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Many assays for oncogenic transformation have been developed ranging from those in established rodent cell lines where morphological alteration is scored, to those in human cells growing in nude mice where tumor invasiveness is scored.
This morphological alteration is accompanied by an increase in the expression of the protein BNIP3 (Bcl2/adenovirus E1B 19 kDa interacting protein 3) as well as a decrease in the abundance of mitofusins 1 and 2, two proteins involved in mitochondrial fusion.
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This morphological alteration was not apparent after single-agent treatment.
The nuclear morphological alteration was observed by staining cells with Hoechst33342.
The most drastic morphological alteration was observed in the tpm1Δ mutant.
The morphological alteration was observed in control and AgNPs treated HeLa cancer cells.
Differential mitochondrial membrane potential decrease, mitochondrial enzymatic dysfunction, and mitochondrial morphological alteration are exhibited in two cell lines.
No morphological alteration was observed in the pulmonary tissue of mice exposed to 10 μmol/kg of (PhTe 2, for 7 or 14 days, when compared with the control group (data not shown).
The expression of such morphological alterations is associated with genomic instability.
Sententious morphological alterations were noticed in esophagitis control group when monitored morphologically and consequent administration of lycopene manifested pronounced protection against the same.
Dark- or light-grown BMS cells showed no distinctive differences in visual fluorescence intensity or vacuolar morphology (Fig. 8 C, D), suggesting that the observed morphological alterations are either a consequence of the expression of the R and C1 regulators, of the accumulation of anthocyanins or of distinctive properties of the vacuoles in which anthocyanins accumulate.
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