[Clinical Practice of Multiple Disciplinary Team Care Model Following the Concept of Palliative Care for Advanced Head and Neck Cancer:Report of One Case].

We provided the palliative care of a multiple disciplinary team care mode to a patient diagnosed with advanced head and neck cancer and her caregivers.People-centered integrated health services were provided according to the specific needs and preferences of individuals.The team-based palliative care relieved the suffering and improved the quality of life of the patient and that of her family who were facing challenges associated with life-threatening illness.

The knockdown of LncRNA AFAP1-AS1 suppressed cell proliferation, migration, and invasion, and promoted apoptosis by regulating miR-545-3p/hepatoma-derived growth factor axis in lung cancer.

Lung cancer is one of the most common human cancers. Long noncoding RNA AFAP1-AS1 (LncRNA AFAP1-AS1) and microRNA-545-3p (miR-545-3p) were reported to play important roles in lung cancer development. This study aimed to elucidate the functional mechanisms of AFAP1-AS1 and miR-545-3p in lung cancer. Quantitative real time polymerase chain reaction was carried out to determine the levels of AFAP1-AS1, miR-545-3p and hepatoma-derived growth factor (HDGF). Cell proliferation, apoptosis, migration and invasion were detected by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide assay, flow cytometry, and transwell migration and invasion assays, respectively. Furthermore, the interaction between miR-545-3p and AFAP1-AS1 or HDGF was predicted by bioinformatics analysis software starbase and confirmed by the dual luciferase reporter assay. Western blot assay was used to detect the protein level of HDGF. Besides, murine xenograft model was conducted through injecting A549 cells transfected with sh-AFAP1-AS1. The expression levels of AFAP1-AS1 and HDGF were increased, while miR-545-3p was decreased in lung cancer tissues and cells. AFAP1-AS1 knockdown suppressed lung cancer cell proliferation, migration, and invasion and induced apoptosis. Furthermore, AFAP1-AS1 mediated cell progression through regulating miR-545-3p expression. In addition, miR-545-3p negatively regulated the expression level of HDGF via binding 3'-untranslated region of HDGF. As expected, AFAP1-AS1 knockdown inhibited lung cancer progression via affecting miR-545-3p/HDGF axis. Besides, AFAP1-AS1 knockdown suppressed lung cancer tumor growth in vivo. Collectively, our results suggested that AFAP1-AS1 promoted the development of lung cancer via regulating miR-545-3p/HDGF axis, providing a potential target for the treatment of lung cancer.

Long Non-Coding RNA (lncRNA) Metastasis-Associated Lung Adenocarcinoma Transcript 1 (MALAT1) Promotes Cell Proliferation and Migration by Regulating miR-143-3p and MAGE Family Member A9 (MAGEA9) in Oral Squamous Cell Carcinoma.

BACKGROUND lncRNA MALAT1 is one of the most widely studied lncRNAs associated with various human cancers. The present study explored the functions and potential regulatory mechanisms of MALAT1 in oral squamous cell carcinoma (OSCC). MATERIAL AND METHODS We assessed levels of MALAT1, miR-143-3p, and MAGEA9 expression in OSCC tissues and cell lines by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot assay. Proliferation and migration of CAL-27 cells were detected via CCK-8 and transwell assays, respectively. To study the relationships among MALAT1, miR-143-3p, and MAGEA9, we performed dual-luciferase assay and assessed the results using Spearman correlation analysis. RESULTS QRT-PCR results showed that MALAT1 and MAGEA9 were expressed at higher levels and miR-143-3p was expressed at lower levels in OSCC tissues. Dramatic suppression of cell proliferation and migration abilities were caused by MALAT1 knockdown or miR-143-3p overexpression in CAL-27 cells. MALAT1 directly interacted with and negatively regulated miR-143-3p. Moreover, MAGEA9 was validated as a miR-143-3p target gene and was found to be negatively regulated by it. MALAT1 knockdown suppressed MAGEA9 protein expression and had the same effect as MAGEA9 knockdown. Additionally, MAGEA9 knockdown inhibited CAL-27 cell proliferation and migration abilities. Finally, in OSCC tissues, MALAT1 and miR-143-3p expression were negatively correlated and MALAT1 was positively correlated with MAGEA9 expression, while an inverse correlation between MAGEA9 and miR-143-3p expression was observed. CONCLUSIONS Taken together, our results suggest that MALAT1 functions as a competing endogenous RNA (ceRNA) in promoting OSCC cell proliferation and migration abilities through the miR-143-3p/MAGEA9 axis, thus providing new therapeutic targets for treatment of OSCC.

Effect of lipid metabolism disorder on liver function in patients with malignant tumors after chemotherapy: a case-control study.

BACKGROUND: This study aims to investigate the effect of lipid metabolism disorder on liver function in patients with malignant tumors after chemotherapy. METHOD: A total of 428 patients with malignant tumors with normal liver function in our hospital between May 2013 to June 2018 were divided into an observation group (lipid metabolism disorder, n = 265) and control group (normal lipid metabolism, n = 163). The lipid metabolism levels and liver damage of the two groups were compared before and after chemotherapy. RESULTS: No significant differences in age, gender, body mass index, tumor types, history of surgery, levels of alanine aminotransferase (ALT; an indicator of liver function), and chemotherapy regimen were observed between the two groups. However, the observation group showed increased levels of total cholesterol (P = 0.000), triglycerides (P = 0.000), and low-density lipoprotein (P = 0.01), as well as decreased levels of high-density lipoprotein (P = 0.000) before chemotherapy compared with the control group. Furthermore, patients with lipid metabolism disorders were more likely to develop abnormal liver function after chemotherapy. Moreover, mixed lipid metabolism disorder was more likely to cause severe liver damage after chemotherapy. Additionally, the number of patients with lipid metabolism disorders after chemotherapy (n = 367) was significantly increased compared with before chemotherapy (n = 265) (P < 0.01), indicating that chemotherapy might induce or aggravate an abnormal lipid metabolism. CONCLUSIONS: After receiving chemotherapy, patients with malignant tumors presenting lipid metabolism disorders are more prone to liver damage and lipid metabolism disorders than patients with a normal lipid metabolism.

Advances in Mechanisms for Prevention and Treatment of Pathological Scars with Mesenchymal Stem Cells.

Pathological scars,including keloids and hypertrophic scars,result from aberrations in the process of physiologic wound healing.An exaggerated inflammatory process is one of the main pathophysiological contributors.Pathological scars may cause pain and pruritis,limit joint mobility,and cause a range of cosmetic deformities that affect the patient's quality of life.However,the effectiveness of currently available prevention and treatment measures remains unsatisfactory.Mesenchymal stem cells,among their multifunctional roles,have the functions of immunomodulation and promotion of angiogenesis.Thus,they have been proposed to be a major candidate for cell therapy to treat or prevent pathologicalscars.This article reviews the mechanism and potentials of stem cell therapy in the prevention and treatment of pathological scars.

Histone demethylase KDM2A promotes tumor cell growth and migration in gastric cancer.

Histone demethylase KDM2A has been reported to be dysregulated in lung cancer. However, its function in gastric cancer remains poorly understood. Here, it was found that the expression level of KDM2A was increased in gastric cancer tissues. Moreover, forced expression of KDM2A in gastric cancer cells promoted cell growth and migration, while the knockdown expression of KDM2A inhibited the tumorigenicity of gastric cancer cells. Mechanistically, KDM2A regulated the growth and motility of gastric cancer cells through downregulating the expression of programmed cell death 4 (PDCD4), a known tumor suppressor in the progression of gastric cancer. Taken together, our study suggested that upregulation of KDM2A was very important in the progression of gastric cancer, and KDM2A might be a promising therapeutic target.

[Population Status of Centropus sinensis in Guangxi Province].

OBJECTIVE: T0 understand the population distribution, species abundance and habitats requirement of a medicinal animal, Centropus sinensis, in Guangxi Province. METHODS: Line transect methods were used to census population number and habitat types in 18 counties or cities of Guangxi. RESULTS: Centropus sinensis distributed in all study area, with a higher population density in the south than in the north. Among seven habitat types, the species preferred living in forest-farmland ecotone, while seldom in broad-leaves forest or plantations. CONCLUSION: The results of habitat preference show an advantage to the population recovering for forest-farmland ecotone commonly existing in Guangxi Province. But the speed of population recovering is slowly under illegal hunting pressure. More attention should be paid to protect this species.

Comparison of the Gut Microbial Communities of Domestic and Wild Mallards (Anas platyrhynchos) Based on High-Throughput Sequencing Technology.

Mallards (Anas platyrhynchos) are currently one of the most popular species in rare bird breeding in several southern provinces of China, but there have been no studies comparing the gut microbial communities of domestic and wild mallards. In this study, 16S rRNA gene high-throughput sequencing technology was used to compare the composition and diversity of gut microbial communities in domestic and wild mallards. Alpha diversity analysis showed significant differences in gut microbial communities between the two groups of mallards, and the diversity and richness of gut microbial communities were significantly higher in wild mallards than in domestic mallards. Beta diversity analysis showed that the two groups of stool samples were mostly separated on the principal coordinate analysis (PCoA) plot. In domestic mallards, Firmicutes (68.0% ± 26.5%) was the most abundant bacterial phylum, followed by Proteobacteria (24.5% ± 22.9%), Bacteroidetes (3.1% ± 3.2%), Fusobacteria (2.2% ± 5.9%), and Actinobacteria (1.1% ± 1.8%). The dominant bacterial phyla in wild mallards were Firmicutes (79.0% ± 10.2%), Proteobacteria (12.9% ± 9.5%), Fusobacteria (3.4% ± 2.5%), and Bacteroidetes (2.8% ± 2.4%). At the genus level, a total of 10 dominant genera (Streptococcus, Enterococcus, Clostridium, Lactobacillus, Soilbacillus, Bacillus, Acinetobacter, Comamonas, Shigella, and Cetobacterium) with an average relative abundance greater than 1% were detected in the fecal samples of both groups. The average relative abundance of five potential pathogenic genera (Streptococcus, Enterococcus, Acinetobacter, Comamonas, and Shigella) was higher in domestic mallards than in wild mallards. The enrichment of pathogenic bacteria in the intestinal tract of domestic mallards should be of sufficient concern.

Efficacy of mFOLFOX6 plus bevacizumab regimen in advanced colorectal cancer after deep hyperthermia: a single-center retrospective study.

Background: This study aimed to explore the clinical efficacy and safety of a modified FOLFOX6 (oxaliplatin + leucovorin + 5-fluorouracil) plus bevacizumab regimen after deep hyperthermia in advanced colorectal cancer. Methods: A total of 80 colorectal cancer patients treated at our hospital were selected as research subjects. According to the random number table method, patients were divided into a control group (mFOLFOX6 plus bevacizumab) and a combination group (mFOLFOX6 plus bevacizumab after deep hyperthermia treatment), with 40 patients in each group. After six cycles of treatment, the objective response rate (ORR), disease control rate (DCR), levels of serum tumor markers carcinoembryonic antigen (CEA), vascular epidermal growth factor (VEGF), Karnofsky performance status (KPS) scores, and the occurrence of adverse events were compared between the two groups. Results: After six cycles of treatment, the ORR in the combination group was higher than that in the control group, but the difference was not statistically significant (P>0.05). The DCR in the combination group was significantly higher than that in the control group (P<0.05). The serum CEA levels in the control and combination groups after treatment were significantly lower than those before treatment, and the serum CEA and VEGF levels in the combination group were significantly lower than those in the control group (all P<0.001). The KPS scores in both groups after treatment were higher than those before treatment, and the KPS scores in the combination group after treatment were significantly higher than those in the control group (all P<0.001). The incidence of fatigue and pain in the combination group was significantly lower than that in the control group (P<0.05). Conclusion: mFOLFOX6 plus bevacizumab after deep hyperthermia is effective in advanced colorectal cancer patients, which can effectively improve their quality of life, and the adverse events are controllable and tolerable. A randomized or prospective trial will be required to further prove these data and explore its potentiality, especially if compared to conventional treatment.

Efficacy of the low dose apatinib plus deep hyperthermia as third-line or later treatment in HER-2 negative advanced gastric cancer.

Aim: To observe the efficacy of the low dose apatinib plus deep hyperthermia as third-line or later treatment for patients with human epidermal growth factor receptor 2 (HER-2) negative advanced gastric cancer. Methods: 80 eligible patients with HER-2 negative advanced gastric cancer admitted to Jingjiang People's Hospital Affiliated with Yangzhou University-from March 2021 to March 2022 were selected, and they were divided into the control group (n = 40, apatinib) and experimental group (n = 40, apatinib plus deep hyperthermia) on the basis of random number table method. The levels of serum carcinoembryonic antigen (CEA), carbohydrate antigen 199 (CA199), and vascular endothelial growth factor (VEGF) were monitored, and the efficacy of the two groups was analyzed by referring to Karnofsky performance status (KPS), overall survival (OS) and disease control rate (DCR) before and after treatment. Results: The levels of CEA, CA199, and VEGF in both groups were lower after treatment than before (p < 0.05), and lower (CEA: 8.85 ± 1.36 vs. 12.87 ± 1.23, CA199: 34.19 ± 4.68 vs. 50.11 ± 5.73, VEGF: 124.8 ± 18.03 vs. 205.9 ± 19.91) in the experimental group than in the control group (p < 0.05). The DCR and KPS of the patients in the experimental group were significantly higher (DCR: 62.50% vs. 40.00%; KPS: 83.25 ± 1.15 vs. 76.25 ± 1.17) than in the control group (p < 0.05). In survival analysis, patients with control group had shorter OS than the experimental group. (median 5.65 vs. 6.50 months; hazard ratio [HR], 1.63 [95% confidence interval (CI) 1.02-2.60], p = 0.0396). Conclusion: The application of low-dose apatinib plus deep hyperthermia for patients with HER-2 negative gastric cancer who failed second-line treatment should be a promising option.

Mogroside-rich extract from Siraitia grosvenorii fruits protects against heat stress-induced intestinal damage by ameliorating oxidative stress and inflammation in mice.

Global warming makes humans and animals more vulnerable to heat stress. Heat stress can cause multiorgan dysfunction, especially in the intestine, primarily via oxidative stress and inflammation. Mogroside-rich extract (MGE) is the active ingredient of Siraitia grosvenorii and has significant antioxidant and anti-inflammatory activity. However, whether MGE can alleviate the intestinal damage caused by heat stress has not been explored. In this study, mice were given 600 mg kg-1 MGE followed by exposure to high temperature (40 °C for 2 h per day), and the structures and molecular changes in the ileum were examined. Our findings showed that body weight was decreased by heat stress, while the activity of serum superoxide dismutase (SOD) was increased. We further found that heat stress impaired the intestinal barrier by reducing the number of goblet cells and mRNA levels of the tight junction proteins zona occludens protein 1 (ZO-1), Occludin (OCLD) and recombinant mucin 2 (MUC2 mucin), but it increased the mRNA level of trefoil factor 3 (TFF3). Interestingly, MGE treatment reversed these changes. Furthermore, heat stress increased the activity of SOD in the intestine, downregulated the expression of the oxidative stress-related genes glutathione peroxidase 1 (GPX1), SOD2 and nuclear factor erythroid 2-related factor 2 (NRF2), and upregulated the expression of catalase (CAT). Moreover, heat stress increased tumor necrosis factor-α (TNF-α) levels in the intestine and upregulated the expression of the inflammation-related genes interleukin 10 (IL-10), TNF-α, Interferon-γ (IFN-γ), toll like receptor 4 (TLR4) and nuclear factor-kappa B (NF-kB). However, MGE treatment effectively reduced TNF-α levels and restored the normal activity of SOD and normal mRNA levels for both oxidative stress-related and inflammation-related genes. In summary, our results showed that MGE can protect against heat stress-induced intestinal damage by ameliorating inflammation and oxidative stress.

Giant calcifying epithelial odontogenic tumor after I-125 seed implantation: A case report.

Calcifying Epithelial Odontogenic Tumor (CEOT), also known as Pindborg tumor, is a rare odontogenic benign tumor. It was first reported by Thoma and Goldman in 1946 and defined as an independent tumor by Pindborg in 1957. Herein, we reported a CEOT case involving most of the mandible after I-125 implantation in a 53-year-old man. We cooperated with governmental and hospital departments to resect the tumors, reconstruct the mandible with a fibular flap graft, and properly dispose of the radioactive particles.

Contribution to the knowledge of Chinese Gryllacrididae (Orthoptera) VIII: One new species of Metriogryllacris (Metriogryllacris) amitarum Group from Guangxi.

This paper describes one new species of Metriogryllacris (Metriogryllacris) amitarum group from Guangxi Huaping National Nature Reserve. A key to the species group is provided. The examined specimen is deposited in Guangxi Normal University.

Plasma cfDNA for the Diagnosis and Prognosis of Colorectal Cancer.

Objective: To evaluate the value of cell-free DNA (cfDNA) for the diagnosis and prognosis of colorectal cancer (CRC). Methods: Peripheral blood specimens of 120 CRC patients and 90 healthy volunteers (as a control cohort) were extracted. A quantitative real-time polymerase chain reaction (qRT-PCR) was performed to determine the cfDNA expression. Following correlation analyses for cfDNA and clinical endpoints, a receiver operator characteristic (ROC) curve was established to assess the sensitivity and specificity of cfDNA, CEA, VEGF, and CA125 and for evaluating the disease-free survival (DFS) of patients. Results: The plasma cfDNA level of colorectal cancer patients was significantly higher than that of healthy subjects (P < 0.05), and after chemotherapy, cfDNA level was significantly lower than that before chemotherapy (P < 0.05). CA125/CEA/VEGF expression significantly correlated with cfDNA level, but not with cfDNA integrity. There was also a significant correlation between tumor differentiation and the cfDNA level. cfDNA has a higher ROC value than the current tumor biomarkers. Survival analysis showed that the DFS of the low cfDNA expression group was longer (29.99 ± 0.78 months) than that of the high cfDNA expression group (27.66 ± 1.05 months, P=0.031). Conclusion: The blood cfDNA is associated with the pathological features of CRC clinical cases and represents a possible indicator for CRC diagnosis and prognosis.

An unstructured phylogeographic pattern with extensive gene flow in an endemic bird of South China: collared Finchbill (Spizixos semitorques).

Recent phylogeographical studies indicated that glacial oscillations played a key role on the phylogeographic pattern of extant species. As most studies have previously been carried out on heavily ice-covered regions, such as in European and North American regions, potential effects of climatic oscillations on species that are distributed on ice-free regions are less known. To address this, we investigated the phylogeographic pattern of an avian species endemic to South China, which was not glaciated during the Pleistocene glaciations. By using 2142 bp mitochondrial DNA, we identified 89 haplotypes defined by 39 polymorphic sites. A combination of high haplotype diversity (0.786-1.00) and low nucleotide diversity (0.00132-0.00252) was detected among geographic populations. Explicit genetic divergence was observed between S. s. semitorques and S. s. cinereicapillus but not detected among geographic populations of S. s. semitorques. Divergence time of the two subspecies was dated back to 87 Kyr which is congruent with the interglacial MIS 5. A weak phylogeographic structure due to strong gene flow among geographic populations was identified in this species, suggesting complex topography of South China has not formed barriers for this species.

HMGB1 knockdown increases the radiosensitivity of esophageal squamous cell carcinoma by regulating the expression of molecules involved in DNA repair.

Radiotherapy is an effective therapeutic strategy in esophageal squamous cell carcinoma (ESCC). However, acquired radioresistance of cancer cells leads to radiotherapy failure. The present study aimed to investigate the mechanisms of the effect of high mobility group box 1 (HMGB1) on the radiation sensitivity of ESCC. Small interfering RNA (si) transfection was used to generate three groups of TE-1 cells (TE-1, negative control and TE-1+siHMGB1), and the protein expression levels of HMGB1 in TE-1 cells were detected by western blotting. These groups of TE-1 cells were irradiated with different doses (0, 2, 4, 6 and 8 Gy) of X-rays after transfection. Subsequently, the viability of TE-1 cells was detected using an MTT assay, and the survival fraction of TE-1 cells was observed using a colony formation assay. The apoptotic rate, reactive oxygen species (ROS) content and levels of phosphorylated (p)-histone H2AX at S139 (p-γH2AX) of the cells were detected by flow cytometry. The alterations in mRNA expression levels of nicotinamide adenine nucleotide phosphate oxidase (NOX)1 and NOX5 were detected by reverse transcription-quantitative PCR, while the changes in protein levels of caspase-3, poly(ADP-ribose) polymerase, p-p38, p-ERK1/2 and p-JNK were detected by western blotting. The results revealed that HMGB1 knockdown significantly decreased cell viability, and the apoptosis rate of TE-1 cells transfected with siHMGB1 combined with radiation treatment was increased compared with that in cells with either siHMGB1 transfection or radiation treatment alone. HMGB1 knockdown increased nicotinamide adenine nucleotide phosphate oxidase-mediated ROS production and induced DNA damage via the MAPK signaling pathway, which may promote apoptosis and radiosensitivity after radiation in TE-1 cells. In conclusion, targeting HMGB1 may represent a promising strategy to increase the efficacy of radiation therapy for ESCC.

Novel intergenic KIF5B-MET fusion variant in a patient with gastric cancer: A case report.

BACKGROUND: MET fusion is a key driver mutation, but it is rare in gastric cancer (GC). Several MET (hepatocyte growth factor receptor) inhibitors have been approved for the treatment of MET-positive patients, but the tumor response is heterogeneous. With the development of next-generation sequencing, diverse MET fusion partner genes have been identified. We herein report a fusion variant involving KIF5B-MET in GC. CASE SUMMARY: After thoracoscopic inferior lobectomy plus lymph node dissection under general anesthesia, a "tumor within a tumor" was found in the lung tumor tissue of a 64-year-old non-smoking male patient. Combining the medical history and the results of enzyme labeling, the focal area was considered to be GC. To seek potential therapeutic regimens, an intergenic region between KIF5B and MET fusion was identified. This fusion contains a MET kinase domain and coil-coiled domains encoded by KIF5B exons 1-25, which might drive the oncogenesis. CONCLUSION: Our finding could extend the spectrum and genomic landscape of MET fusions in GC and favor the development of personalized therapy.

Radiomics-based comparison of MRI and CT for differentiating pleomorphic adenomas and Warthin tumors of the parotid gland: a retrospective study.

OBJECTIVE: The objective of this study was to compare the diagnostic performance of magnetic resonance imaging (MRI) and computed tomography (CT) in differentiating pleomorphic adenomas from Warthin tumors using radiomics. STUDY DESIGN: We retrospectively reviewed 626 patients who underwent preoperative MRI or CT for parotid tumor diagnosis. Patient groups were balanced by propensity score matching (PSM) and 123 radiomic features were extracted from tumor images. Radiomic signatures (rad-scores) were generated using a least absolute shrinkage and selection operator logistic regression model. The Canny edge detector was used to define tumor borders (border index). The diagnostic performance of rad-score and border index before and after PSM was evaluated with area under the receiver operating characteristic curve analysis. RESULTS: For differentiation of pleomorphic adenomas and Warthin tumors, rad-score and border index areas under the curve for MRI after PSM were 0.911 (95% confidence interval [CI], 0.871-0.951) and 0.716 (95% CI, 0.646-0.787), respectively; those for CT were 0.876 (95% CI, 0.829-0.923) and 0.608 (95% CI, 0.527-0.690), respectively. Tumor border index on MRI, but not CT, had superior diagnostic performance (P < .05); MRI- and CT-based rad-scores showed similar performance (P >.05). CONCLUSIONS: MRI is superior to CT for tumor margin examination; however, the radiomics features of both modalities showed no difference.

Magnetic resonance image biomarkers improve differentiation of benign and malignant parotid tumors through diagnostic model analysis.

OBJECTIVES: To explore the effectiveness of magnetic resonance image (MRI)-based biomarkers for identifying benign and malignant parotid tumors via diagnostic model analysis. METHODS: This retrospective study included 109 patients (development cohort and validation cohort) who underwent MRI preoperatively, including T1- and T2-weighted images. Parameters based on 2D or 3D texture analysis were extracted from tumor lesions by MaZda software, fisher discriminant and bootstrap method were used to perform parameter reduction, diagnostic models with the selected biomarkers were established along with clinical data, model performance (discrimination and calibration) was furtherly evaluated by internal and external validation, decision curve analysis was applied to measure the improvement of clinical benefits. RESULTS: S(5,5) Entrop, S(0,1) ASM, WavEnHH (s-4), S(1,1,0) Entropy and Perc.10% were significantly associated with the pathological diagnosis of parotid tumor (benign versus malignancy), when adding these biomarkers to the regression analysis, model performance significantly improved in the development cohort (likelihood-ratio-test; p < 0.05, with an increase of AUC from 0.72 (reference model) to 0.85), and these results were maintained in a small external validation cohort. Decision curve analysis indicated that clinical benefit was greater with the application of MRI-based biomarkers. CONCLUSIONS: MRI-based texture analysis is proven to be an effective tool in differentiating benign and malignant parotid tumors, preoperative diagnosis was improved with the selected biomarkers compared to the reference model.

ADCK1 activates the ß-catenin/TCF signaling pathway to promote the growth and migration of colon cancer cells.

As a result of mutations in the upstream components of the Wnt/ß-catenin signaling pathway, this cascade is abnormally activated in colon cancer. Hence, identifying the activation mechanism of this pathway is an urgent need for the treatment of colon cancer. Here, we found an increase in ADCK1 (AarF domain-containing kinase 1) expression in clinical specimens of colon cancer and animal models. Upregulation of ADCK1 expression promoted the colony formation and infiltration of cancer cells. Downregulation of ADCK1 expression inhibited the colony formation and infiltration of cancer cells, in vivo tumorigenesis, migration, and organoid formation. Molecular mechanistic studies demonstrated that ADCK1 interacted with TCF4 (T-cell factor 4) to activate the ß-catenin/TCF signaling pathway. In conclusion, our research revealed the functions of ADCK1 in the development of colon cancer and provided potential therapeutic targets.