© 2004 by Oxford University Press
© 2004 Oxford University Press
CORRESPONDENCE |
Re: Playing the Old Piano: Another Tune for Endocrine Therapy
For the Swiss Group for Clinical Cancer Research (SAKK)
Affiliations of authors: Department of Oncology/Hematology, Kantonsspital St. Gallen, St. Gallen, Switzerland (DK, BT); Centre Pluridisciplinaire d'Oncologie, Lausanne, Switzerland (LP).
Correspondence to: Dieter Koeberle, MD, Department of Oncology/Hematology, Kantonsspital St. Gallen, 9007 St. Gallen, Switzerland (e-mail: dieter.koeberle{at}kssg.ch)
Osipo et al. (1) report the paradoxical action of fulvestrant in estradiol-induced regression of tamoxifen-stimulated breast cancer. In their article, they proposed a two-phase evolution of acquired resistance to tamoxifen. A novel mechanism, called phase II resistance by the authors, was observed after long-term treatment with tamoxifen. The growth of these MCF-7TAMLT breast tumors became dependent on tamoxifen. In the experimental systems, physiologic levels of estradiol were able to induce tumor regression; in this specific hormonal environment, second-line treatment with fulvestrant promoted growth of those tumors.
In an accompanying editorial, which we have read with interest, Hayes (2) suggested that Osipo's data might argue against the use of fulvestrant in patients with tumor progression after aromatase inhibitor therapy was discontinued because of the reappearance of sufficient estrogen levels that could stimulate tumor growth.
Extrapolation of these laboratory results into the clinical setting appears to contradict the results of an ongoing multicenter phase II trial conducted by the Swiss Group for Clinical Cancer Research (SAKK). Patients with advanced breast cancer who progressed on prior endocrine therapy, first with tamoxifen and later with nonsteroidal aromatase inhibitors, were treated with fulvestrant (3). In this population, a clinical benefit with fulvestrant (partial response or stable disease of 
24 weeks) was observed in 34% (Perey L: unpublished observations). The trial will soon close accrual with 93 patients.
Confirmation of our observation is needed, yet we would like to conclude that fulvestrant is an effective second- or third-line treatment for women with endocrine-responsive breast cancer. Conversely, we agree that the data of Osipo et al. are interesting as far as the investigation of endocrine resistance and the development of new drugs to treat patients with breast cancer are concerned.
NOTES
Dr. Thuerlimann was a member of the advisory boards for the development of fulvestrant (i.e., Faslodex) and received honoraria for these activities.
REFERENCES
1 Osipo C, Gajdos C, Liu H, Chen B, Jordan VC. Paradoxical action of fulvestrant in estradiol-induced regression of tamoxifen-stimulated breast cancer. J Natl Cancer Inst 2003;95:1597–608.
2 Hayes DF. Playing the old piano: another tune for endocrine therapy? J Natl Cancer Inst 2003;95:1565–7.
3 Perey L, Thurlimann B, Hawle H, Bonnefoi H, Aebi S, Pagani O, et al. Fulvestrant (‘faslodex') as hormonal treatment in postmenopausal patients with advanced breast cancer progressing after treatment with tamoxifen and aromatase inhibitors [abstract 249]. Breast Cancer Res Treat 2002;76;Suppl 1:S72.
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J Natl Cancer Inst 2004 96: 556-557.
J Natl Cancer Inst 2004 96: 557.
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