HIF1α mRNA expression in hepatocellular carcinoma (HCC) tissues and its relationship with the prognosis in HCC patients is still unclear. We performed this study to investigate the expression of HIF1α mRNA and its correlation with the prognosis in HCC patients.GSE14520 and Oncomine database were used to analyse the differential expression of HIF1α mRNA among HCC tissues and corresponding peritumour tissues or normal liver tissues. The relationship between HIF1α mRNA expression and the clinicopathological features and survival in HCC patients was analysed using the GSE14520 dataset. CCK-8 assay, wound-healing assay, transwell invasion assay, tube formation assay, and subcutaneous xenograft tumour assays using nude mice were used to confirm the function of HIF1α.Expression of HIF1α mRNA was significantly upregulated in HCC tissues (P<0.05 in all cases); this was supported by the results of the Western blotting (P=0.031) and IHC analyses. Our analysis of the clinicopathological features of HCC patients indicated that high HIF1α mRNA expression was strongly related with TNM stage III (P=0.002) and BCLC stage C (P=0.038). Survival analysis demonstrated that HCC patients with high HIF1α mRNA expression had a short overall survival (OS) (P=0.048), but showed no significant difference in recurrence-free survival (RFS) (P=0.066) compared to patients with low HIF1α mRNA expression. We further demonstrated that HIF1α promoted the proliferation, migration, invasion, and angiogenic ability of HCC cells, by using the stably transformed SK-Hep1 and Hep-3B cell lines showing HIF1α overexpression. Finally, xenograft tumour models of nude mice showed that RNA interference-mediated HIF1α silencing suppressed tumour growth and angiogenesis in HCC.Our study suggests that the upregulation of HIF1α mRNA, which is found in HCC tissues and associated with poor prognosis in HCC patients, contributed to the proliferation, migration, invasion, and angiogenic ability of HCC cells.
Rectal cancer is one of the most common malignant tumors and has a high incidence rate and fatality rate. Accurate preoperative T staging of rectal cancer is critical for the selection of appropriate rectal cancer treatment. Various pre-operative imaging methods are available, and the identification of the most accurate method for clinical use is essential for patient care. We investigated the value of biplane transrectal ultrasonography (TRUS) combined with MFI in preoperative staging of rectal cancer and explored the value of combining TRUS plus MFI with CEA/CA199 and MRI.A total of 87 patients from Daping Hospital with rectal cancer who underwent TRUS examination plus MFI were included. Grades of MFI were determined by Alder classification. Among the total patients, 64 underwent MRI and serum CEA/CA199 tests additionally within one week of TRUS. Pathological results were used as the gold standard for cancer staging. Concordance rates between TRUS, MRI, and CEA/CA199 for tumors at different stages were compared.There were no significant differences between the Alder classification and pathological T staging. The concordance rate of TRUS and MFI for rectal cancer T staging was 72.4% (K = 0.615, p < 0.001). Serum CEA and CA199 levels were significantly different in tumors at different stages and increased progressively by pathological stage (p < 0.001); the accuracy rate was 71.88% (K = 0.599, p < 0.001), while that of MRI was 51.56% (K = 0.303, p < 0.001), indicating that TRUS had higher consistency in the preoperative T staging of rectal cancer. The combination of TRUS, MRI, and CEA/CA199 yielded an accuracy rate of 90.6%, which was higher than that of any method alone.Preoperative T staging of rectal cancer from biplane TRUS plus MFI was highly consistent with postoperative pathological T staging. TRUS combined with MRI and serum CEA/CA199 had a greater value in the diagnosis of rectal cancer and a higher diagnostic rate than any examination alone.
Objective
To evaluate the application values of diffusion tensor tractography (DTT) combined with neuronavigation in microsurgery of insular gliomas.
Methods
The clinical data of 27 patients with insular gliomas, admitted to our hospital from March 2013 to October 2017, were analyzed retrospectively. All DTT images were transferred to the neuronavigation system, and the three-dimensional location of tumors and pyramidal tracts were re-constructed. Surgical approaches were designed and excision scopes were defined before the surgery. Techniques on how to distinguish and protect the key blood vessels and pyramidal tracts were discussed. The treatment efficacies were analyzed.
Results
Total lesion resection was achieved in 22 patients (81.5%), subtotal resection in 4 (14.8%), and partial resection in one (3.7%). Postoperative pathology indicated 7 were oligodendrogliomas, and 20 were astrocytomas, including WHO grade I in one, grade II in 18, and grade III in one. One patient had transient aphasia (recovery after two weeks), 2 experienced worsened hemiplegia on opposite side of their bodies (normal after one month), and the left 24 patients remained intact function after operation.
Conclusions
The combination of DTT and neuronavigation is safe and effective in surgical treatment for insular gliomas, which can protect the brain function at greatest degree and maximize lesion resection, and improve the postoperative quality of life.
Key words:
Neuronavigation; Diffusion tensor tractography; Insular; Glioma; Microsurgery
The Copper Metabolism MURR1 Domain (COMMD) family proteins are known to play roles in promoting or inhibiting the proliferation, migration and invasion of tumor cells. However, the role of COMMD3 in hepatocellular carcinoma are still unclear. By investigating the TCGA datasets, we found that the mRNA expression of COMMD3 was significantly upregulated in hepatocellular carcinoma tissue compared with normal liver tissue, which was further supported by Oncomine dataset, Western blot, qRT-PCR, and IHC analysis. Moreover, Kaplan-Meier survival analysis showed that the high expression of COMMD3 was associated with poor overall survival (OS) and disease-free survival (DFS). Consistently, the clinic-pathological analysis found that the overexpression of COMMD3 was correlated with advanced TNM stage, advanced T stage and vascular invasion. By performing multivariate analysis, we found that the expression of COMMD3 was an independent influencing factor on OS and DFS. Furthermore, we knocked down COMMD3 in HCC cells via RNA interference. The results showed that silencing COMMD3 could inhibit the migration, invasion, and angiogenesis of HCC cells. Finally, we established xenograft tumor model in nude mice, and the knockdown of COMMD3 suppressed tumor growth and angiogenesis. In summary, our study showed that the high expression of COMMD3 was correlated with poor prognosis in HCC patients and contributed to migration, invasion and angiogenesis of HCC cells.
Abstract Extracellular vesicles (Evs) participate in the development of rheumatoid arthritis (RA), but the mechanisms remain unclear. This study aimed to determine the mechanism by which microRNA‐34a (miR‐34a) contained in bone marrow mesenchymal stem cell (BM‐MSC)‐derived Evs functions in RA fibroblast‐like synoviocytes (RA‐FLSs). BM‐MSC‐derived Evs and an Evs inhibitor were extracted. A rat model of RA was established. miR‐34a gain‐ and loss‐of‐function experiments were performed, and the inflammation in rat synovial fluid and tissues was detected. The role of miR‐34a in RA‐FLSs was also measured in vitro. The target gene of miR‐34a was predicted using the online software TargetScan and identified using a dual‐luciferase reporter gene assay, and the activation of the ATM/ATR/p53 signalling pathway was assessed. BM‐MSC‐derived Evs mainly elevated miR‐34a expression, which reduced RA inflammation in vivo and inhibited RA‐FLS proliferation and resistance to apoptosis in vitro, while inhibited miR‐34a expression enhanced RA development. In addition, miR‐34a could target cyclin I to activate the ATM/ATR/p53 signalling pathway, thus inhibiting abnormal RA‐FLS growth and RA inflammation. Our study showed that miR‐34a contained in BM‐MSC‐derived Evs could reduce RA inflammation by inhibiting the cyclin I/ATM/ATR/p53 signalling pathway.
Thyroid cancer has low incidence and mortality. While metastatic cancer is the most common type of intracranial cancer, patients with intracranial metastases from thyroid cancer very rarely present with seizures. Here, we describe a case study and review the neurological symptoms and histopathology of intracranial metastases from thyroid cancer.A 38-year-old woman was diagnosed with intracranial metastases from papillary thyroid cancer, with the chief symptom being generalized seizures. The bilateral frontal masses were completely resected in 2 operations, after which the patient was treated with whole-brain radiotherapy and tyrosine kinase inhibitors (TKIs). It has now been over 13 years since thyroid cancer resection and 51 months since she was diagnosed with intracranial metastases from papillary thyroid cancer. The long-term survival might be due to the effective and prompt treatment. Through literature review, we found the incidence of intracranial metastases from different subtypes of thyroid cancer to be inconsistent with epidemiological findings in thyroid cancer.Intracranial metastases of thyroid cancer should be considered when the patient has a history of thyroid cancer with seizures. A combination of surgery, radiation therapy, and TKI drugs may prolong survival.
Myeloid neoplasms (MN) tend to relapse and deteriorate. Exploring the genomic mutation landscape of MN using next-generation sequencing (NGS) is a great measure to clarify the mechanism of oncogenesis and progression of MN.This multicenter retrospective study investigated 303 patients with MN using NGS from 2019 to 2021. The characteristics of the mutation landscape in the MN subgroups and the clinical value of gene variants were analyzed.At least one mutation was detected in 88.11% of the patients (267/303). TET2 was the most common mutation in the cohort, followed by GATA2, ASXL1, FLT3, DNMT3A, and TP53. Among patients with myeloid leukemia (ML), multivariate analysis showed that patients aged ≥60 years had lower overall survival (OS, p = 0.004). Further analysis showed TET2, NPM1, SRSF2, and IDH1 gene mutations, and epigenetic genes (p < 0.050) presented significantly higher frequency in older patients. In patients with myelodysplastic syndrome (MDS) and myelodysplastic neoplasms (MPN), univariate analysis showed that BCORL1 had a significant impact on OS (p = 0.040); however, in multivariate analysis, there were no factors significantly associated with OS. Differential analysis of genetic mutations showed FLT3, TP53, MUC16, SRSF2, and KDM5A mutated more frequently (p < 0.050) in secondary acute myeloid leukemia (s-AML) than in MDS and MPN. TP53, U2AF1, SRSF2, and KDM5A were mutated more frequently (p < 0.050) in s-AML than in primary AML. KDM5A was observed to be restricted to patients with s-AML in this study, and only co-occurred with MUC16 and TP53 (2/2, 100%). Another mutation was MUC16, and its co-occurrence pattern differed between s-AML and AML. MUC16 mutations co-occurred with KDM5A and TP53 in 66.7% (2/3) of patients with s-AML and co-occurred with CEBPA in 100% (4/4) of patients with AML.Our results demonstrate different genomic mutation patterns in the MN subgroups and highlight the clinical value of genetic variants.
In order to identify the relationship between telomerase and the biological effect of radiation injury, and investigate the role of human telomerase catalytic subunit gene (hEST2) reverse transcriptase(RT) segment in the expression of telomerase activity.Tumor HeLa cells, KB cells and A431 cells were employed to measure the change in telomerase activity after 60Co-ray irradiation at RNA level and protein level. Quantitative PCR and Northern blotting were used to determine the expression of hEST2 RT segment that encodes seven motifs of the human telomeres, a PCR-based telomeric repeat amplification protocol (TRAP) was used to assay telomerase activity after exposure to radiation.Both of telomerase activity and the expression hEST2 RT segment were decreased with increasing dosage of radiation. In addition, testing the expression of motifs domain is similar to the measurement of telomerase activity.The detection of the hEST2 RT segment by Northern blotting and quantitative PCR are new methods for testing telomerase activity. Furthermore, radiation can cause a dose-dependent decrease in telomerase activity. The effect of radiation on telomerase is one possible reason for the death of cancer cells after irradiation.
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