Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001511 (Adhesion)
 5,955 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The use of percutaneous transcatheter hepatic arterial chemotherapy and embolization in the treatment of primary liver cancer has become increasingly popular in recent years. The authors employed this method, using a combination of cisplatin, mitomycin C, 5-fluorouracil, and ethiodized oil (Lipiodol) or absorbable gelatin sponge in 30 patients with huge liver cancers (diameter range, 5.6-12.0 cm) as a preliminary treatment before liver resection. Significant tumor regression occurred after this treatment, converting these tumors into resectable lesions that were excised successfully later. Before surgery, chemoembolization was done once every 4-6 weeks. The patients underwent 1-5 treatment sessions (mean, 2.9) and then waited 1-4 months (mean, 2.4 months) before undergoing surgery. Alpha-fetoprotein levels decreased to normal in seven patients. The tumor diameters were reduced by 31.6 +/- 15.2% (2.3 +/- 1.2 cm) and the percent tumor necrotic area ranged from 40-100%. Adhesions of the tumor to the diaphragm and thickening of the hepatoduodenal ligament and gallbladder wall were the primary operative findings, but they did not significantly complicate the surgery. There was one postoperative death from acute pulmonary embolism. The 1-year, 2-year, and 3-year survival rates were 88.89%, 77.03%, and 77.03%, respectively. Although these patients still are being followed to assess their long-term survival, this treatment appears promising for patients with advanced huge liver cancers who hitherto have been denied surgery on grounds of unresectability.
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PMID:Experience with liver resection after hepatic arterial chemoembolization for hepatocellular carcinoma. 838 Jan 23

Several abnormalities in the immune status of patients with hereditary haemochromatosis (HH) have been reported, suggesting an imbalance in their immune function. This may include persistent production of, or exposure to, altered immune signalling contributing to the pathogenesis of this disorder. Adhesion molecules L-, E- and P-Selectin, intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) are some of the major regulators of the immune processes and altered levels of these proteins have been found in pathological states including cardiovascular diseases, arthritis and liver cancer. The aim of this study was to assess L-, E- and P-Selectin, ICAM-1 and VCAM-1 expression in patients with HH and correlate these results with HFE mutation status and iron indexes. A total of 139 subjects were diagnosed with HH (C282Y homozygotes = 87, C282Y/H63D = 26 heterozygotes, H63D homozygotes = 26), 27 healthy control subjects with no HFE mutation (N/N), 18 normal subjects heterozygous for the H63D mutation served as age-sex-matched controls. We observed a significant decrease in L-selectin (P = 0.0002) and increased E-selectin and ICAM-1 (P = 0.0006 and P = 0.0059) expression in HH patients compared with healthy controls. This study observes for the first time that an altered adhesion molecules profile occurs in patients with HH that is associated with specific HFE genetic component for iron overload, suggesting that differential expression of adhesion molecules may play a role in the pathogenesis of HH.
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PMID:Highly sensitivity adhesion molecules detection in hereditary haemochromatosis patients reveals altered expression. 2019 33

Hepatocellular carcinoma (HCC) is the fifth most common solid tumor in the world and the third leading cause of cancer-associated deaths. A Sleeping Beauty-mediated transposon mutagenesis screen previously identified mutations that cooperate with MYC to accelerate liver tumorigenesis. This revealed a tumor suppressor role for Steroid Receptor Coactivator 2/Nuclear Receptor Coactivator 2 (Src-2/Ncoa2) in liver cancer. In contrast, SRC-2 promotes survival and metastasis in prostate cancer cells, suggesting a tissue-specific and context-dependent role for SRC-2 in tumorigenesis. To determine if genetic loss of SRC-2 is sufficient to accelerate MYC-mediated liver tumorigenesis, we bred Src-2-/- mice with a MYC-induced liver tumor model and observed a significant increase in liver tumor burden. RNA sequencing of liver tumors and in vivo chromatin immunoprecipitation assays revealed a set of direct target genes that are bound by SRC-2 and exhibit downregulated expression in Src-2-/- liver tumors. We demonstrate that activation of SHP (Small Heterodimer Partner), DKK4 (Dickkopf-4), and CADM4 (Cell Adhesion Molecule 4) by SRC-2 suppresses tumorigenesis in vitro and in vivo. These studies suggest that SRC-2 may exhibit oncogenic or tumor suppressor activity depending on the target genes and nuclear receptors that are expressed in distinct tissues and illuminate the mechanisms of tumor suppression by SRC-2 in liver.
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PMID:SRC-2-mediated coactivation of anti-tumorigenic target genes suppresses MYC-induced liver cancer. 2964 18