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The *biology of ER+/HER2- breast cancer* is complex. The estrogen receptor positivity indicates that the cancer cells respond to estrogen, which promotes their growth. Hormone therapies like tamoxifen and aromatase inhibitors are designed to block or reduce estrogen's effect on these cancer cells, effectively slowing down or stopping their growth. However, cancer cells can develop resistance to these therapies over time, leading to recurrence. The absence of HER2 overexpression means that these cancers do not benefit from HER2-targeted therapies like trastuzumab (Herceptin), which are highly effective in HER2-positive breast cancers. Other molecular factors, such as the expression of Ki-67 (a marker of cell proliferation), the grade of the tumor, and the presence of specific gene mutations, can also influence the behavior of ER+/HER2- breast cancers and their likelihood of recurrence.
