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The FHIT gene product is highly expressed in the cytoplasm of renal tubular epithelium and is down-regulated in kidney cancers.

G H Xiao,Fuzi Jin,Andres J. Klein–Szanto,Tamra Goodrow,M. Linehan,Raymond S. Yeung-1997-12-01-PubMed
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TL;DRAbstract

Loss of heterozygosity and homozygous deletion of the 3p14.2 region in human cancers implies the existence of a tumor suppressor gene. One such candidate is the fragile histidine triad (FHIT) gene. To investigate the role of FHIT gene product in tumorigenesis, we generated specific polyclonal antibodies to the human protein and studied its expression in normal and tumor tissues. Immunoblot analysis revealed highly variable expression of pFhit in normal adult human tissues. The highest steady-state level of pFhit was found in kidney and brain, whereas breast, intestine, and skeletal muscle expressed only trace amounts. Within the kidney, the pattern of pFhit immunoreactivity was confined to the tubular epithelium and absent in the glomeruli. Immunofluorescence analysis and biochemical fractionation have sublocalized pFhit to the cytosolic compartment. Compared with normal kidney, pFhit was found to be down-regulated in a subset of primary renal cell carcinoma. Two of 12 renal cell carci

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Loss of heterozygosity and homozygous deletion of the 3p14.2 region in human cancers implies the existence of a tumor suppressor gene. One such candidate is the fragile histidine triad (FHIT) gene. To investigate the role of FHIT gene product in tumorigenesis, we generated specific polyclonal antibodies to the human protein and studied its expression in normal and tumor tissues. Immunoblot analysis revealed highly variable expression of pFhit in normal adult human tissues. The highest steady-state level of pFhit was found in kidney and brain, whereas breast, intestine, and skeletal muscle expressed only trace amounts. Within the kidney, the pattern of pFhit immunoreactivity was confined to the tubular epithelium and absent in the glomeruli. Immunofluorescence analysis and biochemical fractionation have sublocalized pFhit to the cytosolic compartment. Compared with normal kidney, pFhit was found to be down-regulated in a subset of primary renal cell carcinoma. Two of 12 renal cell carci

Keywords

BiologyKidneyLoss of heterozygosityCarcinogenesisTumor suppressor geneGene productPathologyMolecular biology

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