Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rous sarcomas were induced in 6-week-old chickens of several genetically different stocks: inbred lines C, 6(1), 6(3), and 7(2); crosses of inbred lines (6(3) X 7(2)) F4 and (6(1) X 15(1)) F2 X 6(1); and reciprocal crosses (15(1) X 100) F1 X 15(1) and (15(1) X 100) F1 X 100. The resulting tumors were scored for size six times during a 10-week period. Females that had completely regressed their sarcomas were placed in individual laying cages and examined weekly for reappearance of a tumor. After death, the probable cause was determined by necropsy. The major causes of death in the pooled sample of 49 females were fatty liver hemorrhagic syndrome (24.6%), reproductive disorder (14.2%), Marek's disease (12.2%), and lymphoid leukosis (6.1%). Elapsed time between tumor regression and death from any cause ranged from 21 days to 1930 days (5.3 years). One tumor recurred, this in a bird which eventually died with a massive sarcoma in the left wingweb and Rous metastasis in liver tissue. These data provide evidence of specific resistance to neoplastic disease.
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PMID:Causes of mortality in chickens that regressed a Rous sarcoma virus-induced tumor. 301 Feb 65

Insulin resistance is associated with increased incidence and enhanced progression of cancers. However, little is known about strategies that can effectively ameliorate insulin resistance and consequently halt cancer progression. Herein, we propose that the transcription factor Nrf2 (also known as Nfe2l2) may be such a target, given its central role in disease prevention. To this end, we developed a mouse that overexpresses the Notch intracellular domain in adipocytes (AdNICD), leading to lipodystrophy-induced severe insulin resistance and subsequent development of sarcomas, as a model reflecting that Notch signaling is deregulated in cancers and shows positive associations with insulin resistance and fatty liver disease in humans. Nrf2 pathway activation was achieved by knocking down Keap1, a repressor of Nrf2, in the AdNICD background. Constitutively enhanced Nrf2 signaling in this setting led to prevention of hepatic steatosis, dyslipidemia, and insulin resistance by repressing hepatic lipogenic pathways and restoration of the hepatic fatty acid profile to control levels. This protective effect of Nrf2 against diabetes extended to significant reduction and delay in sarcoma incidence and latency. Our study highlights that the Nrf2 pathway, which has been induced by small molecules in clinical trials, is a potential therapeutic target against insulin resistance and subsequent risk of cancer.
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PMID:Nrf2 prevents Notch-induced insulin resistance and tumorigenesis in mice. 2951 34