ERBB2 amplification is associated with tamoxifen resistance in steroid-receptor positive breast cancer

Borg, Åke; Baldetorp, Bo; Fernö, Mårten; Killander, D.; Olsson, Håkan; Rydén, Stefan; Sigurðsson, Helgi

doi:10.1016/0304-3835(94)90194-5

Cited by 224 publications

(112 citation statements)

References 17 publications

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“…EGFR overexpression could be a primary event in inducing transformation or a secondary modi®cation facilitating growth and transformation, which had been demonstrated in in vitro systems (Di Fiore et al, 1987b). Together with other genetic alterations such as c-erbB-2 overexpression or estrogen receptor status, EGFR overexpression, due in large part to gene ampli®cation, correlates with a poor prognosis for overall patient survival (Al-Kasspooles et al, 1993;Borg et al, 1991;Fox et al, 1994;Gramlich et al, 1994). Furthermore, EGFR overexpression can cooperate with other tyrosine kinase receptors to induce cell transformation (Mullaney and Skinner, 1992).…”

Section: Discussionmentioning

confidence: 99%

Mammary gland specific hEGF receptor transgene expression induces neoplasia and inhibits differentiation

et al. 2000

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Section: Discussionmentioning

confidence: 99%

Mammary gland specific hEGF receptor transgene expression induces neoplasia and inhibits differentiation

et al. 2000

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“…In addition, several studies (Borg et al, 1994;Tetu and Brisson, 1994;Sjogren et al, 1998), and two randomized trials (Carlomagno et al, 1996;Stal et al, 1997), have demonstrated that c-erbB2 overexpression in the primary breast cancer reduced the benefit from adjuvant tamoxifen.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of c-erbB2 is an independent marker of resistance to endocrine therapy in advanced breast cancer

et al. 1999

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The present study investigated the interaction between c-erbB2 overexpression and the response to first-line endocrine therapy in patients with advanced breast cancer. The primary tumours of 241 patients who were treated at first relapse with endocrine therapy were assessed for overexpression of c-erbB2 by immunohistochemistry. c-erbB2 was overexpressed in 76 (32%) of primary breast cancers and did not correlate with any other prognostic factor. The overall response to treatment and time to progression were significantly lower in patients with c-erbB2-positive tumours compared to those that were c-erbB2-negative (38% vs 56%, P = 0.02; and 4.1 months vs 8.7 months, P < 0.001, respectively). In multivariate analysis, c-erbB2 status was the most significant predictive factor for a short time to progression ( P = 0.0009). In patients with ER-positive primary tumours treated at relapse with tamoxifen ( n = 170), overexpression of c-erbB2 was associated with a significantly shorter time to progression (5.5 months vs 11.2 months, P < 0.001). In conclusion, overexpression of c-erbB2 in the primary tumour is an independent marker of relative resistance to first-line endocrine therapy in patients with advanced breast cancer. In patients with ER-positive primary tumours, the overexpression of c-erbB2 defines a subgroup less likely to respond to endocrine therapy. © 1999 Cancer Research Campaign

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“…they increase the expression of ERBB2 (Warri et al, 1991;Antoniotti et al, 1992). This may represent an undesirable side e ect of these drugs in breast cancer treatment (Borg et al, 1994) and understanding how oestrogen acts on ERBB2 may lead to eventual separation of antioestrogenic e ect from stimulation of ERBB2, hence allowing the development of more e ective drugs.…”

Section: Introductionmentioning

confidence: 99%

AP-2 transcription factors in the regulation of ERBB2 gene transcription by oestrogen

et al. 2000

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Transcription of the ERBB2 oncogene is repressed by oestrogen in human breast cancer cells. We show that a 218 bp fragment of the human ERBB2 gene promoter is responsive to oestrogen in transient transfection in ZR75.1 and SKBR.3 cells when the oestrogen receptor is expressed. Deletion analysis of this fragment shows that a sequence located at the 5' end, which is known to mediate ERBB2 overexpression in breast cancer, is also responsible for the oestrogen response. This sequence binds AP-2 transcription factors and appears functionally identical to an element of the oestrogen-dependent enhancer described in the ®rst intron of human ERBB2. We observed that oestrogen treatment down-regulates expression of AP-2 proteins but does not a ect the DNA binding activity of AP-2. Constitutive expression of AP2b or AP-2g, but not AP-2a, abrogates the estrogenic repression. Our results demonstrate that AP-2 transcription factors are implicated in the oestrogenic regulation of ERBB2 gene expression and suggest a complex interplay involving the di erent AP-2 isoforms and other unidenti®ed factors. Oncogene (2000) 19, 280 ± 288.

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ERBB2 amplification is associated with tamoxifen resistance in steroid-receptor positive breast cancer

Cited by 224 publications

References 17 publications

Mammary gland specific hEGF receptor transgene expression induces neoplasia and inhibits differentiation

Mammary gland specific hEGF receptor transgene expression induces neoplasia and inhibits differentiation

Overexpression of c-erbB2 is an independent marker of resistance to endocrine therapy in advanced breast cancer

AP-2 transcription factors in the regulation of ERBB2 gene transcription by oestrogen

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