pS2 and response to adjuvant hormone therapy in primary breast cancer

Spyratos, Frédérique; Andrieu, Catherine; Hacène, K.; Chambon, Pierre; Rio, Marc

doi:10.1038/bjc.1994.73

Cited by 23 publications

(14 citation statements)

References 18 publications

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“…As reported in previous studies, we noted a correlation between pS2 and ER and PgR (Foekens et al, 1990;Predine et al, 1992;Spyratos et al, 1994). There was also a weak association of Cath D with both ER and PgR, as already found in several studies (Cazin et al, 1993;Gion et al, 1995), but not all (Granata et al, 1991).…”

Section: Discussionsupporting

confidence: 68%

“…In the overall population, pS2 was weakly positively correlated with FSH and LH levels and negatively to E 2 and Pg. This is probably because of the correlation between pS2 and menopausal status that was noted in our study as in previous reports (Foekens et al, 1990;Predine et al, 1992;Spyratos et al, 1994) because, in premenopause, no correlations were found between E2, Pg, gonadotrophin and pS2. However, in the subset of ER+ premenopausal women, pS2 was correlated with the E2 level, suggesting that pS2 expression, like Cath D, could be increased by E2 in some ER+ breast tumours.…”

Section: Discussionsupporting

confidence: 54%

“…Cath D and pS2 have recently been analysed as markers of prognosis or hormone dependency in breast cancer (Henry et al, 1989;Foekens et al, 1990;Tandon et al, 1990;Schwartz et al, 1991;Rochefort et al, 1992;Pujol et al, 1993;Spyratos et al, 1994). Therefore, determinations of these markers at surgery could theoretically be proposed to guide clinicians in adjuvant therapy.…”

Section: Discussionmentioning

confidence: 99%

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Time at surgery during menstrual cycle and menopause affects pS2 but not cathepsin D levels in breast cancer

Pujol

et al. 1999

Br J Cancer

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Many studies have addressed the clinical value of pS2 as a marker of hormone responsiveness and of cathepsin D (Cath D) as a prognostic factor in breast cancer. Because pS2 and Cath D are both oestrogen induced in human breast cancer cell lines, we studied the influence of the menstrual cycle phase and menopausal status at the time of surgery on the levels of these proteins in breast cancer. A population of 1750 patients with breast cancer, including 339 women in menstrual cycle, was analysed. Tumoral Cath D and pS2 were measured by radioimmunoassay. Serum oestradiol (E2), progesterone (Pg), follicle-stimulating hormone (FSH) and luteinizing hormone (LH) levels at the day of surgery were used to define the hormonal phase in premenopausal women. There was a trend towards a higher mean pS2 level in the follicular phase compared with the luteal phase (17 ng mg −1 and 11 ng mg −1 respectively, P = 0.09). Mean pS2 was lower in menopausal patients than in women with cycle (8 ng mg −1 and 14 ng mg −1 respectively, P = 0.0001). No differences in mean Cath D level were observed between the different phases of the menstrual cycle, or between pre- and post-menopausal women. In the overall population, pS2 was slightly positively associated with E2 and Pg levels and negatively associated with FSH and LH, probably reflecting the link between pS2 and menopausal status. In premenopausal women, no association was found between pS2 and E2, Pg, FSH or LH levels. There were no correlations between Cath D level and circulating hormone levels in the overall population. However, in the subgroup of premenopausal women with ER-positive (ER+) tumours, E2 was slightly associated with both pS2 and Cath D, consistent with oestrogen induction of these proteins in ER+ breast cancer cell lines. There are changes in pS2 level in breast cancer throughout the menstrual cycle and menopause. This suggests that the choice of the pS2 cut-off level should take the hormonal status at the time of surgery into account. In contrast, the level of Cath D is unrelated to the menstrual cycle and menopausal status. 1999 Cancer Research Campaign

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Section: Discussionsupporting

confidence: 68%

Section: Discussionsupporting

confidence: 54%

Section: Discussionmentioning

confidence: 99%

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Time at surgery during menstrual cycle and menopause affects pS2 but not cathepsin D levels in breast cancer

Pujol

et al. 1999

Br J Cancer

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“…As expected, PCR products were amplified in anti-ER␣ as well as anti-p300 ChIPs, primarily in chromatin preparations of E2-treated cells (lanes 4 and 10). These results are consistent with a ligand-dependent binding of ER to the pS2 promoter, as previously demonstrated by gel-shift analyses of estrogen responsive promoters (29). Lack of amplification of promoter sequences of GAPDH, which is not an ER target, demonstrated the specificity of results.…”

Section: Hada3 Is Present In Activator Complexes Bound To the Ere Of supporting

confidence: 77%

“…The chromatin immunoprecipitations were carried out with pre-immune (negative control), anti-hADA3, anti-ER␣, and anti-p300 (positive controls) antibodies, and the associated DNA was used as a template for the PCR amplification of the pS2 promoter sequences incorporating a known ERE (29). As shown in Fig.…”

Section: Hada3 Is Present In Activator Complexes Bound To the Ere Of mentioning

confidence: 99%

Human ADA3 Binds to Estrogen Receptor (ER) and Functions As a Coactivator for ER-mediated Transactivation

Meng

Zhao²,

Nag³

et al. 2004

Journal of Biological Chemistry

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We have recently identified the hADA3 protein, the human homologue of yeast transcriptional coactivator yADA3, as a novel HPV16 E6 target. Using ectopic expression approaches, we further demonstrated that hADA3 directly binds to the 9-cis retinoic acid receptors ␣ and ␤, and functions as a coactivator for retinoid receptor-mediated transcriptional activation. Here, we examined the role of endogenous hADA3 as a coactivator for estrogen receptor (ER), an important member of the nuclear hormone receptor superfamily. We show that ADA3 directly interacts with ER␣ and ER␤. Using the chromatin immunoprecipitation assay, we also show that hADA3 is a component of the activator complexes bound to the native ER response element within the promoter of the estrogen-responsive gene pS2. Furthermore, using an ER response element-luciferase reporter, we show that overexpression of ADA3 enhances the ER␣-and ER␤-mediated sequence-specific transactivation. Reverse transcription-PCR analysis showed an ADA3-mediated increase in estrogen-induced expression of the endogenous pS2 gene. More importantly, using RNA interference against hADA3, we demonstrate that inhibition of endogenous hADA3 inhibited ER-mediated transactivation and the estrogeninduced increase in the expression of pS2, cathepsin D, and progesterone receptor, three widely known ERresponsive genes. The HPV E6 protein, by targeting hADA3 for degradation, inhibited the ER␣-mediated transactivation and the protein expression of ER target genes. Thus, our results demonstrate that ADA3 directly binds to human estrogen receptor and enhances the transcription of ER-responsive genes, suggesting a broader role of mammalian hADA3 as a coactivator of nuclear hormone receptors and the potential role of these pathways in HPV oncogenesis.

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Cytosolic levels of TFF1/pS2 in breast cancer: their relationship with clinical–pathological parameters and their prognostic significance

Corte

Tamargo

Alvarez

et al. 2005

Breast Cancer Res Treat

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pS2 and response to adjuvant hormone therapy in primary breast cancer

Cited by 23 publications

References 18 publications

Time at surgery during menstrual cycle and menopause affects pS2 but not cathepsin D levels in breast cancer

Time at surgery during menstrual cycle and menopause affects pS2 but not cathepsin D levels in breast cancer

Human ADA3 Binds to Estrogen Receptor (ER) and Functions As a Coactivator for ER-mediated Transactivation

Cytosolic levels of TFF1/pS2 in breast cancer: their relationship with clinical–pathological parameters and their prognostic significance

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