HER-2/neu (ERB-B2), a member of the receptor tyrosine kinase superfamily, is altered by gene amplification and/or protein overexpression in a wide variety of human epithelial malignancies. Such alterations activate signaling systems that promote cell growth, angiogenesis, cancer metastases, and other procarcinogenic pathways (1). These HER-2 abnormalities are found in approximately one third of breast cancers. HER-2 “status” is a loose and suboptimal term that is commonly used to describe the degree of HER-2 gene amplification and/or the extent of Her-2 protein overexpression. HER-2 status has been used as a marker for breast cancer prognosis (in addition to the classic markers lymph node status, tumor size, type and grade, hormone receptor status, and proliferation rate), because, in the majority of cases, HER-2 alterations independently portend a worse outcome. In addition, associations have been found between the degree of HER-2 expression or gene copy number and the likelihood that a patient may derive benefit from some chemotherapy regimens, i.e., predictive value (2–4). Statistically significant interactions between HER-2 status and chemotherapeutic agents other than anthracyclines have also been reported (5). Given these chemotherapeutic/HER-2 interactions and new anti-HER-2 therapeutic agents, it is no longer always correct to assume that cancers with an altered HER-2 status will have a poor outcome. As noted, HER-2 has become an important target for novel therapeutic strategies, such as trastuzumab (Herceptin), a monoclonal antibody that acts as an HER-2 antagonist. This agent has shown promise in treating a subset of patients with otherwise chemorefractory, late-stage breast cancer. Many recently opened breast cancer trials combine Herceptin with other agents to treat various stages of disease.
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Ann D. Thor (2001) studied this question.