mg, respectively.

Bone destruction is one of the clinical features of chronic otitis media with cholesteatoma. Bone resorption may be due to the epithelial debris accumulated in the cholesteatoma epidermal sac that acts as foreign body material inducing a destructive granulation tissue and creates pressure on the bony middle ear. This compressive force then induces bone resorption. The present study was designed to replicate certain conditions similar to those in cholesteatoma leading to bone resorption. Four types of materials were implanted into the middle ear cavity of rats: (1) laminaria, an expandable seaweed material, (2) preswollen laminaria, (3) keratin powder suspension, and (4) surgical grade silicone, which when bent exerts pressure on the bulla wall. The placement of laminaria segments in the middle ear cavity of rats was followed by swelling of the implanted materials within 7 days. The bulla bone response was by neo-osteogenesis as well as active bone resorption. The new bone was observed on the external and/or internal surface of the tympanic bone. The cochlear bone also showed extensive bone resorption in the animals. Osteogenesis was rarely observed on the capsule of the cochlea. We also observed no bone resorption at sites without presence of inflammatory connective tissue between laminaria and bone. The typical multinucleated osteoclasts were often seen at the resorption area but the majority of bone resorption sites were characterized by the presence of mononuclear cells and other inflammatory cells. Preswollen laminaria, keratin powder, and silicone strips induced minimal bone resorption. No resorption was observed in the bony cochleas of these experimental groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Fibronectin was localized in human cholesteatoma tissues by immunohistochemical methods. The avidin-biotin-peroxidase complex staining method was used with specific fibronectin antibody. Fibronectin appeared to be localized in the matrix of the cholesteatoma studied, particularly on the surface of the cell membranes and the nuclei of the basal cells and in connective tissue. Fibronectin was not seen in the granular layer or in the keratin area. Fibronectin was found on the surface of granulation tissue, mononuclear cells, fibroblasts and endothelial cells of blood vessels. These findings were confirmed by the immunofluorescent staining method. Our previous study showed that fibronectin induced a migration of keratinocytes, macrophages and fibroblasts demonstrated by the Boyden's chamber chemotaxis assay. Macrophages and fibroblasts were shown to produce collagenase, a bone resorption factor, in cholesteatomatous tissue. The present study showed the presence of fibronectin in the matrix of cholesteatoma and granulation tissue, suggesting that fibronectin might play an important role in the clinical development and invasive behavior of cholesteatoma.