The relationship of cyclin-dependent kinase inhibitor 3 (CDKN3) with tumours has previously been presented in a number of publications. However, the molecular network and interpretation of CDKN3 through the cell cycle between non-malignancy associated hepatitis/cirrhosis and hepatocellular carcinoma (HCC) have remained to be elucidated. Here, we have constructed and analysed significant high expression gene CDKN3 activated and inhibited cell cycle networks from 25 HCC versus 25 non-malignancy associated hepatitis/cirrhosis patients (viral infection HCV or HBV) in GEO Dataset GSE10140-10141, by combination of a gene regulatory network inference method based on linear programming, and decomposition procedure using CapitalBio MAS 3.0 software, based on integration of public databases including Gene Ontology, KEGG, BioCarta, GenMapp, Intact, UniGene, OMIM, and others. Comparing the same and differently activated and inhibited CDKN3 networks with GO analysis, between non-malignancy associated hepatitis/cirrhosis and HCC, our results suggest a CDKN3 cell cycle network (i) with stronger DNA replication and with weaker ubiquitin-dependent protein catabolism as common characteristics in both non-malignancy associated hepatitis/cirrhosis and HCC; (ii) with more cell division and weaker mitotic G2 checkpoint in non-malignancy associated hepatitis/cirrhosis; (iii) with stronger cell cycle and weaker cytokinesis, as a result forming multinucleate cells in HCC. Thus, it is useful to identify CDKN3 cell cycle networks for comprehension of molecular mechanism between non-malignancy associated hepatitis/cirrhosis and HCC transformation.
The aim is to setup single distinguished molecular network. We constructed FOS proliferating network from 22 colorectal samples of the same GEO dataset by GRNInfer tool and DAVID based on linear programming and a decomposition procedure with integrated Kappa statistics and fuzzy heuristic clustering. In the control, we found no proliferating subnetwork. In CRC, we identified one FOS proliferating module (SFRP2, ADAMTS1, SYNPO2, VIP, ADAM33 inhibition to FOS and MGP, FOSB activation to FOS. FOS activation to IGFBP5, LGI1, GAS1 and FOS inhibition to VIP). These results may be useful for developing novel prognostic markers and therapeutic targets in CRC.
Single-photon emission computed tomography/computed tomography should be included in the differential diagnoses when lesions show elevated technetium Tc 99m-labeled methylene diphosphonate uptake on WBS. Compared with a WBS alone, a more accurate diagnosis of IF can be obtained using SPECT/CT, which resulted not only in fewer equivocal lesions but also in a higher diagnostic accuracy.
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