BH1 + TNF-α treatment exaggerated this response, leading to a stronger accumulation of G1 phase cells, associated with a depletion of G2 phase cells.
IC261 caused a significant parallel depletion of G1 phase and cell cycle arrest in G2/M phase (Supporting Information Fig S5).
Cell cycle analysis by a flow cytometer showed that gefitinib treatment (10 μ M) resulted in the depletion of S phase cells from 16.5 to 3.2%, accumulation of G0 G1 phase cells (83.4 96.8%) and virtually no change in G2 M phase cells.
Fibroblasts were harvested 2, 6, and 24 hr after 1.5 Gy, which are times of maximal initial G2 arrest with minimal reduction in S phase, maximal G1 arrest with recovery of mitosis, and sustained G1 arrest with depletion of S phase and mitosis, respectively.
In addition to specimen mass change, the extent of internal oxidation and the depletion of β phase in the substrate were evaluated.
In addition, bortezomib and topotecan treatments provoke a more evident depletion of G1 phase cells from HCT-116, whereas doxorubicin tends to lead to an accumulation of cells in G1 in HKE-3.
They use the extinction curve and the depletion of gas-phase metals as quantities to be compared with observations.
In addition, NVP-AUY922 induced a temporary depletion of S-phase cells.
Intriguingly, they lead to different biological responses: depletion of S-phase indicating growth arrest upon nutlin3a treatment, mainly G1/S arrest induced by 5-FU and induction of apoptosis as a major response to RITA.
This tool allowed us to confirm a transition to the G1 phase and a depletion of the S/G2/M phases in the tumour cells implanted in pre-irradiated mammary glands, thus supporting a transition from the proliferative to migratory phenotypes.
