Disease relevance of Liver Neoplasms

• Risk of cirrhosis and primary liver cancer in alpha 1-antitrypsin deficiency [1].
• Concurrent feeding of phenobarbital and DENA for 10 weeks produced cancer of the liver in 77 percent of the animals, but only 9 percent had metastases in the lung [2].
• Highly elevated levels of immunoreactive gamma GT were detected in the sera of patients with primary hepatoma, metastatic liver cancer, pancreatic cancer, and certain types of lung cancer [3].
• Issues of safety are under constant review, but justified concerns about high doses of tamoxifen acting as a promoter of liver cancer in rats or as a promoter of endometrial cancer in women have not, as yet, proved to be of clinical relevance [4].
• Inhibition of 4-hydroxyphenylpyruvate dioxygenase may prevent the development of liver cirrhosis and abolish or diminish the risk of liver cancer [5].

Psychiatry related information on Liver Neoplasms

• These results, although confirming that age is a risk factor for hepatocellular carcinoma in cirrhosis, indicate that alcohol abuse, male sex, and concurrent hepatitis B and C virus infection do not involve a higher risk of developing liver cancer [6].

High impact information on Liver Neoplasms

• We investigated whether IKKbeta is involved in chemically induced liver cancer, a model not involving overt inflammation [7].
• The adult FAH-/- mouse will serve as useful model for studies of the pathophysiology and treatment of hereditary tyrosinaemia type I as well as hepatic cancer [8].
• Functional inactivation but not structural mutation of p53 causes liver cancer [9].
• A high alpha-fetoprotein value at enrollment was also a risk marker for liver cancer [10].
• Control rats treated with nitrite only, or untreated, did not develop liver neoplasms [11].

Chemical compound and disease context of Liver Neoplasms

• We conclude that aminopyrine metabolism is depressed in most patients with hepatic neoplasm and that the ABT affords a useful method for detecting malignant tumors of the liver [12].
• Thorium dioxide and liver cancer [13].
• Administration of phenobarbital, begun 1 week after cessation of DENA intake and terminated at week 20, led to liver cancer in 64 percent of the rodents [2].
• No liver cancers or increase in colon, rectal, ovarian, or other tumors was observed in the tamoxifen group [14].
• Survey of thorotrast-associated liver cancers in Japan [15].

Biological context of Liver Neoplasms

• Disruption of beta-catenin pathway or genomic instability define two distinct categories of liver cancer in transgenic mice [16].
• The deleted in liver cancer 2 (DLC2) gene, located at chromosome 13q12.3, is a recently identified tumor suppressor gene [17].
• Transfection of the cDNA into PLC/PRF/5 liver cancer cells resulted in reduced cell-cell adhesiveness, based on both morphology and results of Ca(2+)-dependent cell aggregation assay [18].
• We followed the expression of several glutathione S-transferase subunits in altered foci, liver neoplasms and metastases produced in male Fischer 344 rats by a modified Solt-Farber protocol, to determine whether components of the resistant phenotype are lost during neoplastic progression [19].
• Rho GTPase-activating protein deleted in liver cancer suppresses cell proliferation and invasion in hepatocellular carcinoma [20].

Anatomical context of Liver Neoplasms

• RESULTS: With 62 liver cancers and 128 nonhepatobiliary cancers, patients with HH were at a 20-fold risk of liver cancer (SIR, 21; 95% confidence interval [CI], 16-22) but an almost unaltered risk of all other cancers (SIR, 1.2; 95% CI, 1.0-1.4), including nonelevated risks for several gastrointestinal tract cancers [21].
• In the in vitro MTT assay, cPrG-HCl inhibited the growth of 6 liver cancer cell lines (Huh-7, HCC-M, HCC-T, dRLh-84, and H-35, hepatocellular carcinoma; HepG2, hepatoblastoma) in a dose- and time-dependent manner [22].
• The increase of IGF-II mRNA in some liver cancers is consistent with an autocrine mechanism conferring a selective growth advantage to tumorous liver cells [23].
• After exclusion of study subjects exposed to Thorotrast, no association was seen between treatment with phenobarbital and cancer of the liver (odds ratio, 1.0; 95% confidence interval, 0.1-8.0) or biliary tract (odds ratio, 0.8; 95% confidence interval, 0.1-4.2) [24].
• The epithelial cell adhesion molecule CEACAM1 (carcinoembryonic antigen cell adhesion molecule-1) is down-regulated in colon, prostate, breast, and liver cancer [25].

Gene context of Liver Neoplasms

• The Cul4A gene is amplified in human breast and liver cancers, and loss-of-function of Cul4 results in the accumulation of the replication licensing factor CDT1 in Caenorhabditis elegans embryos and ultraviolet (UV)-irradiated human cells [26].
• BACKGROUND & AIMS: Wnt/beta-catenin activation is observed in normal liver development, regeneration, and liver cancer [27].
• We showed a switch from MAT1A to MAT2A gene expression in human liver cancer cells that may offer a growth advantage [28].
• Genotypic and phenotypic characterization of a putative tumor susceptibility gene, GNMT, in liver cancer [29].
• In conclusion, in liver cancers ADAM9 and ADAM12 expression is associated with tumor aggressiveness and progression [30].

Analytical, diagnostic and therapeutic context of Liver Neoplasms

• An enzyme immunoassay for anti-HCV was used to test serum taken from 185 cases with HCC, 35 cases with metastatic liver cancer (MLC), and 432 hospital controls [31].
• Aminopyrine metabolism was assessed by the aminopyrine breath test (ABT) in 153 patients with malignant disease, of whom 75 had hepatic neoplasm and 78 had none [12].
• Early diagnosis of hepatocellular carcinoma remains a key goal in improving the poor prognosis of this form of liver cancer [32].
• METHODS: We compared the expression of GS messenger RNA (mRNA) and protein in tumorous and nontumorous liver from 34 patients with primary liver cancers, using a combination of Northern blot, dot blot, western blot, and determination of GS enzyme activity [33].
• Promotion of liver cancer development by brief exposure to dietary 2-acetylaminofluorene plus partial hepatectomy or carbon tetrachloride [34].

References