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In Reply:

Royal Marsden NHS Foundation Trust, London, United Kingdom

Jack Cuzick, Chris Wale

Wolfson Institute of Preventive Medicine, Barts and The London Queen Mary's School of Medicine and Dentistry, London, United Kingdom

Tony Howell

Christie Hospital NHS Trust, Manchester, United Kingdom

Joan Houghton, Michael Baum

University College London Hospitals NHS Trust, London, United Kingdom

Aman Buzdar

The University of Texas M.D. Anderson Cancer Center, Houston, TX

We read with interest the data and comments of Ponzone et al regarding our hypothesis-generating article¹ on the possible differential sensitivity of anastrozole and tamoxifen to breast cancer based on progesterone receptor (PgR) status. Their focus is on the possible explanation of our results by human epidermal growth factor receptor 2 (HER-2) status being higher in PgR– tumors and HER-2–positive tumors being possibly more sensitive to aromatase inhibitors than to tamoxifen. Although the HER-2 positivity rates in their ER+ patients are higher than we generally find, we concur with their view that it is unlikely that this correlation with HER-2 fully explains our data. In a separate series of 617 ER+ patients, we found 19.5% of the PgR– tumors were HER-2+ compared with just 7.3% in the PgR+ group.² It seems implausible that an effect in only about one fifth of the PgR– patients could explain the profound effects on the outcome seen. We are currently collecting the archival tumors blocks from the Anastrozole or Tamoxifen Alone or in Combination (ATAC) trial to allow systematic centralized analysis of these key parameters. However, we would like to take this opportunity to emphasize that the data that we presented were an unplanned retrospective subgroup analysis and that the extent to which the observations are generalizable depends on their reproducibility in independent studies.

Authors' Disclosures of Potential Conflicts of Interest

Although all authors completed the disclosure declaration, the following authors or their immediate family members indicated a financial interest. No conflict exists for drugs or devices used in a study if they are not being evaluated as part of the investigation. 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.

Authors Employment Leadership Consultant Stock Honoraria Research Funds Testimony Other Mitch Dowsett AstraZeneca (A); Novartis (B) AstraZeneca (A); Novartis (A); Pfizer (A) AstraZeneca (C); Novartis (C) Jack Cuzick AstraZeneca (B); Eli Lilly (A); Novartis (A) Tony Howell AstraZeneca (B); Eli Lilly (A); Novartis (A) AstraZeneca (B); Novartis (A); Pfizer (A) Joan Houghton AstraZeneca (C) AstraZeneca (B) Michael Baum AstraZeneca (B) AstraZeneca (B) Aman Buzdar AstraZeneca (A); Pfizer (A); Genentech (A) AstraZeneca (C); Pfizer (C); Genentech (C)

Dollar Amount Codes (A) < $10,000 (B) $10,000-99,999 (C) > $100,000 (N/R) Not Required

REFERENCES

1. Dowsett M, Cuzick J, Wale C, et al: Retrospective analysis of time to recurrence in the ATAC trial according to hormone receptor status: An hypothesis-generating study. J Clin Oncol 23:7512-7517, 2005[Abstract/Free Full Text]

2. Dowsett M, Houghton J, Iden C, et al: Benefit from adjuvant tamoxifen therapy in primary breast cancer patients according to oestrogen receptor, progesterone receptor, EGF receptor and HER2 status. Ann Oncol (in press)

Related Correspondence

• Progesterone Receptor and Human Epidermal Growth Factor Receptor 2 Status: An Independent Influence on the Efficacy of Endocrine Therapy in Breast Cancer?
  Riccardo Ponzone, Furio Maggiorotto, Claudio Robba, Luca Fuso, and Piero Sismondi
  JCO 2006 24: 1481-1482 [Full Text]

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