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Michaela J. Higgins, James M. Rae, David A. Flockhart, Daniel F. Hayes and Vered Stearns

Many women with hormone receptor–positive breast cancer will receive tamoxifen at some point in their treatment course. Tamoxifen is biotransformed to the potent antiestrogen endoxifen almost exclusively through the cytochrome P450 (CYP) 2D6 isoform. Although prospective data are lacking, the balance of evidence available currently suggests that a single nucleotide polymorphism in the CYP2D6 gene, particularly the presence of 2 null alleles, predicts for reduced tamoxifen metabolism and possibly poorer outcome than expected in patients with a wild-type genotype. Studies evaluating the impact of genetic polymorphisms that result in CYP2D6 with reduced or no activity on long-term outcome have been mostly retrospective and conducted on archival tissues or those obtained previously in prospective studies of tamoxifen. Until data are available from retrospective examinations of the large prospective trials already conducted, or adequately powered prospective analyses, transforming this information into guidelines for individual patients remains challenging. The authors do not currently recommend routine testing for CYP2D6 genotype for making clinical decisions regarding tamoxifen. Use of concomitant strong or intermediate inhibitors of CYP2D6 should be avoided when alternate medications are available. Ongoing research is directed toward identifying other polymorphisms that may influence the efficacy and safety of tamoxifen, other hormonal agents, and chemotherapies used to treat breast cancer. The hope is that in the future, not only tumor-associated factors but also germ-line host genetics can be used to determine whether a woman should receive treatment, and with which specific agents, to prevent breast cancer recurrence or death or avoid drug-related toxicities.

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Davinia S.E. Seah, Ines Vaz Luis, Erin Macrae, Jessica Sohl, Georgia Litsas, Eric P. Winer, Nancy U. Lin and Harold J. Burstein

experienced progression and/or switched to endocrine treatment. Abbreviations: HR, hormone receptor; TNBC, triple-negative breast cancer. Table 2 Proportion of Patients on Chemotherapy for More than 3 Months by Line and Subtype In this

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reviews current endocrine treatment strategies and recent and ongoing studies of combination therapies in metastatic HR+, HER2-negative (HER2−) breast cancer. ET The estrogen receptor (ER) plays a fundamental role in the development and progression

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Julie R. Gralow, J. Sybil Biermann, Azeez Farooki, Monica N. Fornier, Robert F. Gagel, Rashmi Kumar, Georgia Litsas, Rana McKay, Donald A. Podoloff, Sandy Srinivas and Catherine H. Van Poznak

effectively counteracts cancer treatment induced bone loss (CTIBL) in premenopausal breast cancer patients receiving adjuvant endocrine treatment with goserelin plus anastrozole versus goserelin plus tamoxifen-bone density subprotocol results of a randomized

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Erin Currin, Lanell M. Peterson, Erin K. Schubert, Jeanne M. Link, Kenneth A. Krohn, Robert B. Livingston, David A. Mankoff and Hannah M. Linden

initiation of endocrine treatment, suggesting lower ER expression. Finally, after progression on sequential chemotherapy, both FDG-PET and FES-PET showed high uptake diffusely in bone and marrow, indicating active disease with high ER expression. These images

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Janice S. Kwon, Gary Pansegrau, Melica Nourmoussavi, Geoffrey L. Hammond and Mark S. Carey

limited improvements in DFS and OS from extended endocrine treatment strategies and the potential detrimental impact of premature menopause from OA/AI, a decision analytic model is the most feasible strategy to evaluate long-term survival associated with

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Ingrid A. Mayer

no overall survival advantage was seen. However, everolimus remains an option in second- or third-line endocrine treatment of ER-positive metastatic breast cancer. “Agents blocking PI3K, either pan or selective PI3K inhibitors, are currently in

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Amelia B. Zelnak and Ruth M. O'Regan

-analysis on the interaction between HER-2 expression and response to endocrine treatment in advanced breast cancer . Clin Cancer Res 2005 ; 11 : 4741 – 4748 . 3. Cristofanilli M Valero V Mangalik A . Phase II, randomized trial to compare

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James L. Mohler

1997 ; 337 : 295 – 300 . 4. Widmark A Klepp O Solberg A . Endocrine treatment, with or without radiotherapy, in locally advanced prostate cancer (SPCG-7/SFUO-3): an open randomised phase III trial . Lancet 2009 ; 373 : 301 – 308

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Erica L. Mayer, Nancy U. Lin and Harold J. Burstein

response to endocrine treatment in advanced breast cancer . Clin Cancer Res 2005 ; 11 : 4741 – 4748 . 72. Xia W Gerard CM Liu L . Combining lapatinib (GW572016), a small molecule inhibitor of ErbB1 and ErbB2 tyrosine kinases, with therapeutic