Dehydroepiandrosterone inhibits the progression phase of mammary carcinogenesis by inducing cellular senescence via a p16-dependent but p53-independent mechanism

Table 2 Effects of DHEA and DHEA 8354 on SA-β-Gal cells, BrdU-labeled cells and apoptosis

Treatment	Dose (mg/kg diet)	No. of tumors^a	SA-β-Gal cells (%)	BrdU-labelled cells (%)	Apoptosis (%)
Control	0	10	0.4 ± 0.2	15.6 ± 4.8	0.7 ± 0.4
DHEA	125	9	1.9 ± 1.8^b	9.9 ± 4.2^c	1.6 ± 0.4^d
	1,000	15	3.3 ± 2.0^b	2.2 ± 1.2^c	3.2 ± 2.0^d
DHEA 8354	125	8	0.7 ± 0.4	13.5 ± 4.4	1.1 ± 0.4
	1,000	10	2.8 ± 1.0^b	5.3 ± 1.8^c	1.5 ± 0.5^d

^aOne tumor per animal was examined once; ^b,c,dthe differences in values between treated and control tumors are significant (p < 0.05; Student's t test). BrdU, bromodeoxyuridine; DHEA, dehydroepiandrosterone; SA-β-Gal, senescence-associated β-galactosidase (mean ± SD%) values.

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