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Lymphoma is one of the most common malignant tumor of the hematologic system. The genome instability is not only an important molecular basis for the development of lymphoma, but also has important value in the diagnosis and prognosis of lymphoma. There are 2 types of genome instability: Microsatellite instability (MSI/MIN) at gene level and chromosomal instability at chromosome level. Through the study on genes associated with lymphoma, the unstable genes associated with lymphoma could be found, meanwhile the mechanism of its occurrence and development of lymphoma could be explored, and the important basis of molecular biology could also be provided in the field of current hot lymphoma precision medical research.
Assuntos
Humanos , Instabilidade Genômica , Linfoma/genética , Instabilidade de Microssatélites , Repetições de Microssatélites , NeoplasiasRESUMO
The link between nonresolving inflammation and cancer is well documented. On the one hand, epidemiologic evidence supports that approximately 25% of all human cancer worldwide is caused by nonresolving inflammation. On the other hand, inflammatory cells are found in the microenvironment of most, if not all, tumors. In the tumor micro-environment, inflammatory cells and molecules influence almost every aspect of cancer. MicroRNAs (miRNAs) participate in the initiation and progression of nonresolving inflammation-related cancer by regulating the key genes and related signaling pathways. Further investigation into the molecular mechanisms by which miRNAs carry out their functions will be of great value in the prevention, early diagnosis, and treatment of tumors.
Assuntos
Humanos , Doença Crônica , Inflamação , Genética , Alergia e Imunologia , Mediadores da Inflamação , Alergia e Imunologia , MicroRNAs , Genética , Neoplasias , Genética , Microambiente TumoralRESUMO
The research team on the National Key Scientific Program of China: "Transcriptomic regulation and molecular mechanism research of polygenic tumor at different stages" has focused on the field of transcriptomics of 4 common polygenic tumors, including nasopharyngeal carcinoma(NPC), breast cancer, colorectal cancer, and glioma. Extensive laboratory work has been carried out on the expression and regulation of tumor transcriptomics; identification of tumor suppressor/susceptible genes; mechanism of tumor epigenetics including miRNAs, and comparative study of specific gene/protein cluster of tumor transcriptomics and proteomics. Genes including SPLUNC1, LTF, BRD7, NOR1, BRCA1/2, PALB2, AF1Q, SOX17, NGX6, SOX7, and LRRC4 have been identified as the key transcriptional regulation genes during the stage of tumor initiation and invasion. Accordingly,the NPC gene signal regulation network of "SPLUNC1-miR-141-target genes", the breast cancer interaction signal pathway of "miR-193b-uPA",the glioma signal network of "miR-381- LRRC4-MEK/ERK/AKT", and the miRNA-target gene network of colorectal cancer metastasis related gene NGX6 have been thoroughly elucidated. These fruitful Results imply that the changes of key molecules in crucial signal pathway will cause severe dysfunction in signal transduction and gene regulation network in polygenic tumors, indicating that in the category of pathogenesis,these tumors may further classify as the "Disease of gene signal transduction and gene regulation network disorder". The researches have laid solid foundation for revealing the molecular mechanism and transcriptomic regulation of polygenic tumors at different stages.
Assuntos
Animais , Humanos , Neoplasias Encefálicas , Genética , Patologia , Neoplasias da Mama , Genética , Patologia , Neoplasias Colorretais , Genética , Patologia , Regulação Neoplásica da Expressão Gênica , Redes Reguladoras de Genes , Glioma , Genética , Patologia , MicroRNAs , Genética , Herança Multifatorial , Neoplasias Nasofaríngeas , Genética , Patologia , Proteínas de Neoplasias , Genética , Estadiamento de Neoplasias , Neoplasias , Genética , Transcrição Gênica , Transcriptoma , Proteínas Supressoras de Tumor , GenéticaRESUMO
Objective To investigate the function and mechanism of miR-149 in nasopharyngeal carcinoma (NPC).Methods The expression of miR-149 was examined by real-time PCR and calculated by 2-△△Ct method. The cell proliferation was analyzed by MTT assay. The cell migration and invasion were shown by the wound healing assay and transwell migration assay, and the expression of E-cadherin was detected by Western blot. Results The expression of miR-149 was higher in NPC cell lines 5-8F and 6-10B than that in normal immortalized nasopharyngeal epithelial NP69. MTT assay showed that miR-149 promoted the proliferation of NPC cell lines. The wound healing assay showed miR-149 promoted the mobility and invasion of NPC cell lines. Inhibition of miR-149 reduced the ability of NPC cell lines to proliferate and invade. miR-149 downregulated the expression of E-cadherin, whereas antagomir which mediated knockdown of miR-149 significantly upregulated the expression of E-cadherin. Conclusion miR-149 might be involved in the invasion and metastasis of NPC through regulation of epithelial-mesenchymal transition (EMT).
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Objective To evaluate the clinical application of the tissue Doppler imaging (TDI) in investigating the cardiac longitudinal systolic function in the patients with type 2 diabetes mellitus. Methods Forty-two patients with type 2 diabetes mellitus and 25 volunteers underwent TDI. The long axis myocardial peak systolic velocity (Sm), displacement (Dm) and strain rates (SRs) of 18 segments in different left ventricular walls were measured.Results The Dm and SRs of left ventricular wall in diabetic group dramatically decreased (P<0.01). Meanwhile, the diabetic combined hypertension group had much lower Sm of ventricular middle segments than the control group (P<0.05).Conclusion The stain rate and tissue tracking are sensitive and reliable to evaluate the early local cardiac systolic function in the patients with diabetes mellitus. TDI can be used as an noninvasive method to detect early systolic dysfunction.
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OBJECTIVE@#To identify the function of neural cell adhesion molecule (NCAM) mutation in the genesis of human glioma.@*METHODS@#Mutations were found through polymerase chain reaction-single strand conformation polymorphism, and then the changed DNA fragments were purified and multiplied and sent to Shanghai for sequencing. Blast and ORF finder were used to find out the amino changes in NCAM.@*RESULTS@#An A-C transversion was found at position 1 126 in NCAM's 7 exon in a patient with glioblastoma from 43 astrocytoma.@*CONCLUSION@#Structural change in the protein caused by point mutation may be the reason for tumorigenesis of astrocytoma.