Incidence of invasive breast cancer by hormone receptor status from 1992 to 1998
- PMID: 12506166
- DOI: 10.1200/JCO.2003.03.088
Incidence of invasive breast cancer by hormone receptor status from 1992 to 1998
Abstract
Purpose: Between 1987 and 1998, breast cancer incidence rates rose 0.5%/yr in the United States. A question of potential etiologic and clinical importance is whether the hormone receptor status of breast tumors is also changing over time. This is because hormone receptor status may reflect different etiologic pathways and is useful in predicting response to adjuvant therapy and prognosis.
Methods: Age-adjusted, age-specific breast cancer incidence rates by estrogen receptor (ER) and progesterone receptor (PR) status from 1992 to 1998 were obtained and compared from 11 population-based cancer registries in the United States that participate in the National Cancer Institute's Surveillance, Epidemiology, and End Results (SEER) Program.
Results: From 1992 to 1998, the overall proportion of breast cancers that were ER-positive and PR-positive increased from 75.4% to 77.5% (P =.0002) and from 65.0% to 67.7% (P <.0001), respectively, continuing trends observed before 1992. These increases were limited to women 40 to 69 years of age. The proportions of ER-positive/PR-positive tumors increased from 56.7% to 62.3% (P =.0010) among 40- to 49-year-olds, from 58.0% to 63.2% (P =.0002) among 50- to 59-year-olds, and from 63.2% to 67.9% (P =.0020) among 60- to 69-year-olds.
Conclusion: From 1992 to 1998, the proportion of tumors that are hormone receptor-positive rose as the proportion of hormone receptor-negative tumors declined. Because the incidence rates of hormone receptor-negative tumors remained fairly constant over these years, the overall rise in breast cancer incidence rates in the United States seems to be primarily a result of the increase in the incidence of hormone receptor-positive tumors. Hormonal factors may account for this trend.
Comment in
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The ups and downs of the estrogen receptor.J Clin Oncol. 2003 Jan 1;21(1):3-4. doi: 10.1200/JCO.2003.10.008. J Clin Oncol. 2003. PMID: 12506162 No abstract available.
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