Originally published as JCO Early Release 10.1200/JCO.2009.23.0607 on May 18 2009

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Reply to R.S. Mehta et al

University of Alberta, Edmonton, Alberta, Canada

John Hanson

Cross Cancer Institute, Edmonton, Alberta, Canada

Maggie Cheang, Torsten Nielsen

Genetic Pathology Evaluation Centre; Vancouver Coastal Health Research Institute; British Columbia Cancer Agency; and University of British Columbia, Vancouver, British Columbia, Canada

Charles Perou

Lineberger Comprehensive Cancer Center and Departments of Genetics and Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, Chapel Hill, NC

Charles Dumontet

L'Institut National de la Santé et de la Recherche Médicale, U590; Hospices Civils de Lyon; and Université Lyon, Lyon, France

John Reed, Maryla Krajewska

Burnham Institute for Medical Research, La Jolla, CA

Isabelle Treilleux

L'Institut National de la Santé et de la Recherche Médicale, U590; and Centre Léon Bérard, Lyon, France

Matthieu Rupin

Cancer International Research Group, Paris, France

Emmanuelle Magherini

sanofi-aventis, Paris, France

John Mackey

Cross Cancer Institute, Edmonton, Alberta, Canada

Miguel Martin

Hospital Universitario San Carlos, Madrid, Spain

Charles Vogel

Lynn Cancer Center, Boca Raton, FL

We would like to thank Mehta et al¹ for their insightful comments on and elaboration of those points to which we alluded in our article.² We are in substantial agreement with most of them. We agree there is convincing evidence that the standard regimen of paclitaxel once every 3 weeks is inferior to the regimen of docetaxel once every 3 weeks used in the BCIRG (Breast Cancer International Research Group) 001 trial,^3,4 and we apologize for omitting the study by Sparano et al.⁴ This is probably the reason why we found benefit in docetaxel once every 3 weeks when administered to the human epidermal growth factor receptor 2–negative, hormone receptor–positive population, whereas Hayes et al⁵ did not in the CALGB (Cancer and Leukemia Group B) 9344 trial of paclitaxel once every 3 weeks. We also agree that the subgroup of women with hormone receptor–positive breast cancer with low Ki-67 proliferation index (luminal A) is probably the same group identified by multigene assay that did not benefit from first-generation chemotherapy regimens, because there is proven high concordance between classification systems.⁶ As regards the assertion by Mehta et al that standard therapy for all women with breast cancer should not be altered as a result of our findings, we do not advocate an immediate change, and we do state that these data are hypothesis generating only.² However, there is increasing support for the concept of all subtypes of breast cancer requiring targeted/individualized treatments.⁷ Although the impulse to apply the most aggressive treatment in all women is a laudable application of the equity principle, we must remain open to more individualized therapy, if only to be mindful of the original Hippocratic oath: "Above all, do no harm."

AUTHORS' DISCLOSURES OF POTENTIAL CONFLICTS OF INTEREST

Although all authors completed the disclosure declaration, the following author(s) indicated a financial or other interest that is relevant to the subject matter under consideration in this article. Certain relationships marked with a "U" are those for which no compensation was received; those relationships marked with a "C" were compensated. For a detailed description of the disclosure categories, or for more information about ASCO's conflict of interest policy, please refer to the Author Disclosure Declaration and the Disclosures of Potential Conflicts of Interest section in Information for Contributors.

Employment or Leadership Position: Emmanuelle Magherini, sanofi-aventis (C) Consultant or Advisory Role: Judith Hugh, sanofi-aventis (U); John Mackey, sanofi-aventis (U); Miguel Martin, sanofi-aventis (C) Stock Ownership: Charles Perou, University Genomics; Emmanuelle Magherini, sanofi-aventis Honoraria: John Mackey, sanofi-aventis; Miguel Martin, sanofi-aventis; Charles Vogel, sanofi-aventis Research Funding: Judith Hugh, sanofi-aventis; Torsten Nielsen, sanofi-aventis; Charles Dumontet, sanofi-aventis; John Reed, sanofi-aventis; Charles Vogel, sanofi-aventis Expert Testimony: None Other Remuneration: None

REFERENCES

1. Mehta RS, Jackson D, Schubbert T: Metronomic schedule of paclitaxel is effective in hormone receptor–positive and hormone receptor–negative. breast cancer 27:3067, 3068; 2009.

2. Hugh J, Hanson J, Cheang MC, et al: Breast cancer subtypes and response to docetaxel in node-positive breast cancer: Use of an immunohistochemical definition in the BCIRG 001 trial. J Clin Oncol 27:1168, 1176; 2009.[Abstract/Free Full Text]

3. Jones SE, Erban J, Overmoyer B, et al: Randomized phase III study of docetaxel compared with paclitaxel in metastatic breast cancer. J Clin Oncol 23:5542, 5551; 2005.[Abstract/Free Full Text]

4. Sparano JA, Wang M, Martino S, et al: Weekly paclitaxel in the adjuvant treatment of breast cancer. N Engl J Med 358:1663, 1671; 2008.[Abstract/Free Full Text]

5. Hayes DF, Thor AD, Dressler LG, et al: HER2 and response to paclitaxel in node-positive breast cancer. N Engl J Med 357:1496, 1506; 2007.[Abstract/Free Full Text]

6. Fan C, Oh DS, Wessels L, et al: Concordance among gene-expression-based predictors for breast cancer. N Engl J Med 355:560, 569; 2006.[Abstract/Free Full Text]

7. Dinh P, Sotiriou C, Piccart MJ: The evolution of treatment strategies: Aiming at the target. Breast 16:S10, S16; 2007 (suppl 2.

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