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ABSTRACT<br />
Breast cancer evolution and tumor progression are governed by the complex interactions<br />
between steroid receptor [estrogen receptor (<strong>ER</strong>) and progesterone receptor (PgR)] and<br />
growth factor receptor signaling. In recent years, the field of cancer therapy has<br />
witnessed the emergence of multiple strategies targeting these specific cancer pathways<br />
and key molecules (<strong>ER</strong> and growth factor receptors) to arrest tumor growth and achieve<br />
tumor eradication; treatment success, however, has varied and both de novo (upfront) and<br />
acquired resistance have proven a challenge. Recent studies of <strong>ER</strong> biology have revealed<br />
new insights into <strong>ER</strong> action in breast cancer and have highlighted the role of an intimate<br />
cross-talk between the <strong>ER</strong> and H<strong>ER</strong> family signaling pathways as a fundamental<br />
contributor to the development of resistance to endocrine therapies against the <strong>ER</strong><br />
pathway. The aim of this review article is to summarize the current knowledge on<br />
mechanisms of resistance of breast cancer cells to endocrine therapies due to the cross-<br />
talk between the <strong>ER</strong> and the H<strong>ER</strong> growth factor receptor signaling pathways, and to<br />
explore new available therapeutic strategies that could prolong duration of response and<br />
circumvent endocrine resistant tumor growth.<br />
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