It appears that in metastatic breast cancer, the biologic characteristics of liver metastases sometimes differ from those of the primary tumor. This finding may affect treatment choices for metastases. Results of this retrospective study were presented at the 2010 annual meeting of the American Society of Clinical Oncology.
Three key biologic markers are used to determine treatment for breast cancer. These are estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2) status. These markers are expressed as positive or negative and affect the way the cancer grows. Because certain drugs are designed to stop the growth of cancer according to these markers, ER, PR, and HER2 status guide treatment choices.
The treatment of metastatic cancer (cancer that has spread to other parts of the body), is often based on the biologic markers of the primary tumor. Metastatic cancer is not always biopsied to determine its own biologic markers. If, however, metastatic cancer, such as liver metastases, has markers that differ from those of the primary tumor, the original treatment plan may not be as effective.
To evaluate the extent to which characteristics between primary breast tumors and metastases to the liver may differ, researchers in Italy compared tumor biopsies from 255 women.
- Changes in ER status (from ER-negative to ER-positive and vice versa) were observed in 14.5% of liver metastases.
- Changes in PR status were observed in 48.6%.
- Changes in HER2 status were observed in 13.9%.
- Changes in tumor characteristics from primary to metastatic tumors resulted in changes in treatment plan for 12.1% of women.
The researchers concluded that because biologic markers of liver metastases may differ from those of primary breast tumors, biopsy of liver metastases should be considered. Accurate classification of secondary tumors by these markers may influence treatment choices.
Reference: Locatelli MA, Curigliano G, Fumagalli L, et al. Should liver metastases of breast cancer be biopsied to improve treatment choice? Presented at the 2010 annual meeting of the American Society of Clinical Oncology. June 4-8, 2010. Chicago, IL. Abstract CRA 1004.
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