Lack of albumin as genotypic marker of preneoplastic analbuminemic rat hepatocytes transplanted within albumin-positive liver.
نویسندگان
چکیده
In analbuminemic rats, preneoplastic hepatocytes lack the capability to produce albumin. On the other hand, the hepatocytes of F1 hybrids born from parents of analbuminemic rats and normal rats retain their capability to produce albumin, since the analbuminemia is inherited as a recessive trait in rats. We isolated hyperplastic nodule cells from Nagase's analbuminemic rats and transplanted them into the livers of F1 hybrid rats by infusion into the mesenteric vein. The host rats were subjected to a short term dietary 2-acetylaminofluorene and underwent a two-thirds partial hepatectomy to promote the growth of preneoplastic hepatocytes. Within 10 to 13 days after transplantation, may albumin-negative hepatocytic nodules were formed in the albumin-positive host livers. Almost all the albumin-negative nodules expressed conventional biochemical markers for preneoplastic hepatocytes. Eight to 9 weeks after the transplantation, almost the same number of albumin-negative nodules were observed as on days 10-13. However, roughly a half of the albumin-negative nodules showed no biochemical markers. The results indicate that the majority of early preneoplastic lesions revert to become phenotypically normal after removal of the promoting stimuli.
منابع مشابه
Phenotypic reversion in analbuminemic rats due to an altered splicing mechanism
Serum albumin is regarded as an important and indispensable protein, but analbuminemic rats established by Sumi Nagase in 1977 seems to exhibit few symptoms in spite of an almost total lack of albumin in the serum. The albumin gene of analbuminemic rats was found to have a seven-base-pair deletion in an intron, close to exon-intron junction, resulting in the formation of non-functional mRNA in ...
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ورودعنوان ژورنال:
- Cancer research
دوره 48 2 شماره
صفحات -
تاریخ انتشار 1988