PubMed · 4926927
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L W Wannamaker. 1970. Group A Streptococcus.. https://pubmed.ncbi.nlm.nih.gov/4926927/
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We have shown previously that approximately 1 in 10,000 primary hepatocytes isolated from untreated rats undergo clonal growth in soft agar in vitro in response to the synergistic action of nafenopin, a peroxisome proliferator (PP) and epidermal growth factor (EGF), a naturally occurring liver growth regulator. Here, we demonstrate that prior treatment of the animals with the genotoxic hepatocarcinogen diethylnitrosamine (DEN) caused a dose-dependent increase in soft agar colony numbers formed in vitro. These data suggest that the colony assay may offer a method of detecting in vitro hepatocytes transformed in vivo by DEN. It is known that rats treated with DEN develop enzyme altered foci prior to the development of tumours. The majority of these foci express high levels of gamma-glutamyl transpeptidase (GGT). However, foci promoted by PPs do not show this increased enzyme activity. In the present study, the colonies we have generated in vitro mimicked this pattern since the majority (approximately 80%) of the spontaneous colonies expressed GGT whereas colonies promoted by the synergistic action of nafenopin and EGF were mainly (75%) GGT negative. The proportion of colonies positive for GGT were similar using either hepatocytes isolated from control or from DEN-initiated rats. Further studies are required to assess if the hepatocytes selected for clonal expansion by this EGF/nafenopin regime reflect the presumed pre-neoplastic cells induced by genotoxin in vivo and associated with an increased propensity to cancer.
Retinoids modulate cellular proliferation and mediate gene function through a series of nuclear receptors. The retinoic acid nuclear receptor beta (RAR beta) plays an important role in the differentiation of a number of cell types. We now demonstrate that RAR beta expression is confined to normal mammary tissue and is not expressed in either immortalized normal or malignant cell lines. Treatment of RAR beta-transfected MDA-MB-231 cells with 1 microM all-trans-retinoic acid (RA) significantly inhibited monolayer growth of the cells which express recombinant RAR beta. RAR beta-expressing MDA-MB-231 cells formed significantly smaller and fewer colonies in soft agar than the mock-transfected cells. Addition of 1 microM RA stimulated colony size and number in the RAR beta-transfected MDA-MB-231 cells. In contrast to the RAR beta-expressing cells, colony formation by the RAR alpha-expressing cells was similar to the mock-transfected controls and the addition of 1 microM RA to the RAR alpha-transfected cells inhibited colony formation. While demonstrating decreased colony formation in agar, RAR beta-expressing MDA-MB-231 cells failed to exhibit decreased growth in SCID mice. Our results show that RAR beta functions as a negative regulator of growth in breast epithelial cells. In addition, the growth of these cells is differentially regulated by RAR alpha and RAR beta which is most likely the result of the modulation of different genes.
Magnetization-transfer (MT) experiments have been performed at 300 MHz on agar gels, solutions of sodium alginate, bovine nasal cartilage, and postmortem porcine muscle. The experimental results elucidate MT mechanisms between mobile macromolecules (correlation time TC on the order of 10(-8) s) and water, and demonstrate the need to incorporate their effects in the characterization of biological samples. In addition, the results obtained confirm a recently published three-spin-bath theoretical treatment for proton magnetization transfer.