Functional markers and growth behavior of preneoplastic hepatocytes.
نویسنده
چکیده
Functional markers and growth behavior of abnormal hepatocytes at several stages of liver carcinogenesis were studied. Early lesions, i.e., hyperplastic foci and areas, did not accumulate iron in siderotic livers, had persistent glycogen stores, were not more agglutinable by concanavalin A, and were associated with alpha-fetoprotein secretion, but were not independent secretors of high amounts. The cells in the early lesions had an increased mitotic index, but cells from livers with early lesions did not have an increased survival in cell culture or the ability to grow in soft agar. The more developed lesions, hyperplastic nodules, also did not store iron, had persistent glycogen, did not display increased concanavalin A agglutinability, and were not independent secretors of high levels of alpha-fetoprotein. Similarly, nodule cells were proliferative but did not display an increase in survival in cell culture. In addition, both iso- and autotransplantation of nodules into mammary fat pads resulted in persistence but not growth of nodule cells. On the other hand, hepatocellular carcinomas regularly grew upon transplantation. Thus, early lesions and hyperplastic nodules were proliferative lesions did not possess autonomous growth capability comparable to that of hepatocellular carcinomas.
منابع مشابه
Lack of albumin as genotypic marker of preneoplastic analbuminemic rat hepatocytes transplanted within albumin-positive liver.
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...
متن کاملLow selection of preneoplastic hepatocytes after treatment with the 2-acetylaminofluorene diet-partial hepatectomy regimen in the liver of hepatocarcinogenesis-resistant DRH strain rats.
In hepatocarcinogenesis-resistant DRH rats, preneoplastic hepatocytic lesions are smaller than those of usual rats during carcinogenesis. When preneoplastic hepatocytes from DRH and Donryu (original strain of DRH) were reciprocally transplanted into the livers of DRH and Donryu treated with 2-acetylaminofluorene (2-AAF) diet/two-thirds hepatectomy (PH), the Donryu cells formed small colonies wi...
متن کاملPatterns of Ligand Binding to Normal, Regenerating, Preneoplastic, and Neoplastic Rat Hepatocytes1
The binding of epidermal growth factor, asialoorosomucoid, and apoprotein I -ridi lipoproteins to isolated hepatocytes was investigated at various time intervals during the step-by-step development of liver cancer in rats. The degree of binding of the three ligands showed a progressive reduction in early persistent and late persistent putative preneoplastic hepatocyte nodules. This was further ...
متن کاملBiochemical markers associated with the stages of promotion and progression during hepatocarcinogenesis in the rat.
Specific biochemical changes occurring during hepatocarcinogenesis have been sought by many investigators. The development of multistage models for hepatocarcinogenesis in the rodent has renewed interest in such marker alterations in preneoplastic as well as neoplastic hepatocytes. Preneoplastic altered hepatic foci (AHF) exhibit specific histomorphologic changes as viewed with tinctorial stain...
متن کاملPatterns of ligand binding to normal, regenerating, preneoplastic, and neoplastic rat hepatocytes.
The binding of epidermal growth factor, asialoorosomucoid, and apoprotein E-rich lipoproteins to isolated hepatocytes was investigated at various time intervals during the step-by-step development of liver cancer in rats. The degree of binding of the three ligands showed a progressive reduction in early persistent and late persistent putative preneoplastic hepatocyte nodules. This was further d...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید
ثبت ناماگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید
ورودعنوان ژورنال:
- Cancer research
دوره 36 7 PT 2 شماره
صفحات -
تاریخ انتشار 1976