Dissociated overexpression of cathepsin Dand estrogen receptor alpha in preinvasive mammary tumors

Roger, Pascal; Daubes, Jean-Pierre; Maudelondé, Thierry; Pignodel, C; Gleizes, Michel; Chapelle, Jean; Marty-Double, C; Baldet, Piérre; Marès, P.; Laffargue, F; Rochefort, Henri

doi:10.1053/hp.2000.6687

Cited by 270 publications

(355 citation statements)

References 30 publications

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“…We and others have shown that the relative expression of ORa and ORb is significantly altered during breast tumourigenesis Roger et al, 2001), and a similar mechanism has been proposed to underlie tamoxifen resistance in breast cancers (Paech et al, 1997). The current study shows no significant differences in expression of full-length ORb (ORb1) between tamoxifen sensitive and resistant tumours.…”

Section: Discussionsupporting

confidence: 64%

Relationship of coregulator and oestrogen receptor isoform expression to de novo tamoxifen resistance in human breast cancer

et al. 2002

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This study addresses the hypothesis that altered expression of oestrogen receptor-beta and/or altered relative expression of coactivators and corepressors of oestrogen receptors are associated with and may be mechanisms of de novo tamoxifen resistance in oestrogen receptor positive breast cancer. All cases were oestrogen receptor +, node negative, primary breast tumours from patients who later had no disease progression (tamoxifen sensitive) or whose disease progressed while on tamoxifen (tamoxifen resistant). Using an antibody to oestrogen receptor-beta that detects multiple forms of this protein (total) but not an antibody that detects only full-length oestrogen receptor-beta 1, it was found that high total oestrogen receptor beta protein expressors were more frequently observed in tamoxifen sensitive tumours than resistant tumours (Fisher's exact test, P=0.046). However, no significant differences in the relative expression of oestrogen receptor b2, oestrogen receptor b5 and full-length oestrogen receptor b1 RNA in the tamoxifen sensitive and resistant groups were found. Also, when the relative expression of two known coactivators, steroid receptor RNA activator and amplified in breast cancer 1 RNA to the known corepressor, repressor of oestrogen receptor activity RNA, was examined, no significant differences between the tamoxifen sensitive and resistant groups were found. Altogether, there is little evidence for altered coregulators expression in breast tumours that are de novo tamoxifen resistant. However, our data provide preliminary evidence that the expression of oestrogen receptor b protein isoforms may differ in primary tumours of breast cancer patients who prove to have differential sensitivity to tamoxifen therapy.

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Section: Discussionsupporting

confidence: 64%

Relationship of coregulator and oestrogen receptor isoform expression to de novo tamoxifen resistance in human breast cancer

et al. 2002

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“…[42][43][44] In the case of breast, colon and prostate cancer, as well as brain astrocytic tumors, ERb expression has been correlated to a higher tumor differentiation grade, in line with its antiproliferative and differentiating effects. [45][46][47][48] It is of interest that malignant lymphoid cells, as described for the cell lines used in this report, retain ERb expression. This may suggest that malignant transformation of cells of lymphoid origin is not generally associated with the loss of ERb expression and therefore remain as useful targets for therapy by ERb agonists.…”

Section: Discussionmentioning

confidence: 99%

Effect of ligand-activated estrogen receptor β on lymphoma growth in vitro and in vivo

et al. 2011

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Estrogen receptor b (ERb) is expressed in immune cells and studies have suggested an antiproliferative function of ERb. We detected ERb expression in murine T-and human B-cell lymphoma cell lines and analyzed the effects of estradiol and selective ERb agonists on lymphoma growth in culture and in vivo. Treating the cells with estradiol had minor effects on cell growth, whereas the selective ERb agonists diarylpropionitrile (DPN) and KB9520 showed a strong antiproliferative effect. When grafting mice with murine T-cell lymphoma cells, male mice developed larger tumors compared with female mice, a difference that was abolished following ovariectomy, showing estrogen-dependent growth in vivo. To investigate whether lymphoma growth may be inhibited in vivo by ERb agonist treatment, mice grafted with murine lymphoma cells were treated with DPN or KB9520. Both ERb-selective agonists strongly inhibited lymphoma growth. The reduced tumor size seen following either DPN or KB9520 treatment was due to reduced proliferation and increased apoptosis. Our results show an ERb ligand-dependent antiproliferative effect of lymphoma cells expressing endogenous ERb and that lymphoma cell growth in vivo can efficiently be inhibited by ERb agonists. This suggests that ERb agonists may be useful in the treatment of lymphomas.

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“…Only 10-20 % of cells are ERα-positive in normal resting human mammary glands [40][41][42]. This percentage increases in proliferative benign disease, which is often associated with atypical low-grade ductal carcinoma in situ (DCIS).…”

Section: E2 Signaling In Breast Carcinogenesismentioning

confidence: 99%

“…In contrast to ERα, the ERβ levels are decreased in tissues from proliferative ductal hyperplasia to DCIS. whereas in the majority of high-grade DCIS, ER levels are reportedly low or absent [42]. Larger studies are required to determine whether assays for the two ERs may be predictive of risk in premalignant lesions.…”

Section: E2 Signaling In Breast Carcinogenesismentioning

confidence: 99%

RETRACTED ARTICLE: Regulation of estrogen receptor signaling in breast carcinogenesis and breast cancer therapy

Zhou

Qiao

Shetty

et al. 2013

Cell. Mol. Life Sci.

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Estrogen and estrogen receptors (ERs) are critical regulators of breast epithelial cell proliferation, differentiation, and apoptosis. Compromised signaling vis-à-vis the estrogen receptor is believed © Springer Basel 2013 yow4@pitt.edu. ), which predicts for response to endocrine-based therapy; however, innate or acquired resistance to endocrinebased drugs remains a serious challenge. The complexity of regulation for estrogen signaling coupled with the crosstalk of other oncogenic signaling pathways is a reason for endocrine therapy resistance. Alternative strategies that target novel molecular mechanisms are necessary to overcome this current and urgent gap in therapy. A thorough analysis of estrogen-signaling regulation is critical. In this review article, we will summarize current insights into the regulation of estrogen signaling as related to breast carcinogenesis and breast cancer therapy. NIH Public Access

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Dissociated overexpression of cathepsin Dand estrogen receptor alpha in preinvasive mammary tumors

Cited by 270 publications

References 30 publications

Relationship of coregulator and oestrogen receptor isoform expression to de novo tamoxifen resistance in human breast cancer

Relationship of coregulator and oestrogen receptor isoform expression to de novo tamoxifen resistance in human breast cancer

Effect of ligand-activated estrogen receptor β on lymphoma growth in vitro and in vivo

RETRACTED ARTICLE: Regulation of estrogen receptor signaling in breast carcinogenesis and breast cancer therapy

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