G1 phase

Tamoxifen isn't cytotoxic.

It works as a reversible cell cycle inhibitor by decreasing estrogen-mediated protein synthesis, producing a block in the G1 phase and a slowing of cell proliferation.

Tamoxifen raises the risk of an endometrial cancer roughly two to threefold above baseline, along with a higher rate of endometrial polyps and hyperplasia.

The risk climbs with longer duration of use and can be seen with all histologic types.

Moreover, there's a cohort of yeast genes important for growth, such as those required for ribosomal biogenesis.

At the G1 cyclin phase, where the G1 cyclin protein, CLN3 is generated, and that's especially dependent on histone acetylation for the activation.

And as such, the expression of those growth genes is closely coupled to acetyl-CoA as an indicator of a cell's nutritional state.

Thus, when carbon source is abundant, the nucleocytosolic amounts of acetyl-CoA accumulate and facilitate the process of lipid synthesis simultaneously with controlling a full histone acetylome, so that housekeeping gene activity, full transcriptional activity, is now in flux.

But while they're doing their jobs inside, they're also preparing to grow and divide, which happens across three main steps.

The initial step is called G1, or the first gap, and it's actually an intense growth spurt.

At this point, cells are ballooning in size while making new proteins in tiny cell versions of organs called organelles.

The cell cycle is driven by the activity of proteins, and there are related mechanisms called checkpoints, which we'll get into more later, that control the fate of any given cell.