Early vs Late Relapse in ER Positive Breast Cancers
Early vs Late Relapse in ER Positive Breast Cancers
Our findings suggest that patients with highly proliferative (high MKS or high GGI) and high-ER breast cancers (high expression of ER-related genes both adopted from Oncotype DX or from PAM50) have the highest absolute risk for late relapse tumors, despite the fact that their risk of recurrence is modest in the first 5 years on tamoxifen. These tumors could be the best candidates for extended endocrine therapy. Patients with low proliferation and low-ER-related genes also remain at risk for late relapses, and benefit from extended endocrine treatment with aromatase inhibitors should be also assessed.
Early relapses (in the first 2.5 years) are highest in highly proliferative/low-ERS cancers, in particular in node-negative tumors, and this group also had minimal response to neoadjuvant letrozole. These findings suggest that this molecular group is enriched in tumors intrinsically resistant to endocrine therapy (both tamoxifen and letrozole) and in part can explain why upfront AIs were not superior to the sequence of tamoxifen followed by an AI in unselected patients.
Overall, the combined use of markers of proliferation and ER-related genes can inform the design of future adjuvant trials and assist in the selection of patients for extended endocrine treatment.
Conclusions
Our findings suggest that patients with highly proliferative (high MKS or high GGI) and high-ER breast cancers (high expression of ER-related genes both adopted from Oncotype DX or from PAM50) have the highest absolute risk for late relapse tumors, despite the fact that their risk of recurrence is modest in the first 5 years on tamoxifen. These tumors could be the best candidates for extended endocrine therapy. Patients with low proliferation and low-ER-related genes also remain at risk for late relapses, and benefit from extended endocrine treatment with aromatase inhibitors should be also assessed.
Early relapses (in the first 2.5 years) are highest in highly proliferative/low-ERS cancers, in particular in node-negative tumors, and this group also had minimal response to neoadjuvant letrozole. These findings suggest that this molecular group is enriched in tumors intrinsically resistant to endocrine therapy (both tamoxifen and letrozole) and in part can explain why upfront AIs were not superior to the sequence of tamoxifen followed by an AI in unselected patients.
Overall, the combined use of markers of proliferation and ER-related genes can inform the design of future adjuvant trials and assist in the selection of patients for extended endocrine treatment.
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