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    • The site of metastasis in breast cancer

    2021-11-26

    The site of metastasis in breast cancer often contributes to the patient’s OS. Patients with bone metastasis from their breast cancer often have a notably increased survival over RO4929097 sale patients with visceral or RO4929097 sale metastasis. In this analysis, ER+/HER2+ patients were noted to have a higher rate of bone metastasis than ER−/HER2+ patients. Conversely, patients with ER−/HER2+ cancer had significantly more liver metastasis as well as higher rates of metastasis to brain and lung, as well as higher rates of multiple metastases, than patients with ER+/HER2+ cancer. These results are consistent with the findings of many other researchers. Patient with ER−/HER2+ cancer have often been noted to have more visceral metastases as well as metastasis at an earlier time period than comparable patients with ER+/HER2+ cancer.5, 21, 22, 23, 24, 25, 26 In several studies examining the SEER database, although both subtypes had higher rates of bone metastases than to other sites, patients with ER+/HER2+ cancer had higher rates of bone metastasis compared to patients with ER−/HER2+ cancer.22, 25 A recent examination of SEER, although examining only patients presenting with metastatic disease, noted higher rates of bone metastasis in HR+/HER2+ breast cancer compared to either HR−/HER2+ or triple-negative breast cancers. Garcia Fernandez et al noted similar findings, although in a smaller cohort. In a study comparing ER+/HER2+ versus ER−/HER2+ cancer, Smid et al also found higher rates of bone metastasis in the ER+ subgroup. The site of metastasis is often linked to OS in breast cancer, with bone being more favorable than brain or visceral locations. In this large study of SEER and NCDB, ER−/HER2+ patients with bone metastasis had significantly poorer OS than similar ER+/HER2+ breast cancer patients with bone metastasis. Thus, metastasis to the same location confers a different rate of survival based on the receptor subtype of the breast cancer. Interestingly, the significant difference in survival based on site of metastasis and tumor receptor subtype was not replicated in any other sites, with statistically equivalent survival for ER−/HER2+ and ER+/HER2+ patients with brain, liver, and lung metastases as well as multiple metastases. Kast et al described the improved survival for patients with bone metastasis compared to visceral or brain metastases. Thus, clinicians may need to differentiate HER2+ patients with bone metastasis on the basis of hormone receptor status in terms of aggressiveness of systemic therapy. This modern analysis of information in NCDB and SEER supports the notion that patients with ER+/HER2+ breast cancer have better BCSS and OS; interestingly, this survival advantage was not affected by the receipt (or lack thereof) of HER2-targeted therapy. The finding of improved survival for ER+/HER2+ patients over ER−/HER2+ patients is consistent with previously published reports.3, 21, 24, 28, 29 In an examination of metastasis, survival, and receptor subtype, Molnar et al noted similar findings with ER+/HER2+ patients displaying improved OS versus ER−/HER2+, regardless of the receipt of HER2-targeted therapy. Similarly, Lobbezoo et al described improved OS in ER+/HER2+ patients and found receptor status to be an independent prognostic factor for patients with metastatic breast cancer. Sanpaolo et al examined luminal B (ER+/PR+/HER2+) and HER2+ (ER−/PR−) patients and noted significantly improved BCSS and OS for the luminal B subset. They further noted that luminal A patients had improved BCSS and OS compared to the luminal B and HER2+ patients, which may indicate a poorer response to endocrine therapy for the luminal B subset. This improved survival is likely due in part to the preferential bone metastasis in the ER+/HER2+ receptor subgroup. There is also a role for the relationship between hormone receptors and HER2 receptors, and a differential response to therapy. Specifically, there is evidence of cross-talk between the ER and HER2 pathways that can lead to impaired response to endocrine therapy and possible modification of the tumor’s response to HER2-targeted therapy. In both clinical and laboratory studies, this cross-talk has been noted to decrease tamoxifen’s effectiveness.32, 33, 34 More recently, studies examining the response of HER2+ tumors to neoadjuvant HER2+-targeted therapy have noted decreased complete responses in ER+/HER2+ as opposed to ER−/HER2+ patients.35, 36