Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 58-year-old 79 kg male with metastatic liver cancer was scheduled for hepatectomy. Preoperative examination did not reveal any hemostatic abnormalities. Nine hours into the surgery, a vascular clip attached to the middle hepatic vein was disconnected and rapid bleeding followed. Unscheduled intraoperative cell salvage was employed. Despite surgical hemostasis as well as transfusion with fresh frozen plasma and platelets, significant oozing persisted for 10 hours, and cumulative blood loss amounted to 30,000 ml. Therefore, we administered fibrinogen products and recombinant activated factor VLL (rFVIIa, NovoSeven), a potent hemostatic initiator used in treating congenital factor VII deficient patients. After injecting 5 mg of rFVIIa, the bleeding was controlled almost immediately, and the surgery was completed within an hour. Although postoperative computed tomography detected subclinical but extensive thrombosis in the middle hepatic vein, the inferior vena cava, and the deep femoral veins, the thrombus spontaneously dissolved within seven months postoperatively. There was no evidence of metastatic disease 24 months postoperatively. Off-label use of rFVIIa and intraoperatively salvaged autologous blood transfusions are life-saving procedures for cancer patients who have massive bleeding during surgery, although we cannot completely exclude the possibility of serious postoperative thrombotic events and/or hematogenous cancer dissemination.
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PMID:[Successful Anesthetic Management of a Patient with Critical Bleeding during Hepatectomy Using Recombinant Activated Factor VII and Intraoperative Blood Salvage]. 2643 63

Background: Lung adenocarcinoma has a strong tendency to develop into bone metastases, especially spinal metastases (SM). Long noncoding RNAs (lncRNAs) play critical roles in regulating several biological processes in cancer cells. However, the mechanisms underlying the roles of lncRNAs in the development of SM have not been elucidated to date. Methods: Clinical specimens were collected for analysis of differentially expressed lncRNAs. The Kyoto Encyclopedia of Genes and Genomes (KEGG) was used to examine the effects of these genes on pathways. RNA pull-down was utilized to identify the targeting protein of lncRNAs. The effects of lncRNA on its target were detected in A549 and SPCA-1 cells via perturbation of the lncRNA expression. Oncological behavioral changes in transfected cells and phosphorylation of kinases in the relevant pathways, with or without inhibitors, were observed. Further, tumorigenicity was found to occur in experimental nude mice. Results: LINC00852 and the mitogen-activated protein kinase (MAPK) pathway were found to be associated with SM. Moreover, the LINC00852 target S100A9 had a positive regulatory role in the progression, migration, invasion, and metastasis of lung adenocarcinoma cells, both in vitro and in vivo. Furthermore, S100A9 strongly activated the P38 and REK1/2 kinases, and slightly activated the phosphorylation of the JNK kinase in the MAPK pathway in A549 and SPCA-1 cells. Conclusion: LINC00852 targets S100A9 to promote progression and oncogenic ability in lung adenocarcinoma SM through activation of the MAPK pathway. These findings suggest a potential novel target for early intervention against SM in lung cancer.
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PMID:LINC00852 Promotes Lung Adenocarcinoma Spinal Metastasis by Targeting S100A9. 3051 13