P2-05-09: Secondary Inflammatory Breast Cancer: A Possible Model for Post-Surgical Dissemination of Cancer.
Authors: Hashmi S , Zolfaghari L , Levine PH 
Published: June 2012

Abstract
Background: The phenomenon of accelerated tumor growth following surgery has been observed repeatedly and merits further study. Inflammatory breast carcinoma (IBC) is widely recognized as an extremely aggressive malignancy characterized by micrometastasis at the time of diagnosis. It is fast growing, highly angiogenic and angioinvasive, features that are present from its inception. The idea of a dormant cancer cell and awakening of metastatic disease following a surgical/traumatic event may well be exemplified by secondary IBC, a term used to describe the IBC appearing following surgery for a noninflammatory primary breast carcinoma. One possible mechanism can be related to the stimulation of dormant micrometastasis through local angiogenesis occurring as part of posttraumatic healing. It is therefore possible that secondary IBC can be used as a model to support local angiogenesis as an important contributor to the development of an aggressive cancer.
Materials and Methods: Cases of secondary IBC were identified in a review of patients referred to the IBC Registry (IBCR). In this report we document the histories of three patients with secondary IBC as well as two additional patients whose disease presentation also supports the possible occurrence of IBC secondary to breast trauma. Secondary IBC cases were defined as women who had surgery for non-inflammatory breast cancer with recurrence at the previous mastectomy site manifest as skin erythema shown to be associated with pathologically confirmed tumor emboli in the dermal lymphatics.
Results: Two of the patients with secondary IBC developed pathologically confirmed dermal lymphatic invasion two and 42 months after partial mastectomy for non-inflammatory breast cancer. The third had been apparently free of recurrence for seven years when she had reconstructive surgery, which was followed by IBC seven months later. Two additional cases are presented, one in which IBC manifested one month following ductogram procedure and had a contralateral breast IBC recurrence 2 years later. The other patient was diagnosed with IBC one year following nipple piercing and ring removal.
Discussion: Recent publications have focused on the role of surgery in the subsequent development of metastatic breast cancer, many of them focusing on a hormonal mechanism triggered by removal of the primary tumor. We propose local angiogenesis as another possible mechanism for post-surgical dissemination of cancer. In view of the hypothesis that trauma can stimulate angiogenesis which can accelerate tumor growth, the documentation of IBC appearing at the site of a traumatic event merits consideration. Our experience with IBC, noted in the case reports above suggest that local trauma probably mediated in large part by angiogenesis can be an important trigger of IBC. We would therefore suggest that secondary IBC be considered for investigation of one possible mechanism for post-surgical tumor dissemination.
Citation Information: Cancer Res 2011;71(24 Suppl):Abstract nr P2-05-09.