Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0345904 (liver cancer)
 15,188 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The observation of cancer in an individual does not identify the causative agent(s). However, epidemiological data on populations do indicate that a large fraction of human cancers are associated with lifestyle/diet. Such studies may also help identify the etiologic agents but unless there are good dose-response data for humans and/or animal models, the probability of identifying the agent is not high. Cancers may result from endogenous reactions, such as oxidations or from exogenous agents, such as tobacco smoke (lung cancer), sunlight exposure (skin cancer), aflatoxin (liver cancer), and relatively high doses of ionizing radiations (many types of cancers). Many carcinogenic chemicals have been identified in the workplace but, they usually do not affect the overall population. Most cancer causing agents affect cellular DNA and change its coding specificity and act as cancer initiators. The repair of DNA damage ameliorates most of these endogenous and exogenous changes. The important role of DNA repair in controlling the induction of human cancer came from the observation that individuals with the skin cancer-susceptible, human disease xeroderma pigmentosum (XP) were defective in nucleotide excision repair. Endogenous DNA damages are usually damages to individual bases and are usually repaired by systems of glycosylases and endonucleases. It should be useful to investigate the rates of appearance of tumors in normal mice and in mice knocked out for specific repair enzymes because such mice could be used to test the roles of diet and caloric input in affecting particular types of endogenous damages.
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PMID:Human cancer: etiologic agents/dose responses/DNA repair/cellular and animal models. 1137 81

We have previously isolated and characterized a novel human gene HUEL (C4orf1) that is ubiquitously expressed in a wide range of human fetal, adult tissues and cancer cell lines. HUEL maps to region 4p12-p13 within the short arm of chromosome 4 whose deletion is frequently associated with bladder and other carcinomas. Here we present the genomic organization, sizes and boundaries of exons and introns of HUEL. The GC-rich upstream genomic region and 5' untranslated region (UTR) together constitute a CpG island, a hallmark of housekeeping genes. The 3250 bp HUEL cDNA incorporates a 1704 bp ORF that translates into a hydrophilic protein of 568-amino acids (aa), detected as a band of approximately 70 kDa by Western blotting. We have isolated the murine homolog of HUEL which exhibits 89% nucleotide and 94% amino acid identity to its human counterpart. The HUEL protein shares significant homology with the minimal DNA-binding domain (DNA-BD) of the DNA repair protein encoded by the xeroderma pigmentosum group A (XPA) gene. Other notable features within HUEL include the putative nuclear receptor interaction motif, nuclear localization and export signals, zinc finger, leucine zipper and acidic domains. Mimosine-mediated cell cycle synchronization of PLC/PRF/5 liver cancer cells clearly portrayed translocation of HUEL into the nucleus specifically during the S phase of the cell cycle. Yeast two-hybrid experiments revealed interactions of HUEL with two partner proteins (designated HIPC and HIPB) bearing similarity to a mitotically phosphorylated protein and to reverse transcriptase. Co-immunoprecipitation assays validated the interaction between HUEL and HIPC proteins in mammalian cells. HUEL is likely to be an evolutionarily conserved, housekeeping gene that plays a role intimately linked with cellular replication, DNA synthesis and/or transcriptional regulation.
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PMID:The novel human HUEL (C4orf1) protein shares homology with the DNA-binding domain of the XPA DNA repair protein and displays nuclear translocation in a cell cycle-dependent manner. 1190 20